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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The angiotensin II antagonist 1-sar-8-ala-angiotensin II (saralasin) was infused in forty-six patients with hypertension of various aetiology (essential, renal arterial or parenchymal disease, primary hyperaldosteronism), before and/or during sodium volume depletion obtained by chlorthalidone and low sodium diet. When saralasin was infused in twenty-five patients ingesting 130 mmol of sodium per day, including patients with proven renovascular hypertension, the changes in mean arterial pressure and ranged from +10 to -7 mmHg (mean: +0.20 mmHg) and were not related to the plasma renin concentration (PRC) (r = -0.11). During sodium volume depletion, saralasin induced changes in mean arterial pressure, ranging from +21 to -76 mmHg, which were closely related to log PRC (n = 32; r = -0.87). Combined sodium depletion and antagonism of angiotensin II 'normalized' mean arterial pressure (less than or equal to 100 mmHg) in twenty-one of the thirty-two patients, while pressure remained between 106 and 147 mmHg in eleven 'poor' responders, so that pressor mechanisms other than sodium volume and angiotensin must be responsible for the remaining elevation of pressure in these patients. The study indicates that arterial pressure is not dependent on the immediate pressor effects of angiotensin II in sodium replete patients, and in sodium deplete subjects whose PRC remains low, while it is at least partly angiotensin II dependent during sodium volume depletion in the others. The results cast doubts on the clinical usefulness of saralasin in the investigation of patients with hypertension, when studied in the conditions of the present study.
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PMID:Effects of the angiotensin II antagonist 1-sar-8-ala-angiotensin II in hypertension in man. 41 68

Among the newer antihypertensive agents are the beta-blocking drugs, such as propranolol. These agents are useful as second-step drugs to be used if diuretic therapy alone is not effective. In mild to moderately severe hypertension, propranolol, in does of up to 480 mg/day in combination with a thiazide diuretic, has been found to be effective in over 80% of patients on long-term therapy. This degree of response is essentially similar to that noted with a combination of reserpine and a diuretic agent. Although some observers believe that propranolol produces many fewer side effects than the other step 2 drugs (reserpine and alpha-methyldopa), there are some patients who do experience restlessness, insomnia, and depression. Clonidine may be substituted for another step 2 drug, is of moderate potency, but may not be tolerated by a large number of patients because of the severe dry mouth and drowsiness that it produces. Prazosin appears to be a suitable substitute for hydralazine as an effective vasodialator if thiazides plus propranolol or thiazides plus reserpine or alpha-methyldopa are not effective. In some instances, it many be an acceptable second-step drug because of its alpha-adrenoreceptor-blocking properties. The angiotensin II competitive inhibitors or converting enzyme inhibitors may in the future have some place in the management of hypertension.
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PMID:Propranolol and newer antihypertensive drugs in the management of hypertension. 42 60

The renin-angiotensin-aldosterone system in patients with acromegaly was evaluated by infusing [sarcosine1, isoleucine8]angiotensin II, a competitive angiotensin II antagonist, into five acromegalic patients with hypertension and three normotensive acromegalics. The drug was infused at a rate of 600 ng/kg . min for 30 min, 1 h after iv injection of 40 mg furosemide. In addition, before the infusion, plasma samples were obtained for determination of PRA and plasma aldosterone concentration. A significant pressor response to [sarcosine1, isoleucine8]angiotensin II was observed in all eight patients. Preinfusion PRA and plasma aldosterone concentration were significantly lower than in normal controls. It is concluded that in acromegaly, the renin-angiotensin-aldosterone system is suppressed and that this system is probably not involved in maintenance of the high blood pressure observed in some acromegalic patients.
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PMID:Blood pressure response to an angiotensin II antagonist in patients with acromegaly. 42 97

The study concerns the effect of angiotensin II when infused into the systemic and portal blood flow on the general and renal hemodynamics in normal dogs and in hypertensive dogs, as well as the effect of the operation of portacaval transposition (PCT) on the course of renovascular hypertension. When peptide is infused at a rate that causes a moderate pressor effect into the systemic blood flow of normal dogs, an antidiuretic and antinatriuretic effect is obtained, whereas in hypertensive dogs an increase of diuresis, natriuresis, and a less distinct pressor effect are obtained. When angiotensin II is infused into the portal flow, a less distinct pressor and renal effect is seen in dogs with renovascular hypertension. The operation of PCT of the vessels results in a hypotensive effect in the dogs with renovascular hypertension.
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PMID:Portalization of venous blood of kidneys and adrenal glands. Effect in experimental vasorenal hypertension. 42 29

