bluuebunny/crossref_metadata_2025 huggingface dataset:
New-Onset Sustained Ventricular Tachycardia After Cardiac Surgery
Authors: Steinberg Jonathan S. , Gaur Abhishek , Sciacca Robert , Tan Edith
Published: June 2012

Background
—The de novo occurrence of sustained ventricular tachycardia (VT) after CABG has been described, but the incidence, mortality rate, long-term follow-up, and mechanism are not well defined.

Methods and Results
—This prospective study enrolled consecutive patients undergoing CABG at a single institution. Patients were followed up for the development of sustained VT, and a detailed analysis of clinical, angiographic, and surgical variables associated with the occurrence of VT was performed. A total of 382 patients participated, and 12 patients (3.1%) experienced ≥1 episode of sustained VT 4.1±4.8 days after CABG. In 11 of 12 patients, no postoperative complication explained the VT; 1 patient had a perioperative myocardial infarction. The in-hospital mortality rate was 25%. Patients with VT were more likely to have prior myocardial infarction (92% versus 50%,
P
<0.01), severe congestive heart failure (56% versus 21%,
P
<0.01), and ejection fraction <0.40 (70% versus 29%,
P
<0.01). When all 3 factors were present, the risk of VT was 30%, a 14-fold increase. Patients with VT had more noncollateralized totally occluded vessels on angiogram (1.4±0.97 versus 0.54±0.7,
P
<0.01), a bypass graft across a noncollateralized occluded vessel (1.50±1.0 versus 0.42±0.62,
P
<0.01), and a bypass graft across a noncollateralized occluded vessel to an infarct zone (1.50±1.0 versus 0.17±0.38,
P
<0.01). By multivariate analysis, the number of bypass grafts across a noncollateralized occluded vessel to an infarct zone was the only independent factor predicting VT.

Conclusions
—The first presentation of sustained monomorphic VT in the recovery period after CABG is uncommon, but the incidence is high in specific clinical subsets. Placement of a bypass graft across a noncollateralized total occlusion in a vessel supplying an infarct zone was strongly and independently associated with the development of VT.
Detection of Transposition of the Great Arteries in Fetuses Reduces Neonatal Morbidity and Mortality
Authors: Bonnet Damien , Coltri Anna , Butera Gianfranco , Fermont Laurent , Le Bidois Jérôme , Kachaner Jean , Sidi Daniel
Published: June 2012

Background
—Transposition of the great arteries (TGA) is a life-threatening malformation in neonates, but it is amenable to complete repair. Prenatal detection, diagnosis, and early management may modify neonatal mortality and mortality.

Methods and Results
—Preoperative and postoperative morbidity and mortality were compared in 68 neonates with prenatal diagnosis and in 250 neonates with a postnatal diagnosis of TGA over a period of 10 years. The delay between birth and admission was 2±2.8 hours in the prenatal group and 73±210 hours in the neonatal group (
P
<0.01). Clinical condition at arrival, including metabolic acidosis and multiorgan failure, was worse in the neonatal group (
P
<0.01). Once in the pediatric cardiology unit, the management was identical in the 2 groups (atrioseptostomy, PGE
1
infusion, operation date). Preoperative mortality was 15 of 250 (6%; 95% CI, 3% to 9%) in the neonatal group and 0 of 68 in the prenatal group (
P
<0.05). Postoperative morbidity was not different (25 of 235 versus 6 of 68), but hospital stay was longer in the neonatal group (30±17 versus 24±11 days,
P
<0.01). In addition, postoperative mortality was significantly higher in the neonatal group (20 of 235 versus 0 of 68,
P
<0.01); however, the known risk factors for operative mortality were identical in the 2 groups.

Conclusions
—Prenatal diagnosis reduces mortality and morbidity in TGA. Prenatal detection of this cardiac defect must be increased to improve early neonatal management. In utero transfer of fetuses with prenatal diagnosis of TGA in an appropriate unit is mandatory.
Suppression of Atherosclerotic Development in Watanabe Heritable Hyperlipidemic Rabbits Treated With an Oral Antiallergic Drug, Tranilast
Authors: Matsumura Toshiyuki , Kugiyama Kiyotaka , Sugiyama Seigo , Ota Yasutaka , Doi Hideki , Ogata Nobuhiko , Oka Hideki , Yasue Hirofumi
Published: June 2012

Background
—Inflammatory and immunological responses of vascular cells have been shown to play a significant role in the progression of atheromatous formation. Tranilast [
N
-(3,4-dimethoxycinnamoyl) anthranillic acid] inhibits release of cytokines and chemical mediators from various cells, including macrophages, leading to suppression of inflammatory and immunological responses. This study tested whether tranilast may suppress atheromatous formation in Watanabe heritable hyperlipidemic (WHHL) rabbits.

Methods and Results
—WHHL rabbits (2 months old) were given either 300 mg · kg
−1
· d
−1
of tranilast (Tranilast, n=12) or vehicle (Control, n=13) PO for 6 months. Tranilast treatment was found to suppress the aortic area covered with plaque. Immunohistochemical analysis showed that there was no difference in the percentage of the RAM11-positive macrophage area and the frequency of CD5-positive cells (T cells) in intimal plaques between Tranilast and Control. Major histocompatibility complex (MHC) class II expression in macrophages and interleukin-2 (IL-2) receptor expression in T cells, as markers of the immunological activation in these cells, was suppressed in atheromatous plaque by tranilast treatment. Flow cytometry analysis of isolated human and rabbit peripheral blood mononuclear cells showed that an increase in expression both of MHC class II antigen on monocytes by incubation with interferon-γ and of IL-2 receptor on T cells by IL-2 was suppressed by the combined incubation with tranilast.

