bluuebunny/crossref_metadata_2025 huggingface dataset:
Dietary effect on platelet aggregation in men with and without a family history of essential hypertension.
Authors: Nara Y , Kihara M , Nabika T , Mano M , Horie R , Yamori Y
Published: June 2012

Platelet aggregation induced by 5 microM adenosine 5'-diphosphate (ADP) was significantly higher in men with a family history of essential hypertension than in men without such a history when they were fed a low fat-cholesterol diet with low salt. Platelet aggregation activity was remarkably increased in both groups when the diet was changed from low salt into high salt. Platelet aggregation activity was higher in the group with a positive family history of hypertension on the low fat-cholesterol plus high salt diet than in the group without a family history under the same conditions. The activity was slightly increased in both groups when fed a high fat-cholesterol diet with low salt. There was no significant difference in the platelet aggregation between the two groups. The activity was significantly increased in both groups on the high fat-cholesterol diet after the diet was changed from low salt to high salt. Under both the low and high fat-cholesterol diets, the mean blood pressure was significantly elevated in response to excessive salt intake in the group with a family history of essential hypertension, but it was not elevated in the group without such a family history.
Direct action of aldosterone on transmembrane 22Na efflux from arterial smooth muscle. Rapid and delayed effects.
Authors: Moura A M , Worcel M
Published: June 2012

Acute subcutaneous (s.c.) administration of aldosterone increases ex vivo 22Na efflux from rat tail artery smooth muscle, which appears to be due to a specific action on mineralocorticoid receptors. Indeed, this effect is blocked by the antimineralocorticoid compounds RU 28318 [17 beta-hydroxy-3-oxo,7 alpha-propyl(17 alpha)-pregn 4-ene, 21 potassium carboxylate] and spironolactone. The specific glucocorticoid receptor agonist RU 26988 [11 beta,17 beta-dihydroxy-17-(1-propynyl) androesta-1,4,6 trien-3-one] does not modify 22Na efflux. We show here that aldosterone has, at physiological concentrations, a mineralocorticoid specific stimulating effect on passive and sodium pump dependent transmembrane movements of sodium from the rat tail artery smooth muscle. Aldosterone exerts two types of action on sodium transport: 1) a delayed stimulation of ouabain-dependent 22Na efflux and ouabain-independent 22Na efflux, which are completely blocked by actinomycin D; and 2) a very rapid increase of passive 22Na efflux, which is insensitive to actinomycin D and therefore does not seem to depend on transcription of genomic information.
Natriuretic and hypertensive activities reside in a fragment of ACTH.
Authors: Gruber K A , Klein M C , Hutchins P M , Buckalew V M , Lymangrover J R
Published: June 2012

The hypertensive and natriuretic effects of chronic administration of adrenocorticotrophic hormone (ACTH) cannot be duplicated by the administration of glucocorticoids and/or mineralocorticoids. We investigated the effects of a fragment of this hormone (ACTH4-10) and an analog of the fragment (D-Phe7) ACTH4-10 and found them to have pressor and cardioaccelerator actions in rats as determined by bolus intravenous (i.v.) injections of 30 to 1000 nmol/kg. The pressor and cardioaccelerator effects of (D-Phe7) ACTH4-10 were attenuated by alpha-receptor (phentolamine) and beta-receptor (metoprolol) antagonists. The cardiovascular actions of ACTH4-10 were produced in adrenalectomized or ganglionic-blocked (with mecamylamine) rats. At a lower dose (7 nmol/kg i.v.), ACTH4-10 was natriuretic and had a pattern of activity similar to that of a larger ACTH fragment, alpha-melanocyte-stimulating hormone. Extraadrenal effects of the intact ACTH molecule or the in vivo production of an ACTH4-10-like fragment from ACTH may contribute to the hypertensive and natriuretic actions associated with this hormone.
Cardiac hypertrophy and performance of Dahl hypertensive rats on graded salt diets.
Authors: Pfeffer M A , Pfeffer J , Mirsky I , Iwai J
Published: June 2012

The relationship between arterial pressure and left ventricular (LV) functional capacity and LV mass during the natural development of cardiac hypertrophy was assessed in Dahl-resistant (R) and -sensitive (S) hypertensive rats maintained on three dietary NaCl regimens (0.4%, 4.0%, and 8.0% for 9 weeks, then 4.0%) from 5 until 20 weeks of age. In R rats, arterial pressure and LV mass were unaffected by diet. In contrast, S rats demonstrated levels of arterial pressure and LV hypertrophy that were graded according to dietary NaCl. Hemodynamic studies on rats under ether anesthesia demonstrated that the graded pressure elevation in S rats was produced by corresponding increases in total peripheral resistance, as cardiac output did not vary. During acute volume loading, the S rats on all diets achieved the same maximum stroke volume as did R rats, despite the marked increase in the arterial pressure of S rats. An analysis of the ejection fraction/afterload relationship demonstrated preserved contractile state. The ability of the left ventricle to generate pressure was increased in S rats in direct proportion to the degree of LV hypertrophy. Thus, in young adult S rats, cardiac performance was well compensated since pump and contractile functions were maintained and pressure-generating capacity was increased in relation to the degree of LV hypertrophy.
Regional hemodynamic effects of antihypertensive renomedullary lipids in conscious rats.
Authors: Faber J E , Barron K W , Bonham A C , Lappe R , Muirhead E E , Brody M J
Published: June 2012

