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

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.

1977 ◽  
Vol 53 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L. M. H. Wing ◽  
J. L. Reid ◽  
C. A. Hamilton ◽  
P. Sever ◽  
D. S. Davies ◽  
...  

1. A single oral dose of clonidine hydrochloride (300 μg) lowered systolic blood pressure by 20 ± 2 mmHg and diastolic blood pressure by 15 ± 2 mmHg in seven healthy normotensive subjects. 2. Resting supine plasma noradrenaline concentration fell from 2·42 ± 0·47 nmol/l before dosing to a minimum of 0·59 ± 0·18 nmol/l at 6 h. The value subsequently rose and was not significantly different from that before the dose at 12 h. There was a significant reduction in urinary free catecholamine excretion in the first 12 h after dosing. 3. Resting supine plasma renin activity before dosing was 0·95 ± 0·16 pmol of angiotensin I h−1 ml−1 of plasma and rose significantly after clonidine to 3·50 ± 0·39 pmol of angiotensin I h−1 ml−1 of plasma at 6 h. By 12 h plasma renin activity had returned to control values. 4. When the same subjects were studied on a control, drug-free, day under the same conditions, there was no significant change in blood pressure or plasma noradrenaline. Although plasma renin activity rose during this control day, it was significantly lower than after clonidine. 5. In normotensive subjects single doses of clonidine lower blood pressure and are associated with a reduction of sympathetic nervous activity. Delayed elevation of plasma renin activity may be secondary to the fall in blood pressure. There is no evidence for an overshoot of sympathetic activity after a single dose of clonidine.


1981 ◽  
Vol 61 (1) ◽  
pp. 69-73 ◽  
Author(s):  
J. Cunningham ◽  
M. J. Vandenburg ◽  
J. M. P. Holly ◽  
F. J. Goodwin

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.


1978 ◽  
Vol 55 (1) ◽  
pp. 89-96 ◽  
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham ◽  
C. R. Benedict

1. Concentrations of noradrenaline and adrenaline from peripheral venous plasma were measured after 60 min of supine rest in 55 patients on chronic haemodialysis (including six anephric patients) and in 18 normal subjects. In the patients, plasma catecholamine measurements were related to concurrent measurements of blood pressure, pulse rate, plasma renin activity, plasma angiotension II, blood volume and sulphate space. 2. Mean resting peripheral venous plasma noradrenaline concentration was higher by almost twofold, but mean resting plasma adrenaline concentration was lower, in the 49 non-nephrectomized patients than in the normal subjects. In the six anephric patients, resting peripheral venous plasma noradrenaline concentrations were similar to those of normal subjects. 3. Mean resting plasma noradrenaline concentrations in peripheral venous blood were similar in normotensive and hypertensive non-nephrectomized patients; mean plasma adrenaline concentration was higher in the hypertensive patients. A positive correlation was found between plasma adrenaline and plasma renin activity but not between plasma noradrenaline and plasma renin activity. 4. Resting concentrations of both catecholamines were positively correlated with resting pulse rate and inversely related to blood volume. 5. After renal transplantation resting peripheral venous plasma noradrenaline concentrations were normal in eight patients in whom high values had been recorded whilst on chronic haemodialysis. 6. In response to 40° of head-up tilt, plasma noradrenaline increased significantly in six non-nephrectomized patients, whether sodium replete or depleted, and the changes observed in both these states were similar to those of 14 normal subjects studied on a normal diet. 7. Diastolic blood pressure increased on standing in the majority (41/55) of patients: in only four patients was there a fall in diastolic pressure of more than 5 mmHg in the erect position and in two of these blood volumes were low. 8. The cause of increased peripheral plasma noradrenaline concentrations in haemodialysis patients is uncertain.


1976 ◽  
Vol 51 (s3) ◽  
pp. 181s-184s ◽  
Author(s):  
M. Esler ◽  
S. Julius ◽  
O. Randall ◽  
V. Dequattro ◽  
A. Zweifler

1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration. 2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute β-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. An elevated total peripheral vascular resistance at rest and a greater fall in peripheral resistance with α-adrenoreceptor blockade (intravenous phentolamine) suggested the existence of a neurogenic increase in arteriolar resistance. 3. Blood pressure was normalized by ‘total’ autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity. 4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. The elevation of blood pressure is sustained predominantly by neurogenic mechanisms. The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity.


1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta

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.


1980 ◽  
Vol 59 (s6) ◽  
pp. 319s-321s ◽  
Author(s):  
G. Leonetti ◽  
C. Bianchini ◽  
G. B. Picotti ◽  
A. Cesura ◽  
Letizia Caccamo ◽  
...  

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.


1984 ◽  
Vol 35 (6) ◽  
pp. 782-787 ◽  
Author(s):  
Nicolas D Vlachakis ◽  
John Barr ◽  
Manuel Velasquez ◽  
Natalie Alexander ◽  
Robert Maronde

1981 ◽  
Vol 60 (4) ◽  
pp. 399-404 ◽  
Author(s):  
C. J. Mathias ◽  
H. L. Frankel ◽  
I. B. Davies ◽  
V. H. T. James ◽  
W. S. Peart

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enhanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.


1981 ◽  
Vol 61 (2) ◽  
pp. 245-247 ◽  
Author(s):  
B. M. Frier ◽  
R. J. M. Corrall ◽  
J. L. Pritchard ◽  
P. S. Sever

1. The changes in blood glucose, plasma noradrenaline and plasma renin activity were measured in 11 normal subjects and in six tetraplegic subjects with a transection of the cervical spinal cord (preganglionic sympathectomy), in response to acute insulin-induced hypoglycaemia (0.15 unit/kg). 2. After hypoglycaemia, a pronounced rise in plasma noradrenaline was observed in the normal subjects but was absent in the tetraplegic group; plasma renin activity increased markedly in both groups. 3. It is concluded that the stimulation of renin release in response to hypoglycaemia can occur independently of any activation of the sympatho-adrenal system.


1975 ◽  
Vol 49 (5) ◽  
pp. 511-514
Author(s):  
J. Chodakowska ◽  
K. Nazar ◽  
B. Wocial ◽  
M. Jarecki ◽  
B. Skórka

1. The effect of physical exercise on blood pressure, plasma catecholamines and plasma renin activity was studied in fourteen patients with essential hypertension and in eight healthy subjects. 2. Resting plasma noradrenaline and adrenaline and plasma renin activity of the hypertensive patients did not differ from those of the control subjects. 3. In response to graded exercise producing successive heart rates of 120, 140 and 160 beats/min, significantly greater increases of blood pressure were found in the patients than in the control subjects. 4. Plasma noradrenaline increased significantly in both groups at all levels of exercise, the responses being significantly greater in the hypertensive patients. 5. The mean arterial blood pressure was significantly correlated with plasma noradrenaline concentration in the control subjects but not in the hypertensive patients. 6. In the hypertensive group plasma adrenaline increased significantly after exercise at all work loads whereas, in the control group, significant increase occurred only at the highest work load. The differences in the response of the two groups were significant at each work load. 7. Plasma renin activity increased significantly after exercise at the heart rate of 120 beats/min, both in the hypertensive patients and in the control subjects. The magnitude of the response was similar in the two groups.


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