Conclusions
—The results indicate that tranilast suppresses atherosclerotic development partly through direct inhibition of immunological activation of monocytes/macrophages and T cells in the atheromatous plaque.
Pl
A
Polymorphism of Platelet Glycoprotein IIIa and Risk of Restenosis After Coronary Stent Placement
Authors: Kastrati Adnan , Schömig Albert , Seyfarth Melchior , Koch Werner , Elezi Shpend , Böttiger Corinna , Mehilli Julinda , Schömig Kathrin , von Beckerath Nicolas
Published: June 2012

Background
—Platelets play a central role in the process of restenosis after percutaneous coronary interventions. A polymorphism of platelet glycoprotein IIIa (Pl
A
) has been associated with a higher risk of coronary thrombosis. We designed this prospective study to test the hypothesis that Pl
A
polymorphism of glycoprotein IIIa is associated with an increased risk for restenosis after coronary stent placement.

Methods and Results
—The study included 1150 consecutive patients with successful coronary stent placement and 6-month follow-up with coronary angiography. The end point of the study was the incidence of angiographic restenosis (≥50% diameter stenosis) at follow-up. Of the 1150 patients, 72.5% were homozygous for Pl
A1
, 24.7% were heterozygous (Pl
A1/A2
), and 2.8% were homozygous for Pl
A2
. Patients with the Pl
A2
allele demonstrated a significantly higher restenosis rate than did those without (47% versus 38%; OR, 1.42; 95% CI, 1.09 to 1.84). The risk was highest in homozygous carriers of Pl
A2
(53.1% restenosis rate). After adjustment for several clinical and angiographic characteristics, the presence of the Pl
A2
allele remained a significantly independent risk factor for restenosis (adjusted OR, 1.35; 95% CI, 1.07 to 1.70). The influence of the Pl
A2
allele on restenosis was stronger in women. Women with Pl
A2
had a restenosis rate of 52% compared with the 33% incidence among women homozygous for Pl
A1
(OR, 2.21; 95% CI, 1.27 to 3.85).

Conclusions
—This study showed a significant association between the Pl
A
polymorphism of glycoprotein IIIa and the risk of restenosis after coronary stent placement. The risk was more pronounced in patients homozygous for Pl
A2
allele and in female patients.
From Myocarditis to Cardiomyopathy: Mechanisms of Inflammation and Cell Death
Authors: Kawai Chuichi
Published: June 2012

Abstract
—A progression from viral myocarditis to dilated cardiomyopathy has long been hypothesized, but the actual extent of this progression has been uncertain. However, a causal link between viral myocarditis and dilated cardiomyopathy has become more evident than before with the tremendous developments in the molecular analyses of autopsy and endomyocardial biopsy specimens, new techniques of viral gene amplification, and modern immunology. The persistence of viral RNA in the myocardium beyond 90 days after inoculation, confirmed by the method of polymerase chain reaction, has given us new insights into the pathogenesis of dilated cardiomyopathy. Moreover, new knowledge of T-cell–mediated immune responses in murine viral myocarditis has contributed a great deal to the understanding of the mechanisms of ongoing disease processes. Apoptotic cell death may provide the third concept to explain the pathogenesis of dilated cardiomyopathy, in addition to persistent viral RNA in the heart tissue and an immune system–mediated mechanism. Beneficial effects of α
1
-adrenergic blocking agents, carteolol, verapamil, and ACE inhibitors have been shown clinically and experimentally in the treatment of viral myocarditis and dilated cardiomyopathy. Antiviral agents should be more extensively investigated for clinical use. The rather discouraging results obtained to date with immunosuppressive agents in the treatment of viral myocarditis indicated the importance of sparing neutralizing antibody production, which may be controlled by B cells, and raised the possibility of promising developments in immunomodulating therapy.
Prospective Study of
Chlamydia pneumoniae
IgG Seropositivity and Risks of Future Myocardial Infarction
Authors: Ridker Paul M. , Kundsin Ruth B. , Stampfer Meir J. , Poulin Sharon , Hennekens Charles H.
Published: June 2012

Background
—
Chlamydia pneumoniae
has been hypothesized to play a role in atherothrombosis. However, prospective data relating exposure to
Chlamydia pneumoniae
and risks of future myocardial infarction (MI) are sparse.

Methods and Results
—In a prospective cohort of nearly 15 000 healthy men, we measured IgG antibodies directed against
Chlamydia pneumoniae
in blood samples collected at baseline from 343 study participants who subsequently reported a first MI and from an equal number of age- and smoking-matched control subjects who did not report vascular disease during a 12-year follow-up period. The proportion of study subjects with IgG antibodies directed against
Chlamydia
increased with age and cigarette consumption. However, prevalence rates of
Chlamydia
IgG seropositivity were virtually identical at baseline among men who subsequently reported first MI compared with age- and smoking-matched control subjects. Specifically, the relative risks of future MI associated with
Chlamydia pneumoniae
IgG titers ≥1:16, 1:32, 1:64, 1:128, and 1:256 were 1.1, 1.0, 1.1, 1.0, and 0.8, respectively (all probability values not significant). There was no association in analyses adjusted for other risk factors, evaluating early as compared with late events, or among nonsmokers. Further, there was no association between seropositivity and concentration of C-reactive protein, a marker of inflammation that predicts MI risk in this cohort.