Renomedullary tissue has been proposed to exert an antihypertensive endocrine-like action. The antihypertensive polar renomedullary lipids (APRL) and neutral renomedullary lipids (ANRL) are potential mediators of this action. We evaluated the blood pressure and regional hemodynamic responses to APRL administered peripherally (i.v.) and to the central nervous system (CNS) in normal rats and rats with sinoaortic deafferentation (SAD) to remove baroreflex buffering. Rats were chronically instrumented with Doppler flow probes for measurement of mesenteric, renal, and hind-quarter vascular resistance, with arterial pressure and intravenous catheters, and with lateral cerebroventricular cannuli for intracerebroventricular (i.c.v.) administration. Intravenous APRL (0.01 to 1.0 micrograms) produced a dose-dependent decrease in blood pressure, tachycardia, and dilation of all vascular beds studied. The dose-response relationships were shifted to the left in SAD animals. APRL administered i.c.v. had no effect on intact or SAD rats. Pressor and regional vasoconstrictor responses to norepinephrine, angiotensin, and vasopressin were markedly reduced in SAD animals during constant infusion of APRL. In a second group of conscious SAD animals instrumented for blood pressure and heart rate measurements, intravenous ANRL (500 micrograms) decreased both arterial pressure (-45 +/- 16 mm Hg) and heart rate (-50 +/- 16 bpm). When given i.c.v., however, ANRL (10-100 micrograms) had no significant effect on resting blood pressure or heart rate. These studies suggest that APRL and ANRL produce no significant cardiovascular effects that are mediated through the CNS. However, both lipids are potent depressor agents, and APRL exhibits a strong peripheral vasodilator action and nonspecifically reduces reactivity to vasoconstrictor agents.
Decreased uptake of 3H-serotonin and endogenous content of serotonin in blood platelets in hypertensive patients.
Authors: Kamal L A , Le Quan-Bui K H , Meyer P
Published: June 2012

The uptake and content of serotonin in blood platelets were studied in patients with essential hypertension and in five families in which at least one member was hypertensive. Blood was obtained from male and female normotensive volunteers and hypertensive patients who were free of medication. Lineweaver-Burk plots of 3H-serotonin uptake from both control subjects and hypertensive patients were linear, which suggested simple Michaelis-Menten uptake kinetics. The maximal uptake velocity (Vmax) in hypertensive patients was significantly lower than in control subjects (control = 41.7 +/- 3.3 pmol/min/10(8) platelets, n = 17; hypertensive = 26.6 +/- 3.0 pmol/min/10(8) platelets, n = 16; p less than 0.005). The affinity constant (Km) was slightly but significantly lower in hypertensive patients (control = 0.70 +/- 0.08 microM; hypertensive = 0.46 +/- 0.08 microM; p less than 0.05). The serotonin content in blood platelets determined by high pressure liquid chromatography with electrochemical detection was significantly lower in hypertensive patients (control = 165.0 +/- 12.9 nmol/10(11) platelets, n = 29; hypertensive = 105.9 +/- 10.4 nmol/10(11) platelets, n = 27; p less than 0.001). In the five families investigated, the lowered serotonin content was observed in some normotensive members. The reduced number of carriers of serotonin uptake and the slight decrease in the affinity constant observed in platelets of patients with essential hypertension suggest that serotonin metabolism is altered in essential hypertension and that blood platelets may be a useful model in studying the serotonergic modifications at the molecular level.
Tissue and gene specificity of mouse renin expression.
Authors: Field L J , McGowan R A , Dickinson D P , Gross K W
Published: June 2012

The Ren-1 locus of mice encodes the protease renin, which with converting enzyme processes angiotensinogen to the potent vasopressor angiotensin II. Some strains of mice appear to carry a duplication of the renin structural gene (Ren-2) near the Ren-1 locus. Strains with the gene duplication can exhibit as much as 100-fold higher levels of submaxillary gland renin compared to strains with a single gene copy. In contrast, kidney renin levels appear to be unaffected by the gene duplication. Sequence analysis of a 319 bp renin cDNA recombinant isolated from a kidney library from the two-gene strain DBA/2Ha corresponds to a transcript of the Ren-1 gene. Moreover, a single base substitution of A for G at residue #996 in the kidney renin mRNA creates a potential glycosylation recognition site that may, in part, account for the differential glycosylation of kidney and submaxillary gland renins. In addition, our tissue surveys indicate that mature mRNAs from the Ren loci are detectable in adrenal gland and testes, as well as sublingual and parotid salivary glands, and reveal length variation for the renin transcripts in at least the submaxillary gland.
Effect of methyldopa on brain cholinergic neurons involved in cardiovascular regulation. A study in conscious spontaneously hypertensive rats.
Authors: Buccafusco J J
Published: June 2012

