Relationship between the Hypotensive and Renin-Stimulating Actions of Diuretic Therapy in Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 307s-309s ◽  
Author(s):  
G. Leonetti ◽  
Laura Terzoli ◽  
Carla Sala ◽  
C. Bianchini ◽  
Laura Sernesi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Diuretic Therapy ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Hypotensive Activity ◽  
Pressor Responses ◽  
Angiotensin Ii Antagonist

1. The pressor role of renin stimulated by chronic diuretic therapy has been assessed in 31 patients with essential hypertension by infusing the angiotensin II antagonist, saralasin, immediately before and at the end of 2 weeks' treatment with the diuretic, chlorthalidone. 2. Under diuretic therapy the change in blood pressure caused by saralasin was found to be correlated to plasma renin activity values, in such a way that small pressor responses were again observed in patients whose renin was mildly stimulated by the diuretic, whereas a marked depressor response occurred in patients whose renin was markedly increased. 3. On the other hand, the hypotensive effect of chlorthalidone was correlated to values of plasma renin activity under diuretic therapy in an opposite direction: indeed little or no decrease and sometimes an increase in blood pressure were observed in patients with marked renin activation by diuretic therapy. 4. It is concluded that stimulation of renin release by chronic diuretic therapy can be considered a factor limiting the hypotensive activity of diuretic drugs.

Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin

2010 ◽  
Vol 391 (12) ◽  
Author(s):  
M. David Percival ◽  
Sylvie Toulmond ◽  
Nathalie Coulombe ◽  
Wanda Cromlish ◽  
Sylvie Desmarais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cathepsin B ◽  
Plasma Renin ◽  
Renin Activity ◽  
Spontaneously Hypertensive ◽  
Protein Levels ◽  
Arterial Blood ◽  
Gene Compensation

Abstract Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

1978 ◽  
Vol 54 (1) ◽  
pp. 75-83 ◽  
Author(s):  
P. Van Hoogdalem ◽  
A. J. M. Donker ◽  
F. H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Sodium Depletion ◽  
Before And After

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.

Effects of nonhypotensive endotoxemia in conscious rats: role of prostaglandins

1988 ◽  
Vol 254 (3) ◽  
pp. H509-H516 ◽  
Author(s):  
M. Burnier ◽  
B. Waeber ◽  
J. F. Aubert ◽  
J. Nussberger ◽  
H. R. Brunner
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Conscious Rats

A nonhypotensive dose of endotoxin was administered to normal conscious rats to evaluate the vascular and humoral effects of endotoxemia per se. Mean blood pressure and heart rate remained stable during the 45 min infusion of Escherichia coli endotoxin (0.01 mg/min). However, a marked increase in plasma renin activity (4.2 +/- 0.48 vs. 30.2 +/- 6 ng.ml-1.h-1, mean +/- SE, P less than 0.01), plasma epinephrine (0.112 +/- 0.04 vs. 1.71 +/- 0.5 ng/ml, P less than 0.01), and plasma norepinephrine (0.269 +/- 0.028 vs. 1.3 +/- 0.2 ng/ml, P less than 0.001) was observed during infusion in endotoxin-treated rats when compared with the vehicle-treated animals. In addition, the blood pressure response to exogenous norepinephrine was significantly reduced during nonhypotensive endotoxemia. Significant changes in regional blood flow distribution, as assessed by radiolabeled microspheres, were observed in endotoxemic rats; in particular a decrease in renal blood flow (7.39 +/- 0.43 vs. 5.97 +/- 0.4 ml.min-1.g-1, P less than 0.05) and an increase in coronary blood flow (5.01 +/- 0.38 vs. 6.44 +/- 0.33 ml.min-1.g-1, P less than 0.01) were found. The role of prostaglandins in the vascular and humoral alterations induced by nonhypotensive endotoxemia was also examined. Pretreatment with indomethacin (5 mg) prevented the increase in plasma renin activity as well as plasma catecholamine levels. On the contrary, the decreased vascular reactivity and the reduction in renal blood flow observed during endotoxemia were not affected by prostaglandin synthesis inhibition. Thus significant vascular and humoral changes have been found during endotoxemia even in absence of hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of Prostaglandin in the Antihypertensive Mechanism of Captopril in Low Renin Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 141s-144s ◽  
Author(s):  
Keishi Abe ◽  
Toru Ito ◽  
Makito Sato ◽  
Toshiaki Haruyama ◽  
KO Sato ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Hypertensive Patients ◽  
Endogenous Prostaglandin ◽  
Low Renin Hypertension ◽  
Prostaglandin System

1. The role of endogenous prostaglandins in the antihypertensive mechanism of the angiotensin converting enzyme inhibitor, captopril, was investigated. 2. An unequivocal reduction in blood pressure and significant increase in plasma renin activity and urinary prostaglandin E excretion were found after the captopril administration. 3. The changes in blood pressure, plasma renin activity and urinary prostaglandin E excretion induced by captopril were reversed after the inhibition of endogenous prostaglandin synthesis by indomethacin. However, the responses in low renin hypertension were different from those in normal renin hypertension. 4. In low renin hypertensive patients who responded to captopril, the hypotensive effect was abolished after the addition of indomethacin, whereas no marked change in blood pressure was induced by indomethacin in normal renin hypertensive patients. In contrast, plasma renin activity was markedly increased after captopril administration in normal renin hypertension, and no significant change was found in low renin hypertension. 5. Potentiation of the prostaglandin system seems to be a principal factor in the antihypertensive mechanism of captopril in low renin hypertension, and inhibition of the renin-angiotensin system is important in normal renin hypertensives. 6. The increase in renin release after the administration of captopril was inhibited by indomethacin, suggesting that an endogenous prostaglandin system may contribute to the short feedback mechanism of renin release.

