bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reflex Control of Sympathetic Nerve Activity and Heart Rate from Arterial Baroreceptors in Conscious Spontaneously Hypertensive Rats
Authors: Ricksten S. E. , Thorén P. 
Published: August 2015

1. Mean arterial pressure (MAP), heart rate (HR) and splanchnic sympathetic nerve activity were recorded in conscious, 4 months old, male spontaneously hypertensive rats (SHR; n = 9) and matched normotensive Wistar—Kyoto (WKY) rats (n = 8).
2. The reflex bradycardia and reflex inhibition of splanchnic sympathetic nerve activity were studied in each animal during baroreceptor activation. MAP was raised 30–50 mmHg above control with slow, intra-arterial infusion of noradrenaline (1 μg min−1 kg−1 body wt.). There was a significant negative linear correlation between MAP and splanchnic nerve activity and between MAP and HR in all experiments during noradrenaline infusion.
3. The baroreceptor sensitivity with respect to heart rate control was greatly reduced in SHR compared with WKY rats, being 1.5 ± 0.1 beats min−1 mm−1 Hg and 3.7 ± 0.4 beats min−1 mm−1 Hg respectively (P &lt; 0.001).
4. However, baroreceptor sensitivity with respect to control of splanchnic nerve activity, defined as percentage nerve inhibition per mmHg of MAP rise, did not differ statistically between the two groups: 1.8 ± 0.2%/mmHg for SHR and 2.0 ± 0.3%/mmHg for WKY rats.
5. It is suggested that the baroreceptor control of sympathetic ourflow is intact in conscious 4 months old SHR with early established hypertension.
6. It is also suggested that the impaired baroreceptor control of heart rate seen in SHR, and in human essential hypertension, is mainly due to an increased activity of the hypothalamic ‘defence area’, which can selectively block the efferent vagal component of the reflex bradycardia elicited from baroreceptor activation.
Regression of the Baroreceptor Resetting in Hypertension of Long Duration in Rats
Authors: Sumitani Marie , Krieger E. M. 
Published: August 2015

1. The extent of reversal of baroreceptor resetting after pressure normalization was studied in rats with renal hypertension of up to 6 months duration. The aortas of these rats when compared with those of 2 month hypertensive rats were thicker (44%) and had a larger calibre (29%).
2. The more severe morphological alterations found in the 6 month hypertensive rats did not interfere with the reversibility of the resetting process. The entire range of pressure for baroreceptor activation showed a small downward displacement after 1 h and was functioning at a completely normal pressure 6 h after pressure normalization.
3. The data show that reversal of resetting from hypertension is a very rapid process that is independent of the duration of hypertension and the severity of morphological lesions. Moreover, they indicate that reversal is a permanent phenomenon because it was also observed after 2 days of pressure normalization.
Role of the Sympathetic Nervous System in Spontaneous Hypertension: Changes in Central Adrenoceptors and Plasma Catecholamine Levels
Authors: Palermo Anna , Costantini Carlo , Mara Gabriele , Libretti Arnaldo 
Published: August 2015

1. There is evidence that dysfunction of central adrenergic neurons and the peripheral sympathetic nervous system are implicated in the development and maintenance of spontaneous hypertension.
2. Accordingly adrenoceptors of brain areas related to cardiovascular control (hypothalamus and lower brain stem) and plasma catecholamine levels were measured in male spontaneously hypertensive rats and in their normotensive Wistar-Kyoto controls at 11 weeks of age.
3. Assays of β, α1, and α2 receptor binding were performed by using respectively [3H]-dihydroalprenolol, [3H]clonidine and 3H-labelled WB4101 as ligand. Plasma catecholamines were assessed by high performance liquid chromatography with electrochemical detection.
4. No difference was observed on β-receptor binding sites in the two animal groups. On the other hand, α2 receptors were increased by 29% in the lower brain stem and α1 receptors showed an increase of 46% in the hypothalamus of the hypertensive rats. By Scatchard plot analysis, these changes were attributable to variations in the number rather than in the affinity of binding site.
5. Plasma noradrenaline levels were more elevated in the hypertensive rats, and no difference was observed in plasma adrenaline concentrations.
6. The increase in hypothalamic α1 receptors and the probably compensatory increase in lower brain stem α2 receptors suggest enhanced stimulation of the vasomotor centre. Hyperactivity of the peripheral sympathetic nervous system in spontaneous hypertension could therefore be secondary to a dysfunction of central adrenergic neurons projecting to the vasomotor centre of the brain stem.
Heterogeneity of Human Vascular Pre- and Post-Synaptic α-Adrenoceptors
Authors: Stevens M. J. , Rittinghausen R. E. , Moulds R. F. W. 
Published: August 2015