Chemical stimulation of brain cholinergic neurons in many species can produce hypertension. Recent studies in this laboratory have demonstrated that clonidine inhibits this central cholinergic pressor response by inhibiting the biosynthesis of brain acetylcholine. This study was designed to determine whether methyldopa, like clonidine, could inhibit brain cholinergic neurons involved in cardiovascular regulation in freely-moving spontaneously hypertensive rats (SHR). Intravenous (i.v.) injection of methyldopa (50-200 mg/kg) produced a dose-related fall in blood pressure (29/15-54/33 mm Hg) in SHR. Intracerebroventricular (i.c.v.) injection of hemicholinium-3 (HC-3) in SHR evoked a fall in arterial pressure through inhibition of acetylcholine synthesis. Doses of HC-3 (10 micrograms, or 15 micrograms, i.c.v.) and methyldopa (50 mg/kg, i.v.) were administered to produce small reductions in arterial pressure in SHR (7-14 mm Hg diastolic, respectively). When the two agents were injected simultaneously, however, a greater than additive response was obtained (p less than 0.05). Central injection of echothiophate (a long-acting cholinesterase inhibitor) to potentiate brain cholinergic activity resulted in a sustained hypertensive response (greater than 40 mm Hg) in SHR for at least 150 minutes. Simultaneous injection of or pretreatment with methyldopa (100 mg/kg, i.v.) inhibited the pressor response to echothiophate over a time course similar to its antihypertensive response in untreated SHR. Methyldopa, however, was completely ineffective in altering the hypertensive response to central injection of carbachol (1 microgram, i.c.v.). This difference in methyldopa susceptibility between the indirect-acting (echothiophate) and direct-acting (carbachol) cholinergic agonists may be related to an inhibiting effect of methyldopa on brain acetylcholine release.(ABSTRACT TRUNCATED AT 250 WORDS)
Hemodynamic characterization of hypertension induced by chronic intrarenal or intravenous infusion of norepinephrine in conscious rats.
Authors: Kleinjans J C , Smits J F , van Essen H , Kasbergen C M , Struyker Boudier H A
Published: June 2012

The present study was designed to determine the hemodynamic changes underlying the hypertension induced by chronic intrarenal infusion of norepinephrine (NE) in conscious rats. NE was infused for a 5-day period intrarenally with osmotic minipumps via a chronic catheter in the right suprarenal artery at rates of 4 and 36 micrograms . kg-1 . hr-1 or intravenously at a rate of 36 micrograms . kg-1 . hr-1. Control rats received a 1 microliter . hr-1 intrarenal infusion of pyrogen-free 0.9% NaCl. In separate experiments, short-term effects were measured continuously during a 22- to 24-hour intrarenal infusion of 4 and 36 micrograms NE . kg-1 . hr-1 or intravenous infusion of 36 micrograms NE . kg-1 . hr-1. Intrarenal infusion of NE produced a more pronounced long-term hypertensive effect than infusion of the same dose intravenously. This hypertension was characterized by a rapid and sustained increase in total peripheral resistance index (TPRI). Despite of the initial renal vasoconstriction, specifically produced during the first 24 hours of intrarenal NE application, cardiac index (CI) in parallel to stroke volume index (SVI) decreased significantly during intrarenal as well as during intravenous NE infusion. Furthermore, no signs of sodium retention were observed. Both rates of intrarenal NE infusion have been shown previously to produce a significant long-term increase in plasma potassium concentration, and the present study indicates that this is presumably the result of decreased urinary potassium output. It is concluded that chronic hypertension produced by intrarenal or intravenous infusion is not volume-dependent. The relatively greater increase in TPRI during intrarenal NE infusion is attributed to vascular wall receptor sensitization by increased plasma potassium levels resulting from effects of intrarenally present NE on tubular cation exchange mechanisms.
Effect of dietary sodium reduction on red blood cell sodium concentration and sodium-lithium countertransport.
Authors: Cooper R , Trevisan M , Van Horn L , Larbi E , Liu K , Nanas S , Ueshima H , Sempos C , Ostrow D , Stamler J
Published: June 2012

A randomized, crossover trial was carried out on the effect of moderate sodium reduction on red-blood-cell sodium metabolism. The participants were healthy high school students (mean age = 16 years, n = 33). Changes in sodium-lithium countertransport and intracellular sodium concentration were evaluated 24 days after a decrease in dietary sodium from approximately 110 to 40 mEq per day. Dietary sodium restriction had no significant effect on either sodium-lithium countertransport or intracellular sodium concentration.
Diagnosis and treatment of renin-secreting tumors. Report of three cases.
Authors: Baruch D , Corvol P , Alhenc-Gelas F , Dufloux M A , Guyenne T T , Gaux J C , Raynaud A , Brisset J M , Duclos J M , Menard J
Published: June 2012

During the past 10 years, we have found renin-secreting renal juxtaglomerular cell tumors in three hypertensive patients (two women, one man, aged 22, 69, and 21 years, respectively). The major chemical and biological findings revealed the association of severe hypertension with hypokalemia and increased plasma renin activity and plasma aldosterone. The diagnosis of such tumors is difficult, and two of the three patients were followed up for four and five years respectively before undergoing surgery. The pharmacological blockade of the renin system by various agents (beta-blockers, angiotensin II antagonists, and captopril) and its effects on blood pressure and plasma renin activity proved to be unreliable. Renal venous catheterization for renin measurements failed to provide adequate localization of the tumor. Direct radioimmunoassay, however, showed the total plasma renin to be markedly elevated. In addition, renal arteriography showed an avascular area corresponding to the renin-secreting tumor in each of the three patients. All three patients were cured of hypertension and hypokalemia by excision of the tumor.
High blood pressure in older Americans. The First National Health and Nutrition Examination Survey.
Authors: Harlan W R , Hull A L , Schmouder R L , Landis J R , Larkin F A , Thompson F E
Published: June 2012