Plasma noradrenaline, plasma renin and pressor action of exogenous noradrenaline and angiotensin in normotensive subjects and patients with essential hypertension. In normotensive subjects an inverse correlation was observed between the index of sympathetic nervous activity, the plasma noradrenaline concentration during physical exercise, and reactivity to exogenous noradrenaline. The relationship between the index of sympathetic nervous activity and reactivity to noradrenaline was invariably disturbed in age-matched patients with essential hypertension. A multiple regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood pressure (r = 0.91). The data suggest that both factors combined, sympathetic nervous activity and pressor response to noradrenaline, are an important determinant of the arterial blood pressure level. An inverse relationship could also be demonstrated between plasma renin concentration and pressor response to angiotensin II in normotensives and hypertensives. However, this relationship was unaltered in the hypertensives. Therefore angiotensin II does not appear to contribute directly to the high blood pressure.
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PMID:[Pathogenesis of essential hypertension. Plasma noradrenaline, plasma renin and pressor effects of noradrenaline and angiotensin in normotensive patients and patients with essential hypertension]. 46 94

1. In conscious non-pregnant and pregnant ewes and in chronic fetal lamb preparations, the beat by beat relationship between pulse interval and systolic pressure was studied during acute elevations in arterial pressure induced by phenylephrine. Baroreflex sensitivity, which was defined as the slope of the pressure-pulse interval relationship when phenylephrine was used to raise pressure, was abolished by atropine and increased by propranolol. Baroreflex sensitivity was less in pregnant ewes and in foetal lambs compared with non-pregnant ewes. 2. These findings suggest that the vagus nerve is responsible for the reflex bradycardia that occurs in the foetus and the ewe when arterial pressure is increased. 3. In both fetal and adult sheep, actue hypertension due to I.V. injection of angiotensin II was not associated with a consistent and progressive bradycardia, such as was seen with acute hypertension caused by phenylephrine. Angiotensin II has no direct chronotropic effect on heart rate in either the adult or the fetus. 4. No linear relationship between arterial pressure and pulse interval was seen when angiotensin II was used to raise pressure in sheep which were treated with propranolol. Therefore the lack of cardiac slowing with pressor doses of angiotensin II was not due to concomitant activation of the sympathoadrenal system. 5. It is concluded that in both fetal and adult sheep angiotensin II reduces the increase in vagal tone which is responsible for slowing of heart rate in response to acute rises in arterial pressure.
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PMID:The action of angiotensin II on the baroreflex response of the conscious ewe and the conscious fetus. 46 30

Plasma concentrations of angiotensin II (AII) were studied in 36 patients with primary (essential) hypertension and 15 normotensive control subjects during basal (1 h supine rest), upright and frusemide-stimulated (80 mg orally) conditions. Plasma renin activity (PRA) and plasma aldosterone (PA) were determined on the same occasions. AII was then correlated statistically to PRA, PA and 24-hour urinary excretions of aldosterone (Aldo-U), sodium and potassium and to the blood pressure (BP) levels. The AII values in the hypertensive patients were not statistically significantly different from those in the normotensive subjects. A close relationship was found between the AII values and the corresponding PRA values in the hypertensive patients (r=0.65--0.76, p less than 0.001 for all). Correlations between AII and PA, and AII and Aldo-U were not consistently significant. No correlation was found between AII and BP or between AII and 24-hour urinary electrolytes. The findings point to an intact function between PRA and AII but a disturbed AII-aldosterone interrelation in primary hypertension.
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PMID:Angiotensin II in primary hypertension, relationship to plasma renin activity, aldosterone and urinary electrolytes. 47 81

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase ( 5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delay response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.
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PMID:Neurogenic activity--angiotensin II interaction during the development and maintenance of renal hypertension in the rat. 47 45

[1-N4-Dimethyl-asparagine]-angiotensin II was synthesized by Merrifield's solid-phase procedure. The analogue gave rat blood pressure about 70% relative potency to Hypertension (Ciba). Rabbit aorta strips gave intrinsic activity alpha E = 1, a PD2 of 6.92 +/- 0.09 and an affinity relative to [Asn1]-angiotensin II of 6.5%.
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PMID:Synthesis and pharmacological properties of [1-N4-dimethyl-asparagine]-angiotensin II. 47 28

The aim of this report is to offer an explanation for the high incidence of arterial hypertension in women taken hormone contraceptives. The real incidence of this association has been considered in women initially having a normal blood pressure and in others who had high blood pressure before using these contraceptives. The estrogen and progestogen components in hormone contraceptives were analyzed individually in various studies. The most recent investigations seem to indicate that progestogen is the main cause of high blood pressure. Different mechanism that could link hormone contraceptives to high blood pressure were investigated. The renin-angiotensin-aldosterone axis involving the action of estrogens and progestogens on the renin substrate, plasma renin, angiotensin II and aldosterone were analyzed. Another possible mechanism could involve glucocorticoids, altering the metabolism of glucose, pyruvate, cholesterol, and triglycerides, Kidney disease involving renal function, microangiopathic anemia, and renal thromboembolism; hyperactivity of the sympathetic nervous system (noraepinephrine and dopamine-beta-hidroxylase blood levels); prostaglandins; genetic mechanism; and individual mechanism were all taken into consideration. Lastly the priorities of the different systems linking high blood pressure to hormone contraceptives and the relationships between them are analyzed.
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PMID:[Hormonal contraceptives and high blood pressure (author's transl)]. 48 Oct 7


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