1. The effects of various α-receptor agonists and antagonists on pre- and post-synaptic α-receptors of human isolated digital arteries and metacarpal (or metatarsal) veins have been studied.
2. The relative potency of phenylephrine compared with noradrenaline on the postsynaptic receptors was significantly greater in arteries than in veins.
3. The rank order of potency of various α-agonists on postsynaptic receptors was the same in arteries and veins except that in veins adrenaline was more potent than clonidine, whereas the reverse was the case in arteries.
4. Phentolamine showed no selectivity in either antagonizing postsynaptic responses or enhancing stimulation-induced transmitter release by antagonism at presynaptic α-receptors.
5. Yohimbine potently, but not selectively, antagonized postsynaptic responses to noradrenaline and phenylephrine in both arteries and veins, and enhanced stimulation-induced transmitter release to a greater extent in arteries than in veins.
6. Prazosin reduced the maximum response to noradrenaline (but not phenylephrine) to a significantly greater extent in veins than in arteries, and in veins alone shifted the phenylephrine curve to a greater degree than it did the noradrenaline curve. Prazosin did not significantly increase stimulation-induced transmitter release in either arteries or veins.
7. Phenoxybenzamine produced large increases in stimulation-induced tritium outflow which were significantly greater in arteries than in veins (even in the presence of cocaine).
8. It is concluded firstly that the postsynaptic α-adrenoceptors of these tissues are not a homogeneous population and that differing proportions of these receptors are present in the digital arteries and the metacarpal veins, and secondly that the sensitivities of the presynaptic α-adrenoceptors in the two tissues may also be different.
A Monoclonal Antibody for Immunopurification of Human Renin
Authors: Pau B. , Simon D. , Galen F. X. , Devaux C. , Soubrier F. , Ménard J. , Corvol P. 
Published: August 2015

1. A mouse hybridoma secreting an antibody directed against human renin was obtained by fusion of spleen cells with NS 1 myeloma cells. This monoclonal antibody recognizes human and monkey renins but neither hog nor mouse renins nor the acid proteinase cathepsin D.
2. Monoclonal antibody was coupled to Sepharose 4 B. The immunoadsorbent thus obtained was very efficient in purifying both active and inactive human renin from renal or extrarenal sources.
3. Renin enrichment up to 3500-fold was obtained in a single step.
Immunological and Immunofluorescent Studies of Human Angiotensin-Converting Enzyme
Authors: Takada Yasuharu , Unno Masazumi , Hiwada Kunio , Kokubu Tatsuo 
Published: August 2015

1. Human angiotensin-converting enzyme from kidney, lung, small intestine, plasma and urine was found to be immunologically indistinguishable by double immunodiffusion and inhibition of enzyme activity with specific anti-(human kidney enzyme) antibody.
2. Partial inhibition of the enzyme activities from hog, dog and rat sera by the antibody was found, but no inhibition was observed in the enzymes from sheep and bovine sera.
3. Human angiotensin-converting enzyme was located in two types of cells by an immunofluorescent technique using the purified antibody and fluorescein-labelled anti-(rabbit immunoglobulin) antibody. These were the vascular endothelial cells of alveolar capillaries and of pulmonary interstitial small vessels, and the epithelial cells of proximal tubules in the kidney and of mucous membrane in the small intestine.
Relationship between Plasma Renin and Cortisol in Hypertensive Patients
Authors: Atlas S. A. , Case D. B. , Sealey Jean E. , Laragh J. H. 
Published: August 2015