Data from a representative sample of the U.S. adult population obtained during 1971-1975 were analyzed to provide a profile of blood pressure (BP) levels and related nutritional and sociodemographic factors. Older adults (aged 55-74 years) had a twofold greater prevalence of high BP than younger adults (25-54 years), and older black persons had the highest rates. Isolated systolic elevation was uncommon under 54 years of age, but occurred in 5% to 10% of adults over 55 years and was less common than systolic-diastolic elevation. In older adults, body mass (weight/height2) had the strongest relationship to BP of all the nutritional variables. Alcohol consumption and dietary calcium and phosphorus were associated with high BP, but dietary sodium and salt use were not. The serum calcium/phosphorus ratio and serum urate were significantly higher in older adults with high BP. In general, the variables associated with elevated BP in older adults were similar to those in younger adults, although the strengths of the associations differed. Associations of factors useful for nonpharmacologic prevention and management of high BP in older persons were suggested from this survey.
Low sodium cotransport in red cells with physiological internal sodium concentration in essential hypertension.
Authors: Montanari A , Sani E , Canali M , Simoni I , Schianchi P , Borghetti A , Novarini A
Published: June 2012

Ouabain-resistant Na and Li effluxes in erythrocytes from 18 normal subjects and 19 hypertensive subjects were studied in fresh cells that contained about 9 mmol Li and 2.5 or 6.5 mmol Na per liter of erythrocytes after intact cells had been incubated for 5 hours in 110 mM Li, 40 mM Na medium, with or without ouabain 10(-4) M. Outward Na cotransport was estimated at both internal Na concentrations as the furosemide-sensitive unidirectional 22Na efflux from erythrocytes into a Na free-medium containing 75 mM MgCl2. The changes in furosemide-sensitive outward Na transport between the two levels of internal Na were considered as a measure of the response of Na cotransport to the changes in internal Na within its physiological range. At both levels of internal Na, outward Na cotransport was reduced in the majority but not in all of the patients with essential hypertension (p less than 0.05 at 2.5 mmol; p less than 0.001 at 6.5 mmol). The ratio of the changes in Na cotransport to those in internal Na was lower in the hypertensive patients than in the control subjects (17.2 mumol/liter red blood cells/hr/1 mmol in internal Na increase vs 42.2, p less than 0.001). The Li-Na countertransport was increased in a few patients with essential hypertension, with no relationship to cotransport. We conclude that, in essential hypertension, the outward Na + K cotransport is impaired in fresh erythrocytes not treated with PCMBS (2,5 p-chloromercuribenzene sulfonate) or nystatin, even when internal Na is around its physiological range.
Production and characterization of monoclonal antibodies to rat angiotensinogen.
Authors: Clauser E , Baier-Kustermann W , Bouhink J , Corvol P , Menard J , Celio M
Published: June 2012

Three stable monoclonal antibodies to rat angiotensinogen were obtained by fusing myeloma cells with spleen cells from Balb/c mice injected with pure rat angiotensinogen. They were screened by their binding to pure iodinated angiotensinogen and to insolubilized angiotensinogen in a solid phase assay. The titers of the three antibodies varied from 1/3500 to 1/35000, their dissociation constants from 2.5 X 10(-8) M to 3.8 X 10(-10) M, and the sensitivity of the assay ranged from 200 to 10 pmol of pure angiotensinogen. These monoclonal antibodies did not recognize either angiotensin peptides or angiotensinogen from other species, except for mouse angiotensinogen, which cross-reacted with the different antibodies from 0 to 25%. Rat cerebrospinal fluid angiotensinogen, plasma des-angiotensin I-angiotensinogen, and plasma angiotensinogen were equally recognized by these monoclonal antibodies. Contrary to what was observed for a polyclonal antiserum, the monoclonal antibodies failed to inhibit the renin-angiotensinogen reaction in vitro.
Angiotensinogen-producing hepatocellular carcinoma.
Authors: Ueno N , Yoshida K , Hirose S , Yokoyama H , Uehara H , Murakami K
Published: June 2012

This paper describes the first case of an angiotensinogen-producing tumor. The tumor obtained from a hypertensive patient was examined for its renin and angiotensinogen contents. Renin activity was undetectable; however, the angiotensinogen level was extremely high compared with the levels in the tissue surrounding the hepatoma. The presence of angiotensinogen immunoreactivity in the tumor cells was demonstrated by immunohistochemical staining with an angiotensinogen anti-serum. The plasma level of angiotensinogen was also markedly elevated. These results strongly suggest that the hepatoma was an angiotensinogen-producing tumor.
Effect of exercise on cation transport in human red cells.
Authors: Adragna N C , Chang J L , Morey M C , Williams R S
Published: June 2012

To test the hypothesis that environmental as well as genetic factors are important determinants of monovalent cation transport systems in humans, and to explore potential basic mechanisms of the alleged antihypertensive effects of habitual exercise, we studied the effects of a 12-week exercise program (45 minutes, 3-5 times per week) upon several membrane transport parameters in erythrocytes from a population of 63 adult men (30 normotensive subjects and 33 essential hypertensive patients). Subjects were randomly assigned into either an exercise group or a sedentary control group, and clinical and membrane transport parameters were measured at baseline and after 3 months. Exercising subjects demonstrated increases in maximal treadmill work capacity (p less than 0.001) and high-density lipoprotein cholesterol levels (p = 0.009) as well as decreases in heart rate at a fixed submaximal workload (p less than 0.05) and body weight (p less than 0.001) relative to the sedentary group. In conjunction with these well-described effects of exercise conditioning, the exercise group demonstrated a significant decrease in Na+-Li+ countertransport (p = 0.002), without significant changes in any other transport parameters measured. Blood pressure was not significantly altered in either group. We conclude that powerful environmental influences such as exercise training may act in concert with genetic factors to influence monovalent cation transport in humans and must be considered in further investigations of the pathophysiological linkage between altered monovalent cation transport and essential hypertension.
Effect of the protease inhibitor aprotinin on renal hemodynamics in the pig.
Authors: Maier M , Starlinger M , Zhegu Z , Rana H , Binder B R
Published: June 2012

