Acute effect of labetalol on blood pressure in relation to the sympathetic nervous system and plasma renin activity

1984 ◽  
Vol 35 (6) ◽  
pp. 782-787 ◽  
Author(s):  
Nicolas D Vlachakis ◽  
John Barr ◽  
Manuel Velasquez ◽  
Natalie Alexander ◽  
Robert Maronde
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Acute Effect ◽  
Renin Activity ◽  
Sympathetic Nervous

Impaired Response of Plasma Renin Activity to Tilting after Renal Transplantation

1981 ◽  
Vol 61 (1) ◽  
pp. 69-73 ◽  
Author(s):  
J. Cunningham ◽  
M. J. Vandenburg ◽  
J. M. P. Holly ◽  
F. J. Goodwin
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Pulse Rate ◽  
Dominant Role ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous

1. Changes in plasma renin activity, plasma noradrenaline, pulse rate and blood pressure after tilting were measured in normal subjects and in patients with renal transplants. 2. There was a marked difference between the renin responses in the two groups, the increases in plasma renin activity in the control subjects being much greater than those in the transplanted patients. 3. Activation of the sympathetic nervous system after tilting, as indicated by changes in pulse rate, blood pressure and plasma noradrenaline, was similar in the two groups. 4. We conclude that the ability of the transplanted kidney to increase plasma renin activity after tilting is impaired, probably as a result of sympathetic denervation of the kidney during transplantation. The results suggest a dominant role of the sympathetic nervous system in the mediation of renin release after tilting.

scholarly journals Masked Uncontrolled Hypertension Is Accompanied by Increased Out-of-Clinic Aldosterone Secretion

Hypertension ◽  
2020 ◽  
Author(s):  
Mohammed Siddiqui ◽  
Eric K. Judd ◽  
Bin Zhang ◽  
Tanja Dudenbostel ◽  
Robert M. Carey ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Uncontrolled Hypertension ◽  
Aldosterone Secretion ◽  
Urinary Catecholamines ◽  
Serum Aldosterone ◽  
Sympathetic Nervous

Masked uncontrolled hypertension (MUCH) in treated patients is defined as controlled office blood pressure (BP) but uncontrolled out-of-clinic ambulatory BP. Previously, we have shown that patients with MUCH have evidence of heightened out-of-clinic sympathetic nervous system activity. The aim is to test the hypothesis that MUCH patients have higher aldosterone secretion compared with patients with true controlled hypertension. Two hundred twenty-two patients were recruited after having controlled office BP readings at ≥3 clinic visits. Patients taking MR (mineralocorticoid receptor) antagonists and epithelial sodium channel blockers were excluded. All patients were evaluated by clinic automated office BP and morning serum aldosterone and plasma renin activity. Out-of-clinic ambulatory BP monitoring and 24-hour urinary aldosterone, catecholamines, and metanephrines were also measured. Sixty-four patients had MUCH, and the remaining 48 patients had true controlled hypertension. MUCH patients had significantly higher out-of-clinic levels of 24-hour urinary aldosterone, catecholamines, and metanephrines compared with true controlled hypertension. The 2 groups did not differ in serum aldosterone, plasma renin activity, or aldosterone-renin ratio collected in clinic. In addition, 32.8% of MUCH patients had high out-of-clinic 24-hour urinary aldosterone (≥12 µg) but normal clinic serum aldosterone (<15 ng/dL) and aldosterone-renin ratio (<20). Further, in correlation matrix analysis, higher 24-hour urinary catecholamines and metanephrines were associated with higher 24-hour urinary aldosterone and plasma renin activity levels in MUCH patients. Patients with MUCH have higher out-of-clinic urinary aldosterone levels compared with patients with true controlled hypertension. This study suggests that patients with MUCH likely have higher out-of-clinic sympathetic nervous system tone increases aldosterone secretion mediated by increased renin release that may contribute to their higher out-of-clinic BP.

Effects of psychosocial stimuli on plasma renin activity in rats

1976 ◽  
Vol 231 (4) ◽  
pp. 1290-1294 ◽  
Author(s):  
DM Clamage ◽  
CS Sanford ◽  
AJ Vander ◽  
DR Mouw
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Open Field ◽  
Plasma Renin ◽  
Prior Treatment ◽  
Renin Secretion ◽  
Renin Activity ◽  
Renin Substrate ◽  
Sympathetic Nervous

The effects of two types of psychosocial stimuli on plasma renin activity (PRA) were studied in unanesthetized rats, blood being collected by decapitation. Thirty minutes of exposure to a novel environment ("open field") produced statistically significant increases of PRA in rats maintained on either a standard (1% NaCl) or sodium-free diet. No change in plasma renin substrate occurred. Prior treatment with propranolol (approximately 2 mg/kg) reduced the renin response by approximately 50% but did not completely abolish it. Plasma renin activity was also increased significantly by exposure of caged rats to the presence of a hungry cat for 30 min. We conclude that psychosocial stimuli can produce significant increases in renin secretion and that this response is mediated, at least in part, by the sympathetic nervous system.