Conclusions
—In a large-scale study of socioeconomically homogeneous men that controlled for age, smoking, and other cardiovascular risk factors, we found no evidence of association between
Chlamydia pneumoniae
IgG seropositivity and risks of future MI.
Preconditioning in Immature Rabbit Hearts
Authors: Baker John E. , Holman Patricia , Gross Garrett J.
Published: June 2012

Background
—The protective effects of ischemic preconditioning have been shown to occur in adult hearts of all species studied. We determined whether immature hearts normoxic or chronically hypoxic from birth could be preconditioned, the time window or memory of the cardioprotective effect, and the involvement of the K
ATP
channel.

Methods and Results
—Isolated immature rabbit hearts (7 to 10 days old) were subjected to 0, 1, or 3 cycles of preconditioning consisting of 5 minutes of global ischemia plus 10 minutes of reperfusion. This was followed by 30 minutes of global ischemia and 35 minutes of reperfusion. Normoxic hearts (F
io
2
=0.21) subjected to 1 cycle of preconditioning recovered 70±7% of left ventricular developed pressure compared with 43±8% recovery in nonpreconditioned controls. Three cycles of preconditioning did not result in additional recovery (63±8%). Hearts from rabbits raised from birth in hypoxic conditions (F
io
2
=0.12) and subjected to 1 and 3 preconditioning cycles did not show increased recovery (68±8% and 65±5%) compared with nonpreconditioned hypoxic controls (63±9%), although the recovery was greater in chronically hypoxic hearts than in age-matched normoxic controls. Increasing the recovery period after the preconditioning stimulus from 10 to 30 minutes resulted in a loss of cardioprotection. Pretreatment of normoxic hearts for 30 minutes with the K
ATP
channel blocker 5-hydroxydecanoate (300 μmol/L) completely abolished preconditioning (70±7% to 35±9%) but had no effect on nonpreconditioned hearts (40±8%).

Conclusions
—Immature hearts normoxic from birth can be preconditioned, whereas immature hearts hypoxic from birth cannot. Preconditioning in normoxic immature hearts is associated with activation of the K
ATP
channel.
Lack of correlation between serum dopamine-beta-hydroxylase activity and blood pressure in middle-aged men.
Authors: Huttunen J K , Pispa J , Kumlin T , Mattila S , Naukkarinen V , Miettinen T
Published: June 2012

The activity of serum dopamine-beta-hydroxylase (DBH) was measured in 1194 asymptomatic middle-aged men with diastolic blood pressure ranging from 75 to 125 mm Hg during the baseline examination of a multifactorial intervention program for primary prevention of coronary heart disease. No correlation was present between serum DBH activity and systolic (r = -0.01, NS) or diastolic (r = +0.02, NS) blood pressure. No significant differences in serum DBH activity was observed between individuals with blood pressure in the lower, middle or upper deciles. Serum DBH activity was similar in subjects with normal blood pressure, in individuals with widely fluctuating blood pressure and in patients with fixed hypertension. The results suggest that serum DBH activity cannot be used as an aid in the diagnosis of essential hypertension of middle-aged men.
Essential hypertension: an approach to clinical data by the use of models.
Authors: Chau N P , Safar M E , London G M , Weiss Y A
Published: June 2012

A new approach, based on animal circulatory models, was proposed for the study of clinical data in hypertension. Clinical data were identified with steady states in models. From the study of models, possible impairments, susceptible to account for the observed derivations of steady states in men, were analyzed. To be specific, the 1967-Guyton-Coleman model was confronted with a set of data on essential hypertension. The approach afforded a physiological interpretation for statistical results performed on clinical data.
Inhibition of human peptidyl dipeptidase (angiotensin I converting enzyme: kininase II) by human serum albumin and its fragments.
Authors: Klauser R J , Robinson C J , Marinkovic D V , Erdös E G
Published: June 2012

Purified peptidyl dipeptidase (angiotensin I converting enzyme or kininase II) from human lung or hog kidney is inhibited by commercially prepared plasma protein preparations, by human serum albumin and by the additive albumin stabilizer, acetyltryptophan. After the initial steps of purification, albumin was detected by immunodiffusion as a component in human lung peptidyl dipeptidase preparation. Fragment C of albumin (sequence 124-298) is a more potent inhibitor than the parent molecule (Ki = 1.7 X 10(-5)M). Reduction and carboxymethylation of five of the six S-S bridges in Fragment C yield the most potent noncompetitive inhibitor (Ki = 3 X 10(-6)M). Reduction of the sixth bridge raises the K1. This indicates that maintenance of the tertiary structure in Fragment C is of importance for the inhibition. Neither albumin nor Fragment C are substrates of the enzyme. Fragment C and its derivative also inhibit the inactivation of bradykinin by the purified human enzyme and by the peptidyl dipeptidase on the surface of intact cultured human endothelial cells.
Can overnight urine replace 24-hour urine collection to asses salt intake?
Authors: Liu K , Dyer A R , Cooper R S , Stamler R , Stamler J
Published: June 2012