1. Plasma cortisol at 08.00 hours was significantly higher (P &lt; 0.005) in patients with high-renin essential or renovascular hypertension (22.6 ± 1.6 μg/100 ml) than in patients with normal-renin (15.4 ± 1.2) or low-renin (11.9 ± 1.2) forms of hypertension.
2. Plasma cortisol at 12.00 or 16.00 hours did not differ significantly among the three groups; thus the diurnal swing in plasma cortisol was steepest in patients with high plasma renin.
3. Among all patients studied, there was a direct relationship between 08.00 hours plasma cortisol and ambulatory plasma renin activity (r = 0.65, P &lt; 0.001).
4. In patients with high-renin values, 08.00 hours plasma cortisol fell by 39 ± 6% after 10 days treatment with the converting enzyme inhibitor captopril. No consistent decreases were observed in the normal- or low-renin groups.
5. We conclude that the renin—angiotensin system may interact with the pituitary—adrenal axis to influence circulating levels of cortisol. This effect might conceivably contribute to the pathogenesis of certain high-renin states.
ACTH Stimulates Plasma Renin and Angiotensin II in Man
Authors: Oelkers W. , Köhler A. , Belkien L. , Fuchs-Hammoser R. , Maiga M. , Scherer B. , Weber P. C. 
Published: August 2015

1. Adrenocorticotropic hormone (ACTH; 10 i.u./day) was infused for 34 h into normal male subjects. Some subjects were additionally treated with propranolol or indomethacin. Others received sham infusions or hydrocortisone infusions instead of ACTH.
2. ACTH, but not sham or hydrocortisone infusions, led to a significant increase in plasma renin activity and angiotensin II concentration with a lag period of 7–10 h and a maximum response after 24 h. ACTH may be a physiological regulator of renin secretion, perhaps through a ‘trophic’ effect on the juxtaglomerular apparatus.
3. The effect of ACTH on renin is not mediated by a rise in plasma renin substrate, probably not by renal β-adrenoreceptors, but perhaps by prostaglandins.
4. A dissociation between plasma cortisol and aldosterone during ACTH infusion suggests that ACTH, in this dosage, stimulates aldosterone on the second day through renin and angiotensin II, before its secretion is finally suppressed during more prolonged infusion.
Two Forms of Plasma Renin after Activation In Vitro and their Relation to Natural Plasma Renin
Authors: Derkx F. H. M. , Schalekamp M. P. A. , Schalekamp M. A. D. H. 
Published: August 2015

1. Inactive renin in human plasma can be activated by pH 3.3-dialysis (generation of acid-activated renin), by clotting factor XII-mediated prekallikrein to kallikrein conversion after pH has been restored to neutral (generation of acid-kallikrein-activated renin) or by the addition of trypsin (generation of trypsin-activated renin).
2. Natural active renin, acid-kallikrein-activated renin and trypsin-activated renin behave similarly during affinity chromatography on Blue-Sepharose CL-6B and during gel filtration on Sephadex G-100. They also show similar reaction kinetics with similar pH-optimum curves when acting on sheep renin substrate.
3. Acid-activated renin is different. It is retained on Blue-Sepharose columns and it is inactivated at neutral pH during incubation at 37°C. This contrasts with the other forms of renin activated in vitro and with natural active renin. The pH-optimum curve of acid-activated renin, when acting on sheep renin substrate, is also different from that of the other forms of active renin.
4. It is to be proven that the renins generated in vitro by neutral serine proteinases are identical with natural active renin, but clearly they bear more resemblance to natural renin than acid- activated renin does. Our preliminary conclusion is that acid-activated renin is a ‘laboratory renin’, which does not circulate in normal peripheral venous plasma.
α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man
Authors: Morganti A. , Sala Carla , Palermo Anna , Turolo Lucia , Zanchetti A. 
Published: August 2015

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade.
2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin.
3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.
Chemical Renal Medullectomy; Effect upon Reversal of Two-Kidney, One-Clip Hypertension in the Rat
Authors: Bing R. F. , Russell G. I. , Swales J. D. , Thurston H. , Fletcher A. 
Published: August 2015

