Plasma Catecholamines and the Pressor Response to Sar1-Ala8-Angiotensin II in Man

1977 ◽  
Vol 53 (4) ◽  
pp. 341-348
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham ◽  
C. R. Benedict

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemodialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5–6 min, occurred in all normal subjects, patients with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P < 0·02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P < 0·05) and was similar to the response to 5 min of a 40° head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P < 0·005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P < 0·001) and angiotensin II (P < 0·001), directly related to blood volume (P < 0·001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.

1981 ◽  
Vol 61 (s7) ◽  
pp. 65s-68s ◽  
Author(s):  
J. A. Millar ◽  
Kathleen McLean ◽  
J. L. Reid

1. The effect of the calcium antagonist nifedipine on the pressor and aldosterone responses to angiotensin II was studied in six normal subjects. 2. Blood pressure, pulse rate and plasma aldosterone, potassium and cortisol were measured during paired consecutive infusions of angiotensin II (5, 10 and 20 ng min−1 kg−1) on two separate occasions. Nifedipine (20 mg by mouth) was given, 30 min before the second set of infusions. 3. After nifedipine there were reciprocal changes in supine resting blood pressure (−7 mm Hg) and pulse rate (+18 min−1) and a significant decrease in the pressor response to angiotensin II (P &lt; 0.05; Wilcoxon signed rank test). 4. Basal levels of aldosterone were not changed by nifedipine, but the response to angiotensin II was significantly attenuated (P &lt; 0.05). Nifedipine had no effect on plasma potassium or cortisol. 5. Transmembrane movement of calcium is involved in the aldosterone response to angiotensin II in man. Calcium antagonists may lower blood pressure via decreased adrenal responsiveness to angiotensin II as well as by peripheral vasodilatation.


1983 ◽  
Vol 65 (3) ◽  
pp. 227-235 ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
Luisa Gregorini ◽  
G. Leonetti ◽  
G. Parati ◽  
...  

1. Plasma concentrations of noradrenaline and adrenaline were measured radioenzymatically in nine subjects during 4 min pressor and depressor responses (intra-arterial measurements) induced by increasing and reducing sympathetic vasoconstrictor tone via carotid baroreceptor deactivation and stimulation (neck chamber technique). 2. During the pressor response (15 ± 3 mmHg, mean ± se) plasma noradrenaline and adrenaline showed various changes in the different subjects and on average were not significantly increased above control. During the depressor response (−9 ± 2 mmHg) plasma noradrenaline and adrenaline also showed various changes in the subjects and were on average not significantly reduced below control. 3. In contrast the same subjects all showed an increase in noradrenaline and adrenaline (average 76 and 117%) at the fourth minute of a tilting manoeuvre with- a return to pretilting values no more than 4 min after resumption of the supine position. 4. These results suggest that the moderate and/or restricted alterations in sympathetic tone produced by manipulating a single baroreflex, though capable of affecting blood pressure, are not reflected by alterations in plasma catecholamines. To modify these humoral indices significantly, the more drastic or more diffuse alterations in sympathetic activity that may be produced by manipulating low as well as high pressure reflexogenic areas are needed.


1973 ◽  
Vol 44 (6) ◽  
pp. 617-620 ◽  
Author(s):  
L. B. Geffen ◽  
R. A. Rush ◽  
W. J. Louis ◽  
A. E. Doyle

1. Plasma dopamine β-hydroxylase (DβH) amounts were measured by radioimmunoassay in twenty-eight patients, twenty of whom had essential hypertension. There was a positive correlation between resting diastolic blood pressure and plasma DβH concentration. 2. Plasma DβH amounts also correlated significantly with those of plasma noradrenaline (NA) in individual patients. 3. These findings provide further support for the conclusions drawn from studies of plasma catecholamines that the sympathetic nervous system contributes toward the maintenance of the elevated blood pressure in essential hypertension.


1976 ◽  
Vol 51 (s3) ◽  
pp. 193s-196s
Author(s):  
G. A. MacGregor ◽  
P. M. Dawes

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0·25 μg min—1 kg—1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b) normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake); (c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.


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.