Are overnight urine specimens adequate for characterizing the daily salt intake of individuals, i.e., can the overnight specimen replace the 24-hour specimen? Data from 142 male participants of an ongoing trial on the primary prevention of hypertension were used to examine this question with correlation analysis and quantile classification. Estimated correlation between the true mean 24-hour and the true mean overnight sodium excretion was 0.72. Furthermore, 67% of the individuals in the upper third of the distribution of true mean overnight urine sodium were also in the upper third of the distribution of true mean 24-hour sodium. Thus, these data are promising in regard to the use of overnight urine specimens for characterizing the salt intake of individuals. The number of overnight urine collections required to estimate accurately the correlation between an individual's true mean overnight urine sodium and a variable of interest (e.g., blood pressure) was calculated. Given the observed intra- and inter-individual variation, the data indicate that 14 measurements are needed to limit the diminution of the correlation coefficient to 10%.
Arterial baroreceptor reflex control of sympathetic nerve activity in the spontaneously hypertensive rat.
Authors: Judy W V , Farrell S K
Published: June 2012

The combined and individual carotid sinus and aortic baroreceptor control of sympathetic nerve activity (SNA) and mean arterial pressure (MAP) were studied by direct measurement in groups of spontaneously hypertensive rats (SHR) and normotensive Kyoto Wistar rats (WKY) of 5 to 40 weeks of age. The SHR showed a significantly greater SNA and resultant MAP increase as a function of age compared to that of the WKY rats. Both SHR and WKY rats showed a significant rise in SNA and MAP with ablation of all four major baroreceptors. The proportionate change of SNA and MAP after ablation was greater in the younger SHR than in the younger WKY groups and the change in these decreased as a function of age in the SHR. The reflex inhibition of SNA via baroreceptor stimulation also decreased as a function of age in the SHR, due to a 43% loss of aortic inhibitory function; no significant loss of carotid sinus function was found in either the SHR or WKY. The decrement in aortic function occurred after the rapid phase of blood pressure development; therefore baroreceptor dysfunction cannot be the cause of the high SNA and MAP observed in young SHR. An upward resetting of central sympathetic centers was evaluated via the baroreceptor deafferentation; and it appears that the hyperactive sympathetic nervous system and resultant hypertension in the SHR is due to central resetting of sympathetic centers rather than baroreceptor dysfunction.
Variability in 24-hour urine sodium excretion in children.
Authors: Liu K , Cooper R , Soltero I , Stamler J
Published: June 2012

How many 24-hour urine sodium measurements are adequate for characterizing a child's salt intake? Can overnight urine specimens accurately replace 24-hour collections for salt assessment? A sample of 73 6th-8th grade children was taken from two parochial schools in Chicago to investigate systematically these questions. Seven consecutive 24-hour-urine specimens were collected from each child. The estimated ratio of intra- to inter-individual variances was 1.94 for 24-hour-urine sodium. Based on this value, eight 24-hour specimens are necessary to limit to 10% the diminution of the estimated correlation coefficient between 24-hour-urine sodium and blood pressure. Six measurements are required to reduce to 0.01 the probability of misclassifying a child in tertile 1 versus tertile 3. The overnight specimens show a moderate consistency with the 24-hour collections in detecting children with high or low salt intake. For example 92% and 85% of children in the fifth quintile and the third tertile respectively of the true mean overnight sodium have their true mean 24-hour Na in the upper half of the distribution. These results suggest that in a large scale epidemiologic study, overnight specimens may be reasonable alternatives when 24-hour-urine sodium is practically very difficult to collect.
Renal function curve in patients with secondary forms of hypertension.
Authors: Kimura G , Saito F , Kojima S , Yoshimi H , Abe H , Kawano Y , Yoshida K , Ashida T , Kawamura M , Kuramochi M
Published: June 2012

The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (n = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteronism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 +/- 7 to 113 +/- 7 mm Hg (p less than 0.025) in primary aldosteronism but not in renovascular hypertension (130 +/- 6 to 128 +/- 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated x-intercept of the curve was shifted rightward in both primary aldosteronism (111 +/- 7 vs 87 +/- 4 mm Hg; p less than 0.025) and renovascular hypertension (128 +/- 5 vs 95 +/- 2 mm Hg; p less than 0.025) and the slope was depressed in primary aldosteronism (16 +/- 1 vs 40 +/- 17 [mEq/day]/mm Hg; p less than 0.025) but not in renovascular hypertension (130 +/- 75 vs 40 +/- 13 [mEq/day]/mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
Enhanced risk of coronary heart disease mortality in lean hypertensive men.
Authors: Goldbourt U , Holtzman E , Cohen-Mandelzweig L , Neufeld H N
Published: June 2012