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold.
2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter.
3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated.
4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.
β-Endorphin, An Endogenous Depressor Agent in the Rat?
Authors: Petty M. A. , Sitsen J. M. A. , De Jong W. 
Published: August 2015

1. The role of opiates in cardiovascular regulation has been investigated.
2. In urethane-anaesthetized renal hypertensive rats (two-kidney, one-clip Goldblatt model), intracerebroventricular β-endorphin (10 μg) caused a greater fall in mean arterial pressure than in sham-operated controls.
3. Unilateral injection of β-endorphin into the nucleus tractus solitarii of the urethane-anaesthetized rat resulted in a U-shaped dose—response relationship, with a fall in mean arterial pressure and heart rate occurring at low doses. Doses above 10 ng caused a rise in pressure, accompanied by a variable effect on heart rate.
4. The fall in blood pressure and heart rate was prevented by prior subcutaneous administration of naloxone. Naloxone caused an increase in blood pressure when administered alone.
5. These results suggest a depressor role of an endogenous brain opiate, possibly β-endorphin; a site of action is probably the nucleus tractus solitarii.
Central Peptidergic Stimulation in Blood Pressure Control: Role of Enkephalins in Rats
Authors: Yukimura T. , Unger T. , Rascher W. , Lang R. E. , Ganten D. 
Published: August 2015

1. The central blood pressure effects of the enkephalin analogue, d-Ala2-Met-enkephalin were investigated in normotensive rats and in spontaneously hypertensive rats.
2. In conscious Wistar rats, injection of 1.7, 17 and 170 nmol of d-Ala2-Met-enkephalin into the lateral brain ventricle produced dose-dependent blood pressure increases of 5.3 ± 1.8, 10.5 ± 2.8 and 15.3 ± 3.0 mmHg respectively. In contrast, in α-chloralose-anaesthetized rats, the same doses of the enkephalin analogue produced dose-dependent blood pressure falls of −8.9 ± 1.9, −11.1 ± 5.2 and −19.8 ± 8.4 mmHg.
3. The pressor responses to 170 nmol of d-Ala2-Met-enkephalin were blocked by intracerebroventricular pretreatment with the opiate receptor antagonists diprenorphine and naloxone at doses of 10–500 nmol. The depressor effects under anaesthesia were blocked by diprenorphine (10–100 nmol) but not by naloxone.
4. Spontaneously hypertensive rats showed enhanced pressor responses to centrally applied enkephalin when compared with normotensive rats.
5. Central injection of diprenorphine alone produced an initial short blood pressure increase followed by a long-lasting blood pressure fall, which was significantly greater in spontaneously hypertensive rats than in normotensive rats.
6. The results indicate that the central blood pressure effects of enkephalins depend on the state of consciousness and are mediated through naloxone- and diprenorphine-sensitive opioid receptors.
7. The increased sensitivity to centrally applied enkephalins and the depressor responses to the intracerebroventricular injection of diprenorphine suggest a central enkephalinergic contribution to the maintenance of hypertension in spontaneously hypertensive rats.
Does Long-Term Low-Dose Corticosteroid Therapy Cause Hypertension?
Authors: Jackson S. H. D. , Beevers D. G. , Myers K. 
Published: August 2015

1. One hundred and ninety-five patients undergoing low-dose prednisone or prednisolone therapy were investigated. Blood pressure, weight, serum urea, sodium and potassium were recorded before therapy and again after at least 1 year of therapy.
2. The rise in both mean systolic and mean diastolic blood pressure was paralleled by an increase in the prevalence of arbitrarily defined hypertension.
3. There was no relationship between change of blood pressure and either dose of corticosteroid or duration of therapy. Blood pressure before therapy was the main determinant of the change in blood pressure.
4. Mean serum sodium levels rose slightly but serum potassium levels did not change during the follow-up period. There was no significant weight gain.
5. These results indicate that treatment of asthma and rheumatoid arthritis with prednisolone or prednisone in low dose does not cause hypertension or biochemical features suggestive of mineralocorticoid excess.
Neurohumoral Response to Hospitalization in Hypertensive Patients
Authors: De Leeuw P. W. , Van Soest G. A. W. , Punt R. , Hoogma R. P. L. M. , Smout A. J. P. M. , Birkenhäger W. H. 
Published: August 2015