ROLE OF ANGIOTENSIN III IN THE REGULATION OF BLOOD PRESSURE, PLASMA ALDOSTERONE AND PLASMA RENIN ACTIVITY IN RABBIT

1978 ◽  
Vol 89 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Ikuo Saito ◽  
Takao Saruta ◽  
Toyohisa Eguchi ◽  
Kazuoki Kondo ◽  
Ryuichi Nakamura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Pressure Plasma ◽  
Angiotensin Iii ◽  
Pre Treatment

ABSTRACT To evaluate the role of angiotensin III in the control of blood pressure, plasma aldosterone and plasma renin activity (PRA), the pressor, steroidogenic and PRA-suppressing effect of angiotensin III was studied in rabbits with or without simultaneous constant infusion of Ile7-angiotensin III, an analogue of angiotensin III, or Sar1Ala8-angiotensin II, an analogue of angiotensin II, and compared with the effect of angiotensin II. Infusion of 30 ng/kg/min of angiotensin III or angiotensin II produced a twofold increase in plasma aldosterone. Pressor response to angiotensin III was approximately one tenth of that of angiotensin II. Infusion of angiotensin II suppressed the PRA significantly, while infusion of angiotensin III did not suppress it. Angiotensin II or angiotensin III induced-increase in plasma aldosterone was attenuated by the pretreatment with either Ile7-angiotensin III or Sar1Ala8-angiotensin II. Pressor or PRA-suppressing action of angiotensin II was unaffected by the pre-treatment with Ile7-angiotensin III, while it was significantly inhibited by pre-treatment with Sar1Ala8-angiotensin II. This study indicates that angiotensin III or angiotensin III analogues affect the adrenal glands selectively and suggests that there are differences between the receptor sites for angiotensins in vascular smooth muscle, kidney and those in the adrenal cortex.

Blood Pressure Decrease and Responsiveness to Renin-Releasing Stimuli under Increasing Doses of Propranolol in Patients with Essential Hypertension

1974 ◽  
Vol 48 (s2) ◽  
pp. 77s-79s
Author(s):  
G. Leonetti ◽  
G. Mayer ◽  
A. Morganti ◽  
L. Terzoli ◽  
A. Zanchetti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Moderate Hypertension ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Hypertensive Patients ◽  
Small Doses ◽  
Oral Doses

1. Stepwise increases of oral doses of propranolol produced both a significant lowering of blood pressure and suppression of plasma renin activity in sixteen patients with mild or moderate normal-renin essential hypertension. 2. The hypotensive and the renin-suppressive actions of propranolol were differently related to plasma propranolol concentrations. At the lowest propranolol concentrations (15–40 nmol/l), there was almost no decrease in blood pressure whereas plasma renin activity and responsiveness to renin-releasing stimuli (standing, intravenous frusemide) were already strongly depressed (greater than 50%). Therefore in a large number of normal-renin hypertensive patients under small doses of propranolol, the renin-suppressive action of the drug can be dissociated from the hypotensive effect. Dissociation of the two effects, though in the opposite way, was also observed in three of four low-renin hypertensive patients, whose blood pressure was decreased by propranolol without further reduction of the already suppressed plasma renin activity. 3. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, the hypotensive effect of propranolol cannot be attributed to suppression of renin activity. These conclusions do not necessarily apply to high-renin hypertensive patients.

Effect of Increasing Doses of Labetalol on Blood Pressure, Plasma Renin Activity and Aldosterone in Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 401s-404s ◽  
Author(s):  
A. Salvetti ◽  
R. Pedrinelli ◽  
P. Sassano ◽  
F. Arzilli
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Hypotensive Effect ◽  
Inhibitory Effect ◽  
Renin Activity ◽  
Dose Dependent Fashion ◽  
Dose Dependent

1. Four different doses of labetalol (150, 300, 600 and 900 mg/day) were given for 1 week to each of four groups of patients with essential hypertension (six patients for each group). 2. Labetalol decreased mean blood pressure and heart rate to the same extent on the first and the seventh days of treatment. Only standing blood pressure showed a dose-dependent decrement, and heart rate showed a dose-dependent inhibition both in the supine and upright position. 3. Labetalol exerted a net inhibitory effect on plasma renin activity, which was related to basal renin values and was already maximal at the lowest doses. This effect was well maintained in the supine position, although during standing it tended to be less evident with increasing doses. 4. Urinary aldosterone was decreased in a dose-dependent fashion and its changes were largely independent of plasma renin activity. 5. Neither basal values nor changes of renin and aldosterone were related to the hypotensive effect of labetalol. 6. During labetalol treatment urinary sodium excretion fell for 2–3 days and then returned to basal values. The retentive effect of labetalol on sodium was directly related to the decrease of blood pressure, and the successive sodium escape might be explained either by the observed increase of plasma volume (indirectly measured by packed cell volume) or by aldosterone inhibition.

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