A recently presented hypothesis contends that the excess coronary heart disease mortality associated with hypertension is more prominent in lean men than in overweight men. This hypothesis was addressed using data collected in the Israeli Ischemic Heart Disease Study (n = 10,059). The ratios of age-adjusted 15-year death rates in hypertensive and normotensive men were 4.7, 2.8, 2.0, and 1.9 in the Quetelet index groups of less than 2.29, 2.29 to 2.56, 2.56 to 2.83 and greater than 2.83 g/cm2, respectively. The corresponding ratios for all-cause mortality were 2.2, 2.1, 2.0, and 1.7, respectively. The group with the highest all-cause age-adjusted mortality, at 33.6%, was that of the leanest (less than 2.29 g/cm2, bottom 20% of the Quetelet index distribution) hypertensive subjects. The same group also displayed the highest coronary heart disease mortality (age-adjusted rate, 18.2%). The findings persisted for both smokers and nonsmokers and after exclusion of men with coronary heart disease or diabetics at intake, men on antihypertensive medication, or those who died in the first 2 years of follow-up (1963-1965). A multivariate risk score for developing myocardial infarction was calculated, based on levels of age, systolic blood pressure, total cholesterol, high density lipoprotein cholesterol, cigarette smoking, diabetes mellitus, and Quetelet index. This score varied little across the four Quetelet index groups in hypertensive men: 5-year mean estimated risks of myocardial infarction were between 70 and 74/1000. In normotensive men the scores increased from 19/1000 in the leanest subjects to 29/1000 in the overweight ones.(ABSTRACT TRUNCATED AT 250 WORDS)
Ethanol-induced hypertension involves impairment of baroreceptors.
Authors: Abdel-Rahman A A , Wooles W R
Published: June 2012

We studied the effect of 12 weeks of ethanol feeding on arterial blood pressure and baroceptor reflex control of heart rate in Sprague-Dawley and Wistar rats. Baroceptor reflex sensitivity and pressor responsiveness were evaluated by evoking graded rises in mean arterial pressure with increasing doses of phenylephrine and angiotensin II. After 12 weeks of ethanol feeding there was a modest increase in mean arterial pressure with no change in heart rate in both strains. When angiotensin II or phenylephrine was used as the pressor agent, baroreceptor reflex curves (relationships between changes in mean arterial pressure and heart rate) of Wistar rats were shifted upward and had a markedly reduced slope compared with those of control rats, suggesting that impairment of baroreceptor reflex control of heart rate had occurred. This effect was less evident in the Sprague-Dawley rats. Ethanol-fed rats had a higher sympathetic activity, since beta-blockade with propranolol decreased heart rate to a greater degree than that seen in control rats. The pressor response curve of phenylephrine was shifted to the right in control rats challenged with ethanol (0.5 g/kg), implying the presence of alpha-blockade. This shift was not present in ethanol-fed rats, showing that tolerance had developed to this effect of ethanol. These findings show that attenuation of baroreceptor reflex function is associated with ethanol-induced hypertension but do not establish whether this is a cause or an effect of the developed hypertension.
Renal scintigraphic captopril test in the diagnosis of renovascular hypertension.
Authors: Fommei E , Ghione S , Palla L , Mosca F , Ferrari M , Palombo C , Giaconi S , Gazzetti P , Donato L
Published: June 2012

Angiotensin converting enzyme (ACE) inhibitor-induced renal failure has been reported in bilateral renal artery stenosis and in stenosis in solitary kidneys, but not in unilateral renal artery stenosis. In these patients, however, a functional impairment of the kidney ipsilateral to the stenosis can often be detected after ACE inhibition by scintigraphic techniques employing glomerular radionuclide tracers like 99mTc-diethylenetriamine pentaacetic acid (DTPA). Dynamic renal scintigraphy with 99mTc-DTPA before and 1 hour after administration of captopril, 25 mg (renal scintigraphic captopril test; RSCT), was performed in a selected series of 39 hypertensive subjects with suspected renovascular hypertension. Changes in glomerular filtration rate induced by captopril on the individual kidney were estimated by assessing the early (120-180 seconds) DTPA uptake by the kidney. Values were expressed as the ratio between the kidney with the lower uptake and the contralateral one in 34 patients and as the ratio of the kidney counts to the injected dose in five patients with solitary kidneys, aortic coarctation, or both. Compared with precaptopril values, postcaptopril uptake decreased markedly in 14 subjects (-62.42 +/- 30.94 [SD]%; range, -25 to -100%) and decreased modestly or even increased in the other 25 (+0.57 +/- 9.83%; range, +28 to -13%). Of the 14 subjects considered to be RSCT-positive diagnostic workup revealed either established (10) or strongly suspected (2) renal artery stenosis in 12 and aortic coarctation in 2 subjects. In another patient with established renovascular hypertension, results of the RSCT were negative when performed in the supine position but became positive when repeated in the sitting position.(ABSTRACT TRUNCATED AT 250 WORDS)
Pressure dependence of atrial natriuretic peptide during norepinephrine infusion in humans.
Authors: Uehlinger D E , Zaman T , Weidmann P , Shaw S , Gnädinger M P
Published: June 2012

The relative contribution of increased blood pressure (BP) or norepinephrine (NE), or both, to the stimulatory effect of an NE pressor infusion on circulating immunoreactive atrial natriuretic peptide (ANP) was evaluated in 10 healthy young men. They were studied during an infusion of NE, which was applied initially alone and then in combination with sodium nitroprusside. NE infusion rate was increased in four 30-minute intervals to a final dose of 200 ng/kg body weight per minute, leading to 12-fold higher plasma NE levels than were seen during control conditions. This increased mean BP (from a mean basal value of 94 +/- 3 to 119 +/- 4 [SEM] mm Hg; p less than 0.001) and plasma immunoreactive ANP (from 50 +/- 7 to 112 +/- 17 pg/ml; p less than 0.001), whereas heart rate decreased (p less than 0.001). The NE infusion was continued at the highest dose and an additional infusion of sodium nitroprusside was started to titrate mean BP in 30-minute intervals down to control values; a mean sodium nitroprusside dose of 0.95 micrograms/kg/min restored mean BP to 93 +/- 4 mm Hg (p less than 0.001), decreased plasma immunoreactive ANP to basal values (51 +/- 4 pg/ml; p less than 0.001), increased heart rate (p less than 0.001), and left plasma levels of NE largely unchanged. Plasma protein and hematocrit rose about 5 to 6% (p less than 0.001) during the NE infusion and then decreased about 3 to 4% (p less than 0.001 and p less than 0.01) when sodium nitroprusside was added.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood pressure response to potassium supplementation in normotensive adults and children.
Authors: Miller J Z , Weinberger M H , Christian J C
Published: June 2012