Aprotinin, the serine protease inhibitor that also inhibits glandular (urinary) kallikrein, or vehicle was infused into the aorta above the renal arteries of anesthetized pigs. Renal hemodynamic and functional parameters were followed over time and during hemorrhagic hypotension. Both renal cortical blood flow and glomerular filtration rate were maintained in vehicle-treated animals at mean arterial pressures as low as 70 mm Hg. As long as renal cortical blood flow and glomerular filtration rate were maintained during the progressive hypotension, urinary excretion rate of kallikrein (as defined by kinin-generating activity) was increased. In contrast, all aprotinin-treated animals had a decreased excretion rate, and the renal cortical blood flow declined with the mean arterial pressure during hemorrhage. The pattern of glomerular filtration rate and plasma renin activity was comparable in both aprotinin-treated and vehicle-treated hemorrhaged animals. Our findings suggest that the endogenous renal kallikrein-kinin system is required for functional renal vasodilatation to maintain renal cortical blood flow during hemorrhage and is therefore directly or indirectly responsible for adjustment of preglomerular resistance.
Effects of a calcium channel blocker on cardiac output distribution in conscious hypertensive dogs.
Authors: Knight D R , Kirby D A , Vatner S F
Published: June 2012

The effects of nitrendipine, 8 micrograms/kg/minute, were evaluated in six conscious dogs through measurements of arterial pressure and blood flow in the ascending aorta (cardiac output), mesenteric, renal, and iliac arteries before and after induction of chronic perinephritic hypertension. Before hypertension was induced, nitrendipine reduced mean arterial pressure 19 +/- 2.3% (from 95 +/- 3.2 mm Hg), decreased total peripheral resistance (60 +/- 2.6%), and increased cardiac output (108 +/- 10.5%). These values returned to baseline within 15 to 30 minutes. Nitrendipine caused the greatest increase in blood flow in the iliac bed (98 +/- 9.9%), an intermediate increase in the mesenteric bed (37 +/- 3.7%), and the least increase in the renal bed (7 +/- 2.2%). Two to six weeks after induction of hypertension, administration of nitrendipine elicited significant (p less than 0.01) decreases in mean arterial pressure (32 +/- 2.5% from 151 +/- 4.8 mm Hg) and total peripheral resistance (67 +/- 1.3%) compared with its administration in normotensive dogs, while the increase in cardiac output was not significantly changed (111 +/- 10.9%). These changes in arterial pressure and vascular resistances also were prolonged (i.e., hemodynamics returned to baseline after 75-90 minutes). The increase in iliac (99 +/- 16.8%) and renal (9 +/- 6.1%) blood flows after nitrendipine administration in hypertensive dogs was similar to that found in the normotensive dogs, but mesenteric blood flow doubled (84 +/- 8.4%). Thus, in conscious, hypertensive dogs, nitrendipine administration appears to markedly decrease arterial pressure and total peripheral and regional resistances, which also require more time to return to baseline, but appears to increase blood flow by a greater amount only in the mesenteric bed.
Significance of blood pressure in infancy. Familial aggregation and predictive effect on later blood pressure.
Authors: Zinner S H , Rosner B , Oh W , Kass E H
Published: June 2012

Blood pressure was measured in 730 infants and their mothers within 5 days of birth. Paternal blood pressures were obtained where possible, and follow-up measurements were made on participants at 1 week and 1, 6, 12, 18, and 24 months. Infant blood pressures were adjusted for such variables as age, observer, cuff size, and sleep/activity status. Infant blood pressure correlated with maternal blood pressure corrected for age and observer shortly after birth (r = 0.138, p less than 0.001 for systolic pressure; r = 0.169, p less than 0.001 for diastolic pressure). Father-infant correlations were significant only at 1 month after birth (r = 0.179, p = 0.031; r = 0.250, p = 0.002 for systolic and diastolic pressures respectively), and sibling correlations were significant from 6 months after birth (r = 0.173, p = 0.011 for systolic pressure; r = 0.265, p less than 0.001 for diastolic pressure). Blood pressures of infants before 6 months after birth were not consistently predictive of later pressures, but systolic and diastolic blood pressures 6 and 12 months after birth were significantly and positively related to pressures at later ages (for systolic pressures at 6 and 12 months, r = 0.147, p = 0.003; 6 and 18 months, r = 0.218, p less than 0.001; 6 and 24 months, r = 0.212, p less than 0.001). These results indicate that the familial aggregation of blood pressure and blood pressure tracking can be detected early in life.
Autonomic innervation of cerebral blood vessels decreases in renal hypertensive rats.
Authors: Saito A , Lee T J
Published: June 2012

The ultrastructural distribution of the autonomic nerves of brain arteries was investigated in renal (one-kidney, one clip) hypertensive and normotensive Wistar-Kyoto rats. Sympathetic and nonsympathetic nerve terminals were found only in the adventitial layer of brain arteries of renal hypertensive and normotensive rats. In both normotensive and renal hypertensive rats the total nerve endings were dense in anterior cerebral artery, moderately dense in middle cerebral artery, and sparse in basilar artery. In normotensive rats, nonsympathetic nerves outnumbered sympathetic nerves in anterior cerebral, middle cerebral, and basilar arteries. In renal hypertensive rats these two types of nerve terminals in close apposition to smooth muscle decreased in anterior cerebral and basilar arteries, while those in middle cerebral arteries remained unchanged. These results suggest that the potential neurogenic control of cerebral blood vessels as well as the trophic effect of sympathetic nerves on brain blood vessels may decrease in renal hypertensive rats. As this finding contrasts with that in spontaneously hypertensive rats, the pattern of innervation in brain arteries may differ in different types of hypertension.
Cardiac contractile and coronary flow reserves in deoxycorticosterone acetate-salt hypertensive rats.
Authors: Yamamoto J , Tsuchiya M , Saito M , Ikeda M
Published: June 2012

