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.

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

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.

Renin Release during Head-up Tilt Occurs Independently of Sympathetic Nervous Activity in Tetraplegic Man

1980 ◽  
Vol 59 (4) ◽  
pp. 251-256 ◽  
Author(s):  
C. J. Mathias ◽  
N. J. Christensen ◽  
H. L. Frankel ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Nervous Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Head Up Tilt ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system in the release of renin during head-up tilt has been studied in five normal subjects and in four tetraplegic patients with cervical spinal-cord transection above the sympathetic outflow. Blood pressure, heart rate and concentrations of plasma noradrenaline, plasma adrenaline and plasma renin activity were measured during head-up tilt to 45° before and after acute β-adrenoreceptor blockade with intravenous propranolol. 2. In the normal subjects there were minimal changes in blood pressure during head-up tilt and there was a rise in both plasma noradrenaline concentration and plasma renin activity. After propranolol values of plasma renin activity at rest fell with little change occurring during head-up tilt. 3. In the tetraplegic patients there was a substantial fall in blood pressure during head-up tilt. Concentrations of plasma noradrenaline and adrenaline did not change but there was a marked increase in plasma renin activity. Values of plasma renin activity both at rest and during head-up tilt were unaffected by propranolol. 4. We conclude that in tetraplegic patients renin release during head-up tilt may occur independently of sympathetic nervous activity and is probably largely dependent on activation of renal vascular receptors.

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.

Plasma Catecholamines and Plasma Renin Activity at Birth and during the First Days of Life

1980 ◽  
Vol 59 (s6) ◽  
pp. 319s-321s ◽  
Author(s):  
G. Leonetti ◽  
C. Bianchini ◽  
G. B. Picotti ◽  
A. Cesura ◽  
Letizia Caccamo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Umbilical Cord Blood ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Plasma Adrenaline ◽  
Noradrenaline And Adrenaline ◽  
Noradrenaline Levels

1. Plasma noradrenaline and adrenaline concentrations and plasma renin activity were measured in 21 mothers at delivery and in their babies at birth (umbilical cord blood) and on days 1 and 5 of extrauterine life. 2. At birth plasma renin activity was significantly higher in the newborn than in mothers. Plasma renin activity increased further, but not significantly, on day 1 of life and significantly decreased on day 5. On day 5, 10 min head-up tilting caused no change in plasma renin activity. 3. Plasma noradrenaline in the newborn was higher than in mothers at birth and significantly decreased thereafter. Plasma adrenaline levels at birth were similar in the newborn and their mothers and significantly lower in the newborn in subsequent days. Tilting caused no increase in either plasma adrenaline or noradrenaline levels. 4. No correlation was found between plasma noradrenaline and adrenaline levels and plasma renin activity, or between noradrenaline, adrenaline or plasma renin activity and blood pressure.

scholarly journals Altered Neural and Vascular Mechanisms in Hypertension

2011 ◽  
pp. 381-402 ◽  
Author(s):  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
G Proteins ◽  
High Blood Pressure ◽  
Calcium Current ◽  
Calcium Influx ◽  
Dominant Role ◽  
Cardiovascular Complications ◽  
Sympathetic Nervous

Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins. Although there is considerable information on the complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing.

Sign in / Sign up

Export Citation Format

Share Document