To investigate the effect on blood pressure of a modest increase in dietary potassium intake, 38 healthy, free-living families were enrolled in a study involving 4 weeks of potassium supplementation. This was preceded by collection of five baseline measurements of blood pressure and urinary electrolyte excretion and followed by a 4-week recovery period. Although there was a significant increase in urinary potassium excretion during supplementation in both adults and children (p less than 0.001), there were no significant changes in systolic, diastolic, or mean arterial blood pressure. Height and weight increased significantly in children (p less than 0.001), and weight increased in adults (p less than 0.01) over the course of the study. Multivariate analysis of variance of blood pressure controlling for these confounding variables failed to reveal any effect of the potassium supplementation on blood pressure. These results suggest that increasing intake of dietary potassium alone in a healthy, free-living normotensive population is unlikely to have a discernible effect on blood pressure.
Isolation of renin-rich rat kidney cells.
Authors: Johns D W , Carey R M , Gomez R A , Lynch K , Inagami T , Saye J , Geary K , Farnsworth D E , Peach M J
Published: June 2012

Enzymatic dispersion and density gradient (Percoll) sedimentation were used to isolate a population of renin-containing, granule-laden cells (density 1.067 g/ml) from rat kidney cortex. Using immunohistochemistry (light microscopy) and electron microscopy, we defined the presence and ability of these cells to store renin protein(s). A 1000 base pair rat renin complementary DNA was used to show that these cells express the renin gene. The reverse hemolytic plaque assay defined the functional properties of the renin-containing cell. The data are consistent with the postulated inverse relationship between calcium concentration and release of renin. Thus, we have isolated a population of functional rat kidney cells that synthesize, store, and release renin.
Intracellular sodium and the response to nitrendipine or atenolol in African blacks.
Authors: M'Buyamba-Kabangu J R , Lepira B , Lijnen P , Tshiani K , Fagard R , Amery A
Published: June 2012

The relationship between the hypotensive effect of nitrendipine (N), 20 mg/day (n = 17), or atenolol (A), 100 mg/day (n = 17), and the erythrocyte sodium [( Na]i) and potassium [( K]i) concentrations was investigated in hypertensive African blacks during a randomized double-blind study. After 6 weeks, both treatments significantly reduced supine and standing blood pressures; however, the magnitude of the decrease in supine systolic (-22.0 +/- 2.0 vs -12.1 +/- 3.4 mm Hg) and diastolic (-14.1 +/- 1.3 vs -7.6 +/- 2.1 mm Hg) pressures and in standing diastolic pressure (-16.0 +/- 1.7 vs -9.2 +/- 2.0 mm Hg) was more pronounced (p less than 0.05) in the N-treated than in the A-treated group. Pulse rate, plasma aldosterone, and plasma renin activity were lower (p less than 0.05) in the A-treated patients. Neither treatment had significant influence on [Na]i, [K]i, or ouabain-sensitive sodium efflux. The N-induced changes in supine systolic and diastolic pressure correlated (p less than 0.05) with age (r = -0.65 and r = -0.58, respectively) and pretreatment plasma renin activity (r = 0.71). Multiple regression analysis demonstrated a negative association between pretrial [Na]i and the change in systolic pressure during N treatment that was independent of age, pretreatment blood pressure, and change in pulse rate. Age and the change in supine pulse rate were also independently correlated with the change in diastolic pressure during N treatment. The results show a greater antihypertensive efficacy of N than A in the patients entered in this study and suggest that a higher intracellular sodium concentration could predict a better hypotensive response to N.
Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.
Authors: Grassi G , Giannattasio C , Saino A , Sabadini E , Capozi A , Sampieri L , Cuspidi C , Mancia G
Published: June 2012

Cardiopulmonary receptors modulate renin release in several animals species. However, their involvement in reflex control of this humoral substance in humans is controversial. Furthermore, no information is available on the alteration of this control in hypertension. We studied the modulation of plasma renin activity (radioimmunoassay) in 12 normotensive subjects and in 12 age-matched subjects with untreated hypertension of mild or moderate degree. Cardiopulmonary receptors were stimulated by increasing central venous pressure (right atrial catheter) and cardiac volume (echocardiographic measurement) through passive leg raising and deactivated by reducing central venous pressure and cardiac volume through lower body negative pressure. The stimuli were maintained for 20 to 30 minutes, and their degree was set to avoid changes in blood pressure (indirect or direct measurements) and heart rate, thus avoiding involvement of arterial baroreceptors. In normotensive subjects, deactivation of cardiopulmonary receptors induced a progressive rise in plasma renin activity and stimulation of cardiopulmonary receptors induced a progressive fall. The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation. During cardiopulmonary receptor deactivation, the gain corresponded to that obtained by dividing the increase in plasma renin by the reduction in central venous pressure induced by tilting. Cardiopulmonary receptor deactivation and stimulation also induced clear-cut changes in plasma renin activity in hypertensive subjects, but the percent magnitude of the reflex plasma renin activity excursion was less than that in normotensive subjects. These observations indicate that cardiopulmonary receptors modulate plasma renin activity in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
The differential effect of aldosterone and dexamethasone on pressor responses in adrenalectomized rats.
Authors: Yagil Y , Krakoff L R
Published: June 2012