Anti-Hypertensive Effect of Acebutolol: Its Relation to Sympathetic Nervous System Responsiveness and to Plasma Renin and Dopamine-β-Hydroxylase Activities

1976 ◽  
Vol 51 (s3) ◽  
pp. 477s-480s
Author(s):  
A. Fournier ◽  
J. M. Hardin ◽  
J. M. Alexandre ◽  
M. Lombaert ◽  
G. Ronco ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Daily Dose ◽  
Head Up Tilt ◽  
The Common ◽  
System Responsiveness ◽  
Sympathetic Nervous

1. Acebutolol, a β1-receptor blocker, has, at a daily dose of 800 mg, a mild but significant anti-hypertensive effect in moderate sustained essential hypertension with normal or low plasma renin activity. 2. Prediction of its anti-hypertensive effect is better based on the evaluation of the sympathetic nervous system responsiveness to head-up tilt than on the evaluation of plasma renin activity or dopamine-β-hydroxylase. 3. The anti-hypertensive effect of acebutolol is better explained on the basis of inhibition of the sympathetic nervous system activity than on the basis of suppression of plasma renin activity. 4. A positive correlation between plasma renin activity and dopamine-β-hydroxylase in patients on diuretics suggests the common dependence of these two variables on sympathetic overactivity.

Humoral Effects of the Oral Converting-Enzyme Inhibitor Sq 14 225 in Hypertensive Patients in Supine and Tilted Position

1979 ◽  
Vol 57 (s5) ◽  
pp. 149s-152s ◽  
Author(s):  
A. Morganti ◽  
T. G. Pickering ◽  
J. Lopez-Ovejero ◽  
J. H. Laragh
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Hypertensive Patients ◽  
Sympathetic Nervous

1. To evaluate the effects of converting-enzyme inhibition on the sympathetic nervous system, on renin and on the other known regulators of aldosterone secretion, we measured blood pressure, heart rate, plasma noradrenaline, adrenaline, renin activity, aldosterone, cortisol and serum potassium in 15 sodium-repleted hypertensive patients in supine position and during 30 min of 65° head-up tilt before and during treatment with SQ 14 225. 2. SQ 14 225 produced significant decreases in supine blood pressure and plasma aldosterone and significant increments in plasma renin activity and potassium; in contrast, heart rate, noradrenaline, adrenaline and cortisol were unchanged. 3. While in control tilt studies blood pressure was always maintained, during treatment three of 15 patients had vasovagal syncopes. In the remaining 12 blood pressure was maintained during tilt on SQ 14 225; however, while the tilt-induced responses in heart rate and adrenaline were as in control studies, the 30 min increments in noradrenaline were significantly higher. 4. Both before and during treatment the responses of plasma renin activity and aldosterone to tilt were parallel, and correlated with each other, and cortisol and potassium changed only slightly. 5. It is concluded that the SQ 14 225-induced fall in blood pressure occurs without a concomitant rise in sympathetic nervous activity; thus the increase in supine plasma renin activity, being a reflection of the interruption of the angiotensin feedback mechanism on renin release, indicates an effective suppression of angiotensin II formation. 6. During SQ 14 225 the persistence of aldosterone response to tilt and its relationship with renin activity suggest that the enzymatic blockade is over-ridden; however, in the presence of a reduced formation of angiotensin II a more pronounced response of the sympathetic nervous system is required to defend blood pressure against postural changes.

Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis

1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Regular Hemodialysis

Abstract. The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol·kg−1·min−1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 ± 0.52 to 3.39 ± 0.85 nmol·l−1·h−1 predialysis and from 2.78 ± 0.71 to 3.15 ± 0.86 nmol·l−1·h−1 postdialysis, respectively, mean ± sem; P < 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the reninangiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.

Acute Effect of Plasma Exchange on Arterial Blood Pressure and Plasma Renin Activity

1985 ◽  
Vol 9 (3) ◽  
pp. 276-279 ◽  
Author(s):  
L. Moriconi ◽  
C. Palombo ◽  
E. Fommei ◽  
P. Meconi ◽  
R. Puccini ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Exchange ◽  
Arterial Blood Pressure ◽  
Plasma Renin ◽  
Acute Effect ◽  
Renin Activity ◽  
Arterial Blood

Renin, Noradrenaline and Adrenaline Responses to Simulated Altitude

1973 ◽  
Vol 44 (3) ◽  
pp. 243-251 ◽  
Author(s):  
Dr T. A. Kotchen ◽  
R. P. Hogan ◽  
A. E. Boyd ◽  
T.-K. Li ◽  
Helen C. Sing ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Simulated Altitude ◽  
Plasma Adrenaline ◽  
The Third ◽  
Sympathetic Nervous ◽  
Excretion Rates ◽  
Noradrenaline And Adrenaline

1. Plasma renin activity, plasma adrenaline and noradrenaline concentrations, and urinary adrenaline and noradrenaline excretion rates were measured in ten subjects during 3 days of exposure to a simulated altitude of 12 000 ft. 2. In both the supine and standing positions, renin activities were suppressed during all 3 days at altitude. 3. Plasma noradrenaline and adrenaline concentrations were significantly increased by the third day at altitude. 4. Urinary adrenaline excretion tended to be increased during the entire 3 days at altitude, with no significant change between the first and third day. Noradrenaline excretion was significantly increased on the third day. 5. The finding of decreased renin levels suggests that the enhanced activity of the sympathetic nervous system at high altitude does not stimulate renin release.

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system

1995 ◽  
Vol 268 (6) ◽  
pp. H2267-H2273 ◽  
Author(s):  
A. Zanchi ◽  
N. C. Schaad ◽  
M. C. Osterheld ◽  
E. Grouzmann ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Sympathetic Nervous

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

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