Cardiac contractility and coronary flow were compared in conscious rats with established deoxycorticosterone acetate-salt hypertension and in those with sham treatment. The hypertensive rats showed a 32% increase in left ventricular/body weight ratio at 9 weeks of treatment and 42% at 18 weeks of treatment. Resting peak rate of change of pressure (dp/dt) was unchanged at 9 weeks and increased at 18 weeks in hypertensive rats, while isoproterenol-stimulated maximal, propranolol-induced minimal, and Ca2+-stimulated maximal peak dp/dt were greater at 18 weeks. These data indicate the preservation of contractile function. At 18 weeks, the beta-adrenergic receptor-mediated contractile reserve, estimated from isoproterenol-stimulated maximal and resting peak dp/dt, was reduced but the propranolol-induced decrease in peak dp/dt was increased in hypertensive rats compared with sham-treated rats. Thus, at this stage, a greater portion of the total contractile capacity appeared to be mobilized with prolongation of hypertension and progression of left ventricular hypertrophy. No differences were observed in left ventricular and right ventricular coronary flow (microspheres) and left ventricular inner/outer flow ratio at rest and with dipyridamole-induced maximal coronary dilatation, at 9 and 18 weeks. There were no alterations in left or right ventricular coronary flow reserves, as estimated from resting and dipyridamole-induced values. The minimal coronary vascular resistance (normalized for gram of tissue) of both the left and right ventricles was increased at either stage, which suggests the occurrence of structural coronary vascular changes. Thus, basal coronary flow and a coronary flow reserve were uncompromised despite evidence of structural coronary vascular alterations in these hypertensive rats.
Sodium balance in renal failure. A comparison of patients with normal subjects under extremes of sodium intake.
Authors: Koomans H A , Roos J C , Dorhout Mees E J , Delawi I M
Published: June 2012

To gain insight into the factors involved in the maintenance of sodium balance in patients with chronic renal failure, we studied 10 patients with a creatinine clearance of 11.5 +/- 4.0 ml/min after equilibrium on 20 and 120 mEq of sodium per day. The measurements included blood pressure, plasma volume, blood volume, extracellular fluid volume, plasma renin activity, plasma aldosterone, and plasma norepinephrine. For comparison, eight normal volunteers were studied after equilibration on 20, 200, and 1128 mEq of sodium per day. The latter intake was chosen to match the high sodium intake per residual renal function in the patients. In the patients, equilibrium after raised sodium intake was accompanied by a marked increase in blood pressure and blood volume, a moderate fall in plasma renin activity and levels of aldosterone and norepinephrine, and only little expansion of the interstitial space. The 24-hour creatinine clearance rose by 21.2 +/- 7.2%. Fractional sodium excretion (X 100%) was 5.3 +/- 0.8% during the 120 mEq sodium diet. In the normal volunteers, increasing the sodium intake from 20 to 1128 mEq/day evoked no consistent change in blood pressure but caused a comparable rise in blood volume, considerable suppression of plasma renin activity, aldosterone, and norepinephrine, and a much larger increase in interstitial volume. Their creatinine clearance had risen by 22.4 +/- 6.5%, and their fractional sodium excretion during the 1128 mEq sodium intake was 3.9 +/- 0.2%.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise training attenuates stress-induced hypertension in the rat.
Authors: Cox R H , Hubbard J W , Lawler J E , Sanders B J , Mitchell V P
Published: June 2012

The ability of exercise training to block the generation of hypertension produced by chronic stress in the borderline hypertensive rat was tested. Twenty-three male borderline hypertensive rats, F1 offspring of spontaneously hypertensive and Wistar-Kyoto rats, were divided into three groups. Two groups (8 rats per group) were subjected to 2 hours of daily, predictable, uncontrollable tail shock for 12 weeks. One of these groups was also given 2 hours of daily swim stress (exercise trained). A third group served as a maturation control and received neither intervention (n = 7). After 12 weeks of stress, direct recording of blood pressure verified the pattern observed with tail cuff: shock only group, 180/118 +/- 3/3 mm Hg; exercise-trained and shocked group, 166/108 +/- 4/2 mm Hg; and control group, 160/98 +/- 6/4 mm Hg (mean +/- SEM). Systolic and diastolic blood pressures in the shock only group were significantly higher than in both the other groups (p less than 0.05). The control group differed from the exercise-trained and shocked group only in diastolic BP (p less than 0.05). During a short-term stress session plasma norepinephrine levels in the exercise-trained and shocked group were significantly lower than those in the shock only group (555 +/- 56 vs 776 +/- 84 pg/ml; p less than 0.05). These results indicate that an alteration of autonomic function resulted from the exercise training, but its contribution to the resistance of the exercise-trained and shocked rats to stress-induced hypertension is unclear.
Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats.
Authors: Iijima F , Malik K U
Published: June 2012