The effect of selective glucocorticoid or mineralocorticoid replacement on pressor responses to angiotensin I and II and norepinephrine was studied in adrenalectomized rats given high salt intake. Four groups were prepared by 1) adrenalectomy only (n = 5); 2) adrenalectomy plus aldosterone, 6 micrograms/24 hr i.p. (n = 5); or 3) adrenalectomy plus dexamethasone, 10 micrograms/24 hr i.p. (n = 5), using miniosmotic pumps; and 4) sham adrenalectomy (controls; n = 5). Plasma corticosterone was undetectable in all three adrenalectomized groups. Plasma aldosterone concentration was similar in aldosterone-replaced and sham-operated controls. Pressor responses to various doses of angiotensin I, angiotensin II, and norepinephrine were determined in unanesthetized, undisturbed rats. Compared with both control and dexamethasone-replaced rats, pressor responses to all three agonists were significantly reduced in both nonreplaced adrenalectomized and aldosterone-replaced groups. Comparing the ratios of the pressor responses to angiotensin I and angiotensin II in the four groups over the entire dose range suggests that a greater fraction of injected angiotensin I was converted to angiotensin II in nonreplaced adrenalectomized rats than in the other three groups. We conclude that glucocorticoid action markedly contributes to the systemic pressor effect of angiotensin and norepinephrine. However, glucocorticoid deficiency does not impair in vivo conversion of angiotensin I to angiotensin II.
Local generation and release of angiotensin II in peripheral vascular tissue.
Authors: Mizuno K , Nakamaru M , Higashimori K , Inagami T
Published: June 2012

Isolated rat hindlegs were perfused with Krebs-Ringer solution, and immunoreactive angiotensin II (irAng II) released into the perfusate was directly determined using a Sep-Pak C18 cartridge connected to the perfusion system. High performance liquid chromatography clearly demonstrated the presence of angiotensin I (Ang I), angiotensin II (Ang II), and a small amount of angiotensin III. The spontaneous release of irAng II was as high as about 600 pg/30 min, which was stable up to 3 hours. Captopril added to the perfusion medium (10(-9) to 10(-6) M) suppressed irAng II release in a dose-dependent manner (p less than 0.001), and it (10(-6)M) caused a reciprocal increase of irAng I release (p less than 0.05). Oral pretreatment of captopril (50 mg/kg/day) for 1 week suppressed the irAng II release by 31% (p less than 0.02). The same treatment with SA 446, a highly lipophilic angiotensin converting enzyme inhibitor, inhibited the irAng II release by 63% (p less than 0.001). On the other hand, the two inhibitors suppressed the plasma irAng II to very similar extents. Pretreatment with SA 446 plus nephrectomy did not cause any further change in irAng II release as compared with that with SA 446 alone. These results provide direct proof for local generation and subsequent secretion of Ang II by peripheral vascular tissue.
Inhibition of tissue angiotensin converting enzyme. Quantitation by autoradiography.
Authors: Sakaguchi K , Chai S Y , Jackson B , Johnston C I , Mendelsohn F A
Published: June 2012

Inhibition of angiotensin converting enzyme (ACE) in serum and tissues of rats was studied after administration of lisinopril, an ACE inhibitor. Tissue ACE was assessed by quantitative in vitro autoradiography using the ACE inhibitor [125I]351A, as a ligand, and serum ACE was measured by a fluorimetric method. Following oral administration of lisinopril (10 mg/kg), serum ACE activity was acutely reduced but recovered gradually over 24 hours. Four hours after lisinopril administration, ACE activity was markedly inhibited in kidney (11% of control level), adrenal (8%), duodenum (8%), and lung (33%; p less than 0.05). In contrast, ACE in testis was little altered by lisinopril (96%). In brain, ACE activity was markedly reduced 4 hours after lisinopril administration in the circumventricular organs, including the subfornical organ (16-22%) and organum vasculosum of the lamina terminalis (7%; p less than 0.05). In other areas of the brain, including the choroid plexus and caudate putamen, ACE activity was unchanged. Twenty-four hours after administration, ACE activity in peripheral tissues and the circumventricular organs of the brain had only partially recovered toward control levels, as it was still below 50% of control activity levels. These results establish that lisinopril has differential effects on inhibiting ACE in different tissues and suggest that the prolonged tissue ACE inhibition after a single oral dose of lisinopril may reflect targets involved in the hypotensive action of ACE inhibitors.
Stress increases renal nerve activity and decreases sodium excretion in Dahl rats.
Authors: Koepke J P , Jones S , DiBona G F
Published: June 2012