1978 ◽  
Vol 55 (s4) ◽  
pp. 61s-63s ◽  
Author(s):  
T. Philipp ◽  
A. Distler ◽  
U. Cordes ◽  
H. P. Wolff

1. An inverse relationship was found between plasma noradrenaline and reactivity to exogenous noradrenaline in normotensive subjects. 2. The relationship between plasma noradrenaline and reactivity was disturbed in age-matched patients with essential hypertension. 3. A multiple-regression analysis showed a highly significant correlation between adrenergic activity and reactivity to noradrenaline and the mean arterial blood pressure level (r = 0·91). The results suggest that adrenergic activity and pressor response to noradrenaline combined are important determinants of arterial blood pressure. 4. An inverse relationship could also be demonstrated between plasma renin activity and reactivity to exogenous angiotensin II. No difference was observed between normotensive and hypertensive subjects.


1983 ◽  
Vol 6 (5) ◽  
pp. 255-260 ◽  
Author(s):  
D. Ratge ◽  
R. Augustin ◽  
H Wisser

To assess the interaction between adrenergic activity and blood pressure regulation, plasma catecholamines (CA), plasma renin activity (PRA) and plasma aldosteron (PA) were measured in 66 normal subjects and 18 dialysis patients. Prior to dialysis, blood levels of free norepinephrine (NE), epinephrine (E) and PRA were normal, but total (free and conjugated) CA as well as PA were significantly elevated. There was a spectrum of response during hemodialysis. On an average mean arterial blood pressure (MAP) fell during the first two hours of treatment, concomitantly followed by an increase in mean NE level. Whereas PRA and PA were highest at the end of treatment, mean free NE returned promptly to predialysis values through the late dialysis period. Severe hypotensive episodes during dialysis were associated with a baroreceptor-mediated adrenergic stimulation. These results indicate a qualitatively normal reaction of dialysis patients to volume removal and the importance of the renin-angiotensin-system in maintaining blood pressure during dialysis.


1976 ◽  
Vol 51 (s3) ◽  
pp. 461s-463s
Author(s):  
K. Abe ◽  
H. Aoyagi ◽  
M. Yasujima ◽  
S. Miyazaki ◽  
T. Kusaka ◽  
...  

1. The interactions of dopamine, reserpine and methyldopa on blood pressure of normal subjects and of those with essential hypertension were examined. 2. When biosynthesis of noradrenaline from dopamine was blocked by reserpine, dopamine induced a prominent depressor effect in essential hypertension. 3. The long-term treatment with methyldopa induced a marked potentiation of the pressor action of domapine in hypertension, although no significant pressor response was found in normal subjects. 4. It is suggested that methylnoradrenaline may accumulate in peripheral nerve endings of patients with essential hypertension in comparison with normal subjects, and this accumulated methylnoradrenaline potentiates the pressor response to dopamine in essential hypertension.


1980 ◽  
Vol 59 (s6) ◽  
pp. 53s-56s ◽  
Author(s):  
B. A. Schölkens ◽  
W. Jung ◽  
W. Rascher ◽  
A. Schömig ◽  
D. Ganten

1. The mechanisms of central angiotensin II blood pressure effects in conscious dogs on normal or sodium-deficient diets were examined. 2. The biosynthesis of brain angiotensin II in cerebrospinal fluid from its local precursor angiotensinogen was induced in vivo by injection of 0.5 unit of hog kidney renin through a chronically implanted cannula into the third brain ventricle in conscious dogs. 3. Intracerebroventricular administration of renin induced an increase of arterial blood pressure and a marked drinking response under both dietary regimens. Sodium restriction had no effect on the magnitude of the central angiotensin pressor response. 4. Plasma concentrations of renin and angiotensin II decreased, and plasma antidiuretic hormone, noradrenaline, adrenaline and corticosterone increased, in both groups of dogs. 5. Simultaneous intraventricular administrations of captopril with renin inhibited the central renin effects. Intracerebroventricular injections of [Sar1, Val5, Ala8] angiotensin II alone increased plasma renin and angiotensin II concentrations. 6. It is concluded that endogenous brain angiotensin II participates in central mechanisms of blood pressure regulation by the stimulation of the release of antidiuretic hormone, adrenocorticotrophic hormone, adrenaline and noradrenaline.


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.


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