Possible alterations in mesenteric vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin and its relationship to prostaglandins in dexamethasone-induced hypertension in rats were investigated. The animals were treated with dexamethasone or its vehicle (sesame oil) for 1 day (1.8 mg/kg) and for 14 days (1.8 mg/kg/wk). The superior mesenteric artery with its branches was isolated and perfused with Tyrode's solution at a constant flow rate of 5 ml/min. Administration of norepinephrine (1-10 nmol), arginine vasopressin (0.03-0.3 nmol), or angiotensin II (0.1-1 nmol) produced vasoconstriction and increased the output of 6-keto-prostaglandin F1 alpha and prostaglandin E2 in a dose-related manner in mesenteric vessels. Administration of 10 nmol bradykinin or 19 nmol A23187 enhanced the output of prostaglandins without altering vascular tone. The vasoconstrictor response to arginine vasopressin, but not norepinephrine or angiotensin II, was enhanced in mesenteric vessels from rats treated with dexamethasone for 14 days but not for 1 day. In contrast, the output of basal as well as norepinephrine, arginine vasopressin, angiotensin II, bradykinin, or A23187-induced prostaglandin output was significantly reduced in mesenteric vessels from rats treated with dexamethasone for 1 or 14 days. Prostaglandin output in mesenteric arteries from rats treated with dexamethasone for 1 and 14 days was not different. These data indicate that dexamethasone treatment for longer but not for shorter periods results in a selective increase in vascular reactivity of mesenteric vessels to arginine vasopressin that is independent of prostaglandin synthesis. The increase in vascular reactivity to arginine vasopressin during long-term dexamethasone treatment may contribute to the development or maintenance, or both, of glucocorticoid-induced hypertension.
Effects of taurine on stress-evoked hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.
Authors: Yamamoto J , Akabane S , Yoshimi H , Nakai M , Ikeda M
Published: June 2012

Cardiovascular hemodynamics (microspheres) and plasma norepinephrine and epinephrine levels at rest and during short-term shaker stress were investigated in conscious spontaneously hypertensive rats and Wistar-Kyoto rats, with or without oral taurine (1.5%) treatment for 8 weeks. Taurine effects were evaluated by comparing data on the taurine-treated and untreated rats. Taurine affected neither the resting hemodynamics nor the resting plasma catecholamine levels in spontaneously hypertensive and Wistar-Kyoto rats. Taurine slightly but significantly reduced the left ventricular/body weight ratio in the spontaneously hypertensive rats (p less than 0.05) and caused an insignificant 10 mm Hg decrease in the resting mean arterial pressure. Spontaneously hypertensive and Wistar-Kyoto rats responded in a qualitatively similar manner to stress, as evidenced by resistance-dominated increases in mean arterial pressure and increases in heart rate, with a blood flow redistribution from splanchnic, cutaneous, and testicular to skeletal muscle and cerebral circulations and by increases in plasma norepinephrine and epinephrine levels. These changes were more marked in the spontaneously hypertensive rats. Taurine significantly reduced the stress values of mean arterial pressure (untreated, 189 +/- 4 (SE) mm Hg; treated, 166 +/- 4 mm Hg in the spontaneously hypertensive rats; p less than 0.05), while it significantly reduced stress values of heart rate in spontaneously hypertensive and Wistar-Kyoto rats (p less than 0.05). Taurine also blunted the stress values of splanchnic, testicular, and cutaneous vascular resistance in the spontaneously hypertensive rats. There were no or only slight regional effects in the Wistar-Kyoto rats. Taurine substantially decreased plasma levels of norepinephrine (untreated, 615 +/- 76 pg/ml; treated, 383 +/- 49 pg/ml) and epinephrine (untreated, 892 +/- 187 pg/ml; treated, 232 +/- 59 pg/ml) during stress in the spontaneously hypertensive rats. These results indicate that chronic taurine treatment attenuates short-term shaker stress-induced hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.
Effect of dietary sodium on platelet alpha 2-adrenergic receptors in essential hypertension.
Authors: Ashida T , Tanaka T , Yokouchi M , Kuramochi M , Deguchi F , Kimura G , Kojima S , Ito K , Ikeda M
Published: June 2012

To study the aggregation, adhesion, and specific binding of an alpha 2-antagonist, [3H]rauwolscine, to the platelet membrane fractions, platelets were obtained from 30 patients with essential hypertension and nine normotensive subjects fed a high sodium diet (NaCl, 16-18 g/day) for 7 days and thereafter a low sodium diet (NaCl, 1-3 g/day) for 7 days. The patients with essential hypertension were classified as either salt responders (all those who had greater than 7% decrease in mean arterial pressure from the high to low sodium period) or salt nonresponders (all others). In salt responders, the number of alpha 2-adrenergic receptors on platelet membrane fraction was increased from 523.4 +/- 55.4 fmol/mg of protein in the high sodium period to 669.4 +/- 84.0 fmol/mg of protein in the low sodium period (p less than 0.01), whereas it did not change in salt nonresponders. In contrast, the epinephrine-induced platelet aggregation through alpha 2-adrenergic receptors was decreased in nonresponders, from 47.3 +/- 7.4% in the high sodium period to 24.5 +/- 9.3% in the low sodium period (p less than 0.05), while it did not change in responders. No significant change in the number of alpha 2-adrenergic receptors or epinephrine-induced platelet aggregation was observed in the normotensive subjects.
Salt sensitivity in essential hypertension as determined by the cosinor method.
Authors: Bittle C C , Molina D J , Bartter F C
Published: June 2012

