The Effect of Mental Stress on Catecholamines, their Metabolites and Plasma Renin Activity in Patients with Essential Hypertension and in Healthy Subjects

1979 ◽  
Vol 57 (s5) ◽  
pp. 229s-231s ◽  
Author(s):  
W. Januszewicz ◽  
M. Sznajderman ◽  
B. Wocial ◽  
T. Feltynowski ◽  
T. Klonowicz

1. Ten patients with essential hypertension and ten healthy men were submitted to mental stress consisting of Kraepelin's arithmetic test combined with noise. Concentrations of plasma and urine catecholamines and of their metabolites as well as plasma renin activity before and after the test were studied. 2. In both groups a significant increase of noradrenaline and adrenaline in blood and noradrenaline in urine was observed. The urinary excretion of dopamine fell significantly in both groups after stress. 3. After mental stress a significant increase in urinary excretion of 3-methoxy-4-hydroxyphenylglycol was observed in both groups. The excretion of vanillylmandelic acid decreased significantly only in healthy subjects. 4. The plasma renin activity rose significantly in both groups but the increase was more pronounced in healthy subjects.

1974 ◽  
Vol 48 (s2) ◽  
pp. 85s-88s ◽  
Author(s):  
G. Muiesan ◽  
C. Alicandri ◽  
E. Agabiti Rosei ◽  
M. Motolese ◽  
C. Valori

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge. 2. The same procedure was repeated in the same subjects 3–4 days later after pretreatment with oxprenolol. 3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged. 4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values. 5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.


1972 ◽  
Vol 71 (2) ◽  
pp. 321-330 ◽  
Author(s):  
H. Hedeland ◽  
J.-F. Dymling ◽  
B. Hökfelt

ABSTRACT The present study was concerned with the relation of catecholamine production and plasma renin activity. The catecholamine production was measured as the urinary excretion of noradrenaline and adrenaline. Thirteen subjects were studied under basal conditions and also following insulin induced hypoglycaemia both before and during treatment with the imidazoline derivate clonidine. Before clonidine, hypoglycaemia produced a marked increase in catecholamine production and an elevation of plasma renin activity. These parameters were significantly correlated. Treatment with clonidine markedly suppressed noradrenaline production and plasma renin activity. Adrenaline production showed a minor decrease. During clonidine treatment insulin induced pronounced hypoglycaemia. In spite of this the increase in adrenaline production and plasma renin activity was less marked as compared to that before clonidine. There was no longer any significant correlation between catecholamine production and plasma renin activity. Our results indicate that sympathetic amines liberated from the adrenal medulla and/or the sympathetic nerve endings can stimulate renin production.


1981 ◽  
Vol 61 (s7) ◽  
pp. 445s-448s ◽  
Author(s):  
F. W. Amann ◽  
P. Bolli ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler

1. α1-Adrenoceptor-mediated vasoconstriction was studied before and during propranolol therapy in eight normal renin essential hypertensive patients; four were known ‘responders’ and four, age-matched ‘non-responders’ to previous β-receptor blocker monotherapy. Plasma renin activity, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during regional postjunctional α1-adrenoceptor blockade with prazosin. All measurements were done on placebo and again after 6 weeks’ propranolol monotherapy (320 mg/day). 2. Propranolol reduced heart rate and plasma renin activity to the same extent in ‘responders’ and ‘non-responders’. Resting plasma adrenaline concentrations tended to be higher in ‘responders’ before propranolol; they remained unchanged in both groups on propranolol. Plasma noradrenaline concentrations were similar in both groups before and on propranolol. 3. Before propranolol forearm flow was not different in ‘responders’ and ‘non-responders’. Non-specific vasodilatation with sodium nitroprusside produced a similar increase in forearm flow before and after propranolol in both groups. 4. Prazosin-induced increments in forearm flow tended to be higher in ‘responders’ before propranolol. After propranolol the vasodilator effect of prazosin was attenuated in ‘responders’ but it remained unchanged in ‘non-responders’ (P < 0.01). 5. In patients with normal renin essential hypertension the antihypertensive response to propranolol monotherapy is paralleled by a decrease in postjunctional α1-adrenoceptor-mediated vasoconstriction.


1981 ◽  
Vol 61 (1) ◽  
pp. 107-110 ◽  
Author(s):  
M. S. Golub ◽  
M. L. Tuck ◽  
D. B. Fittingoff

1. The plasma aldosterone responses to exogenous angiotensin II and adrenocorticotropic hormone (ACTH) were studied before and after 1 month of propranolol therapy (120–240 mg/day) in eight patients with essential hypertension. 2. Basal supine plasma renin activity was decreased (P < 0.001) after propranolol, whereas plasma aldosterone was unchanged. After 3 h of upright posture the increases in both plasma renin activity and aldosterone were decreased (P < 0.05) after propranolol. 3. Plasma aldosterone responses to exogenous angiotensin II and ACTH were not significantly different after propranolol. Serum and urinary electrolytes and plasma cortisol were also unaffected by propranolol therapy. 4. It is concluded that changes in adrenal sensitivity are not responsible for maintaining unchanged supine plasma aldosterone concentrations after β-adrenoceptor antagonism in essential hypertension.


1978 ◽  
Vol 102 (1) ◽  
pp. 120-122 ◽  
Author(s):  
Pauli Yuitalo ◽  
Heikki Vapaatalo ◽  
Timo Metsä-Ketelä ◽  
Timo Pitkäjärvi

1975 ◽  
Vol 13 (26) ◽  
pp. 101-103

Thiazide diuretics such as bendrofluazide and chlorothiazide have been used for nearly 20 years in the treatment of hypertension. They have been regarded as rather weak antihypertensive agents which could be used alone only in mild hypertension and otherwise as adjuvants to more potent drugs in more serious cases.1 There are however some patients with ‘essential’ hypertension who are very sensitive to diuretics and in whom the pressure may be brought down to normal by a thiazide2 or spironolactone3 even when it is initially considerably raised. Furthermore a few patients who are responsive to thiazides are strikingly unresponsive to non-diuretic antihypertensive drugs. Patients particularly likely to respond to a thiazide diuretic4 or spironolactone3 commonly have low plasma renin activity and this occurs in about 25% of patients with essential hypertension.5 Since plasma renin activity is not routinely estimated it is simplest to identify these patients by observing the response to an adequate trial of a thiazide.


1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.


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