Changes In Plasma Angiotensin Research Articles

Pressor effect of tonin in anephric animals.

Tonin was injected intravenously to normal rats without effect on blood pressure. Twenty-four hours after bilateral nephrectomy, tonin produced a dose-dependent pressor effect in rats which was abolished by the angiotensin antagonist [Sar1-Ala8]-angiotensin II. Vascular response to angiotensin II was slightly increased after nephrectomy. Plasma angiotensin II increased significantly after injection of tonin and disappeared biexponentially with a half-life of less than 1 min for the fast component and 9 min for the slow component. The change in plasma angiotensin II correlated with the elevation in mean blood pressure. No difference in inhibitory power of plasma on tonin activity could be shown between intact and nephrectomized rats. In vitro, the initial velocity of generation of angiotensin II by tonin acting on plasma increased after addition of semipurified rat renin substrate and was significantly greater in plasma of nephrectomized rats. In nephrectomized rabbits, but not in intact ones, a dose-dependent pressor effect was produced by tonin. These data demonstrate the in vivo production of angiotensin II by tonin in an animal model with elevated substrate levels. Together with the in vitro data, these results suggest a role for substrate concentration in the expression of tonin enzymatic activity in vivo.

Role of various vasodepressor systems in the acute hypotensive effect of captopril in man.

The acute hypotensive effect of captopril 25 mg was investigated in 26 hypertensive patients (11 with essential and 15 with renal arterial disease). Intra-arterial blood pressure was recorded continuously and arterial blood was sampled for renin, angiotensin I and II, aldosterone, kininase II, catecholamines and prostaglandins. Captopril led to an increase in plasma renin activity, active and total plasma renin concentration and angiotensin I, a decrease in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2 alpha and no change in plasma (nor) adrenaline, dopamine and inactive renin concentration. The hypotensive effect of captopril was related to the changes in plasma angiotensin II level and inversely to the changes in prostaglandin E2; the correlation coefficients were low, respectively 0.61 and -0.44. It is likely that the acute hypotensive effect of captopril to some extent is related to changes in plasma angiotensin II and in prostaglandins E2 and F2 alpha. There is no evidence for a role of the adrenergic systems in the hypotensive response.

Efficacy of an oral angiotensin-converting enzyme inhibitor (captopril) in severe hypertension

The antihypertensive effect of captopril was assessed during short- and long-term periods in ten patients with elevated blood pressure readings that were uncontrollable by standard therapy (supine diastolic blood pressure of greater than 100 mm Hg with a regimen of propranolol hydrochloride, hydralazine hydrochloride, and hydrochlorothiazide). When given alone, captopril therapy was unable to normalize the blood pressure in any patient. The addition of hydrochlorothiazide to the captopril therapy normalized the blood pressure in one patient and sharply improved the blood pressure in four others. The blood pressure in the remaining patients responded inadequately to this combination. The addition of propranolol to captopril and hydrochlorothiazide reduced the blood pressure further in most cases (seven on the ten patients had normal blood pressure readings while they received these three drugs). In four patients, the blood pressure response to the added propranolol was unrelated to changes in plasma angiotensin II concentration. Captopril was helpful in the management of refractory hypertension in most cases.

Efficacy of an Oral Angiotensin-Converting Enzyme Inhibitor (Captopril) in Severe Hypertension

The antihypertensive effect of captopril was assessed during short- and long-term periods in ten patients with elevated blood pressure readings that were uncontrollable by standard therapy (supine diastolic blood pressure of greater than 100 mm Hg with a regimen of propranolol hydrochloride, hydralazine hydrochloride, and hydrochlorothiazide). When given alone, captopril therapy was unable to normalize the blood pressure in any patient. The addition of hydrochlorothiazide to the captopril therapy normalized the blood pressure in one patient and sharply improved the blood pressure in four others. The blood pressure in the remaining patients responded inadequately to this combination. The addition of propranolol to captopril and hydrochlorothiazide reduced the blood pressure further in most cases (seven on the ten patients had normal blood pressure readings while they received these three drugs). In four patients, the blood pressure response to the added propranolol was unrelated to changes in plasma angiotensin II concentration. Captopril was helpful in the management of refractory hypertension in most cases.

Essential hypertension: abnormal renal vascular and endocrine responses to a mild psychological stimulus.

We have assessed the influence of a mild emotional stimulus on arterial blood pressure, heart rate, renal blood flow, plasma renin activity (PRA), and plasma aldosterone concentration in 24 normal subjects, eight of who had a parent with hypertension, and in 15 patients with essential hypertension. A nonverbal IQ test, Raven's Progressive Matrices, was employed as the stimulus. In 11 of the 15 hypertensives, arterial blood pressure rose transiently by 7 mm Hg or more, but in only three of 16 normal subjects (x2 = 7.23, p less than 0.01). Transient moderate increases in heart rate were also more common in the hypertensives (p less than 0.01). Renal blood flow rose in 11 of 16 normal subjects and fell in each of the 15 patients with essential hypertension (x2 = 15.1; p less than 0.005). As opposed to the transient changes in arterial pressure and heart rate, the fall in renal perfusion was sustained. The PRA fell in 10 of the 16 normal subjects with a negative family history and rose in 14 of 15 patients with essential hypertension (p less than 0.005). Changes in plasma angiotensin II concentration and in plasma aldosterone were in accord with the changes in PRA, but plasma cortisol did not change. Both the renal vascular response and the change in PRA were intermediate in normal subjects in whom family history was positive for hypertension. For the entire group of 39 subjects there was statistically significant agreement between the direction of the renal vascular response and the directional change in PRA: renal blood flow rose when PRA fell and fell when PRA rose (p less than 0.005). We conclude that there is an abnormality in the control of both the renal circulation and of renin release in patients with essential hypertension in response to psychological provocation, and that a similar process is present in some normotensive subjects whose parents have hypertension.