1. To investigate whether reduced activity of pressor systems could explain the spontaneous drop in pressure upon hospitalization, 51 subjects with uncomplicated essential hypertension were admitted to hospital. Sodium intake was fixed at 55 mmol/day.
2. Blood samples for noradrenaline, adrenaline, active renin, angiotensin II and aldosterone were drawn on each morning of the first 3 days of hospitalization; blood pressure was measured at 2 h intervals and values were averaged for each day.
3. Subjects were divided in two groups depending on whether they became normotensive (group 1; n = 12) or remained hypertensive (group 2; n = 39). This distinction was thought to reflect mild and more severe hypertensive groups respectively.
4. Although both groups showed a comparable fall in blood pressure during hospitalization, noradrenaline levels fell more consistently in group 1, whereas adrenaline levels fell only in group 2. The components of the renin—angiotensin—aldosterone system rose, but more conspicuously in group 1.
5. It is concluded that withdrawal of sympathetic activity can only partly explain the hypotensive response to hospitalization. The renin—angiotensin system behaves only passively and appears to be counterproductive to alterations in blood pressure.
Metoprolol and Pindolol in Hypertension: Different Effects on Peripheral Haemodynamics
Authors: Svensson A. , Gudbrandsson T. , Sivertsson R. , Hansson L. 
Published: August 2015

1. Thirty-six patients with essential hypertension, were randomly allocated to double-blind treatment with either metoprolol (100–200 mg/day) or pindolol (5–10 mg/day). The effects upon blood pressure and peripheral blood flow were determined. Both drugs reduced blood pressure significantly.
2. Heart rate was significantly reduced by metoprolol but not by pindolol.
3. Vascular resistance at maximal dilatation was not changed by either compound.
4. At rest, pindolol reduced vascular resistance in the calf by 14% (P &lt; 0.05) but metoprolol tended to increase the resistance slightly. The difference in effect was also significant (P &lt; 0.005).
5. During leg muscle work there were no changes in vascular resistance in the forearm with either compound.
6. We conclude that pindolol appears to reduce blood pressure at least partly through vascular mechanisms, in contrast to metoprolol. The response to sympathetic stimulation induced by physical exercise does not differ between metoprolol- and pindolol-treated patients.
β-Receptor-Blocking Agents May Reverse or Prevent Diuretic-Induced Increases in Serum Low-Density Lipoprotein Cholesterol
Authors: Meier A. , Schiffl H. , Weidmann P. , Mordasini R. , Riesen W. , Bachmann C. 
Published: August 2015

1. The effect of treatment with a thiazide-like diuretic alone or combined with a β-adrenoceptor blocker on serum lipoproteins was investigated in 35 patients with essential hypertension.
2. In group I (18 patients), serum low-density lipoprotein cholesterol was increased (P &lt; 0.001) during monotherapy with chlorthalidone (100 mg/day) but not during combined chlorthalidone-β-blocker therapy.
3. This tendency was similar in subgroups studied with an inverse sequence of drug administration. In subgroup IA (11 men), a 22% increase (P &lt; 0.01) in low-density lipoprotein cholesterol after 6 weeks of chlorthalidone was reversed after use of a β-blocker as well as chlorthalidone; in subgroup IB (five men, two post-menopausal women), low-density lipoprotein cholesterol was increased by 41% (P &lt; 0.05) above placebo values 6 weeks after withdrawal of the β-blocker from combination therapy.
4. In group II (18 men), low-density lipoprotein cholesterol was increased by 13% (P &lt; 0.025) after 4 weeks of monotherapy with clopamide (5 mg/day) but restored to control levels 4 weeks after addition of pindolol (10 mg/day).
5. No significant changes occurred during any treatment phase in high-density lipoprotein cholesterol.
6. Certain β-receptor blocking agents may prevent or reverse diuretic-induced increases in serum low-density lipoprotein cholesterol.