The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, renal sympathetic nerve activity, and renal function were examined in conscious Dahl salt-sensitive (DS) and Dahl salt-resistant rats (DR) on low (0.4%) and high (8%) NaCl diets. Air stress increased renal sympathetic nerve activity and decreased urine flow rate and urinary sodium excretion in conscious Dahl rats on a high sodium diet, but it had no effect in rats on a low sodium diet. Mean arterial pressure did not change during air stress in any group. Renal denervation prevented the antidiuretic and antinatriuretic responses to air stress in DS and DR on a high NaCl diet. An increased renal tubular reabsorption of sodium and water appeared to mediate the antinatriuretic and antidiuretic responses to air stress, since glomerular filtration rate and renal plasma flow were unchanged. Thus, environmental stress increases renal sympathetic nerve activity and decreases urinary sodium excretion more in Dahl rats on a high NaCl diet than on a low NaCl diet. On a high NaCl diet, these responses are greater in DS than in DR.
Effects of moderate hypertension on cardiac function and metabolism in the rabbit.
Authors: Taegtmeyer H , Overturf M L
Published: June 2012

To study the early effects of hypertension on the heart, we examined isolated hearts from rabbits with slowly developing hypertension of up to 64 weeks in duration after unilateral nephrectomy and renal artery stenosis. Normotensive animals kept under identical conditions served as controls. Mean arterial blood pressure rose from 83 to 155 mm Hg in the hypertensive group of longest duration, but the ratio of left ventricular weight to body weight was not different between the experimental and control groups. Although left ventricular hypertrophy was not present, left ventricular peak systolic pressure of perfused hearts was significantly higher in hypertensive than in normotensive hearts. Furthermore, while in hypertensive hearts the left ventricular end-diastolic volume was increased, the peak systolic pressure did not respond to an increase in left ventricular end-diastolic volume. Functional changes were accompanied by metabolic changes in the left ventricle. Rates of glucose utilization were increased and rates of ketone body utilization were decreased in hypertensive hearts. Activities of key enzymes of carbohydrate metabolism (phosphorylase, hexokinase, phosphofructokinase, and lactate dehydrogenase) were increased, while those of ketone body metabolism (3-oxoacid-CoA transferase, acetoacetyl-CoA synthase) were decreased and those of the citric acid cycle (citrate synthase, 2-oxoglutarate dehydrogenase) were not different between groups. In summary, moderate hypertension for a period of more than 1 year resulted in functional and metabolic changes of the left ventricle in hypertensive animals that were already manifest at 8 weeks of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypotensive action of parathyroid hormone in hypoparathyroid and hyperparathyroid rats.
Authors: Baksi S N
Published: June 2012

Experimental and clinical data suggest an association between chronic hyperparathyroidism and hypertension, but acute infusion of parathyroid hormone causes vasodilation and hypotension. These observations imply that chronic and acute parathyroid states affect blood pressure through different mechanism(s), either by modification of vascular receptors or by an ionophoretic effect of parathyroid hormone. The effect of parathyroid status induced by dietary calcium manipulations or by surgical ablation of the parathyroid gland on the hypotensive response of parathyroid hormone infusion was studied in rats. At 4 weeks of age 24 male rats were divided into four equal groups. Three groups were sham-operated, and one group was thyroparathyroidectomized. Only the thyroparathyroidectomized group was treated with thyroxine, 10 micrograms/kg/day. The control and thyroparathyroidectomized groups were raised on a 1.4% calcium diet; the other two groups were raised on 0.005% and 2.8% calcium diets. After 8 weeks on the diets, parathyroid hormone was infused through a venous cannula at 5 and 10 micrograms/kg doses and blood pressure was measured through arterial cannulas. The results indicate that hyperparathyroidism and hypocalcemia induced by the low calcium diet attenuated the hypotensive response to parathyroid hormone compared with responses in rats raised on a 1.4% calcium diet. In hypoparathyroid rats (2.8% Ca diet) with hypercalcemia, the hypotensive response was also reduced. However, in hypoparathyroid (thyroparathyroidectomized) rats with hypocalcemia, the hypotensive response was enhanced. The data suggest that chronic parathyroid status, as well as hypercalcemia, alters the hypotensive response to parathyroid hormone infusion, presumably by altering the vascular parathyroid hormone receptors or by some other mechanism.
The reproducibility of average ambulatory, home, and clinic pressures.
Authors: James G D , Pickering T G , Yee L S , Harshfield G A , Riva S , Laragh J H
Published: June 2012

The reproducibility of ambulatory, home, and clinic blood pressures was compared in 13 untreated mildly hypertensive and 14 normotensive subjects. Each subject had two sets of daily ambulatory recordings, home self-measured readings (over 6 days), and clinic measurements taken 2 weeks apart. Comparisons over the 2 weeks within and among the methods of measurements were made using a repeated-measures analysis of variance. The results showed that there was no consistent average change in the ambulatory or home pressures and no change in clinic diastolic pressures, but the clinic systolic pressure of the hypertensive subjects dropped 6 mm Hg (p less than 0.05), while that of the normotensive subjects showed no significant change. Test-retest correlations of each of the three methods were similar in magnitude, indicating a similar level of reliability. Test-retest correlations of the ambulatory standard deviations, however, were low, indicating a low reliability of this measure of daily pressure variability. These results suggest that the reproducibility of ambulatory pressures may be as good or better than that of home or clinic measurements. They also suggest that the average ambulatory pressure may be preferable as the measurement in clinical trials, since it may be less influenced by measurement anxiety, particularly in hypertensive subjects.