Change in the Renin Dependency of Blood Pressure Induced by Volume Depletion and/or Propranolol Therapy in Hypertensive Patients

1976 ◽  
Vol 51 (s3) ◽  
pp. 189s-192s
Author(s):  
G. G. Geyskes ◽  
P. Boer ◽  
J. Vos ◽  
E. J. Dorhout Mees
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin ◽  
Special Importance ◽  
Volume Depletion ◽  
Blood Pressure Elevation ◽  
Hypertensive Patients ◽  
Angiotensin Ii Antagonist ◽  
Different Types ◽  
Propranolol Therapy

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113). 2. The P113-induced fall of the blood pressure did correlate with the log PRA (r = 0·888, P < 0001). This correlation was found irrespective of different types of hypertension and treatment schedules. 3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency. 4. No indication was found that a given PRA is of special importance for blood pressure elevation in different patients. 5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.

Changes in Blood Pressure in Relation to Vascular and Plasma Renin after Renin Injection in Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 153s-156s ◽  
Author(s):  
M. Loudon ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Aortic Tissue ◽  
Relative Importance ◽  
Bilateral Nephrectomy ◽  
Single Intravenous Injection ◽  
Angiotensin Ii Antagonist ◽  
Renal Origin

1. To assess the relative importance of vascular as opposed to plasma renin, groups of conscious rats received a single intravenous injection of partially purified rat renin 18 h after bilateral nephrectomy. Blood pressure was monitored continuously and plasma and aortic renin concentrations were determined at 1, 3, 6 or 9 h after injection. In separate groups of rats the effect of the competitive angiotensin II antagonist, saralasin, on blood pressure was measured 3 or 6 h after renin injection. 2. Blood pressure remained elevated for up to 6 h after renin injection, returning to normal by 9 h. Saralasin infusion reversed the rise in blood pressure at both 3 and 6 h after injection. 3. Aortic renin concentration followed the pattern of the pressor response whereas plasma renin concentration had returned to subnormal values by 3 h. 4. Circulating renin of renal origin is taken up by aortic tissue. The pressor response to exogenous renin in rats after bilateral nephrectomy is not related to changes in plasma renin but is similar in duration to the persistence of aortic renin-like activity and can be blocked by saralasin at both 3 and 6 h after injection.

Blood pressure and endocrine effects of single doses of CS-866, a novel angiotensin II antagonist, in salt-restricted hypertensive patients

1997 ◽  
Vol 15 (12) ◽  
pp. 1809-1812 ◽  
Author(s):  
Kurt Püchler ◽  
Jürg Nussberger ◽  
Petra Laeis ◽  
Peter U. Witte ◽  
Hans R. Brunner
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Endocrine Effects ◽  
Hypertensive Patients ◽  
Angiotensin Ii Antagonist

Effects of Felodipine and Metoprolol on Blood Pressure, Plasma Renin, Angiotensin II, Aldosterone and Catecholamines in Hypertensive Patients

Drugs ◽  
1987 ◽  
Vol 34 (Supplement 3) ◽  
pp. 170-175 ◽  
Author(s):  
P. Lijnen ◽  
R. Fagard ◽  
J. Staessen ◽  
E. Moerman ◽  
A. De Schaepdryver ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Pressure Plasma

Effect of Sotalol on Haemodynamics and Renin—Angiotensin—Aldosterone System in Hypertensive Patients

1976 ◽  
Vol 51 (1) ◽  
pp. 9-17 ◽  
Author(s):  
A. Verniory ◽  
M. Staroukine ◽  
F. Delwiche ◽  
M. Telerman
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Excretion Rate ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Receptor Blocking ◽  
Plasma Angiotensin

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.

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.

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