A method of data reduction for the statistical examination of mean arterial pressure in essential hypertensive subjects to determine salt sensitivity was examined. A computerized method was used to estimate the best-fitting cosine curve for data collected every 30 minutes for 24 hours. The effect of sodium loading on the cosinor parameters (mesor, amplitude, and acrophase) in 45 subjects with essential hypertension and five normotensive control subjects was assessed. Twenty-five percent of the essential hypertensive subjects in the study were found to be salt-sensitive with a statistically significant increase in their mesors with sodium loading (p less than 0.05). The non-salt-sensitive group was found to contain a subpopulation with a statistically significant decrease in their mesor with sodium loading (p less than 0.05). Sodium loading appears to affect the lability of mean arterial pressure independently of mesor changes.
Pulmonary vascular overreactivity in systemic hypertension. A pathophysiological link between the greater and the lesser circulation.
Authors: Fiorentini C , Barbier P , Galli C , Loaldi A , Tamborini G , Tosi E , Guazzi M D
Published: June 2012

This study was undertaken to test whether the emphasized systemic vasomotion during sympathetic activation in hypertension is shared by the pulmonary circulation. To this end, 10 normotensive and 29 primary hypertensive subjects were investigated during adrenergic stimulation by mental arithmetic and cold pressor test. Both stimuli induced a systemic pressor reaction in both groups, which was mediated through an increase in cardiac output and a mild reduction in vascular resistance during arithmetic and through a predominant rise in systemic vascular resistance during cold. Each of these changes was emphasized in the hypertensive population as compared with the normotensive one. Pressure in the pulmonary artery remained unchanged during cold and was slightly raised (systolic) during arithmetic in normotensive subjects. On the contrary, in hypertensive subjects systolic and diastolic pulmonary pressures were consistently augmented by both stimuli, and pulmonary arteriolar resistance (dyn sec cm-5) rose from 92 in the baseline to 125 (p less than 0.01) during arithmetic and to 124 (p less than 0.01) during the cold test. This reaction is interpreted as reflecting a neurally mediated vasoconstriction and not as the consequence of mechanical or chemical changes, since no difference was observed in pulmonary wedge pressure, pleural pressure, arterial blood gas levels, and pH between controls and hypertensive subjects in the steady state and during either stressful stimulation. Baseline pulmonary arteriolar resistance was also found to correlate positively with systemic vascular resistance in the hypertensive group. When pressure changes occurred, the time course was similar in the two circuits; resistance increased to a proportionally similar degree in the two districts during the cold stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)
Evidence for a predominantly central hypotensive effect of alpha-methyldopa in humans.
Authors: Bobik A , Jennings G , Jackman G , Oddie C , Korner P
Published: June 2012

We examined the time course and extent to which central and peripheral mechanisms contribute to the short-term effects of a 500-mg oral dose of alpha-methyldopa on supine mean arterial pressure, cardiac output, and total peripheral resistance, as well as its effects on total urinary excretion of norepinephrine and its metabolites, in five subjects with essential hypertension. Total peripheral resistance was reduced significantly 1 hour after alpha-methyldopa administration and remained so for the ensuing 7 hours of the study (p less than 0.05). A small but significant reduction in mean arterial pressure occurred 7 hours after the dose (p less than 0.05), while cardiac output did not change significantly. Total 24-hour urinary norepinephrine and metabolite excretion was reduced by 8.1 mumol (35% compared with placebo). The relative distribution of urinary norepinephrine metabolites was unaffected by alpha-methyldopa, and the catecholamine metabolites of alpha-methyldopa, alpha-methylnorepinephrine and alpha-methylnormetanephrine did not account for this reduction. Competitive inhibition of methyldopa transport across the blood-brain barrier and into the central nervous system by large oral doses of isoleucine antagonized most of the effect of alpha-methyldopa. The effects on total peripheral resistance were completely abolished, and small, insignificant changes during the 7-hour study were similar to those observed after placebo. Changes in mean arterial pressure were not significant; however, 24-hour total urinary norepinephrine and metabolite excretion increased by 6.1 mumol to 22.7 mumol (24.7 mumol excreted after placebo). Adding benserazide to the alpha/methyldopa-isoleucine dose regimen in an attempt to inhibit any residual, presumably peripheral, effects of alpha-methyldopa caused little, if any, further antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise hemodynamics and oxygen delivery in human hypertension. Response to verapamil.
Authors: Cody R J , Kubo S H , Covit A B , Müller F B , Lopez-Ovejero J , Laragh J H
Published: June 2012

To characterize the hemodynamic response to exercise and the effects of calcium channel antagonism in hypertensive subjects, invasive exercise hemodynamics were performed in the baseline state after intravenous infusion of verapamil and after 5 to 7 days of oral verapamil in 10 subjects with moderate to severe hypertension. We also assessed oxygen delivery and use and the response of the sympathetic nervous system by measuring plasma norepinephrine levels at rest and during exercise. Both routes of administration were associated with significant reductions of mean arterial pressure and systemic vascular resistance at rest and peak exercise (p less than 0.05). Changes in heart rate were not statistically significant. Following oral administration of verapamil, stroke volume increased significantly in both the resting and exercise states. Pulmonary wedge pressure did not increase; in fact, the Frank-Starling relationship of cardiac performance actually was improved. Oxygen delivery and use were unchanged with both routes of administration. There was no significant difference in rest and exercise plasma norepinephrine levels following verapamil therapy. Thus, verapamil resulted in a significant reduction of mean arterial pressure, mediated by a significant reduction of systemic vascular resistance, following both intravenous and short-term oral administration. This reduction occurred without expression of left ventricular dysfunction and was not at the expense of increased oxygen use or enhanced sympathetic nervous systemic activity.