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

The "effective" contribution of angiotensin II in blood pressure regulation was investigated in 6 patients on maintenance hemodialysis who were hypertensive at the time of the study (MAP 133 +/- 5 mmHg). Saralasin, a specific angiotensin II inhibitor, was infused at 0.5 and 2.5 microgram/kg/mn three hours before andone hour after hemodialysis. Before hemodialysis, a mean arterial pressure decrease of 13.2 to 19 p. 100 was obtained in 5 patients, arterial pressure being normalized in three of them. After hemodialysis, saralasin induced a normalization of arterial pressure in these 5 subjects. One patient, who was resistant to the saralasin infusion before and after the hemodialysis procedure, can be considered as purely volume-dependent. The renin-angiotensin system is probably one of the primary determinant of dialysis-resistant hypertension. However, a negative response to saralasin should encourage to control hypertension by more vigorous ultrafiltration during dialysis.
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PMID:[Arterial hypertension and maintenance hemodialysis: effects of specific inhibition of angiotensin II by saralasin acetate]. 10 Nov 76

The possibility that mean arterial pressure (MA) might be maintained by an effect of angiotensin II or its precursors on the central nervous system in rats made hypertensive by occluding the aorta between the renal arteries was investigated. Aortic coarctation produced severe hypertension (MAP greater than 150 mmHg) and plasma renin activity values (radioimmunoassay) at least 10 times normal within 2-6 days after surgery. [Sar1, IIe8]angiotensin II, an angiotensin II antagonist administered centrally via an intracerebroventricular (icv) injection (10-100 mug), lowered the MAP in a dose-dependent manner. Peripheral administration of [Sar1, IIe8]angiotensin II (bolus injection) at 100 mug intra-arterially was ineffective, but the antagonist did lower arterial pressure when infused intravenously for 1 h at 4 times this dose. Less than Glu-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, a converting enzyme inhibitor, and pepstatin, a renin inhibitor, were ineffective via an icv injection. These results suggest that angiotensin II is in part responsible for the elevation in blood pressure following aortic coarctation in rats. Both central and peripheral administration of [Sar1, Ile8]-angiotensin II lowered mean arterial pressure but the antagonist lowered arterial pressure at lower doses and produced a more rapid decline in arterial pressure when administered into the central nervous system then when administered intra-arterially or intravenously.
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PMID:Central antihypertensive effects of inhibitors of the renin-angiotensin system in rats. 18 43

Uninephrectomized, saline-fed male Sprague-Dawley rats were given DOCA 5 mg per week alone or together with progesterone 20 mg per week for 6 weeks (phase I). Subsequently, the doses of DOCA and progesterone were doubled and the rats were studied for an additional 6 wk (phase II). Progesterone prevented DOCA-induced hypertension during phase I. Phase II blood pressures were higher in DOCA-progesterone-treated animals than in controls, but remained lower than in animals treated with DOCA alone. At the end of phase II the animals were killed, and blood samples and skeletal muscle samples were taken for analysis of electrolyte content. DOCA-treated animals were found to have an increased rate of potassium excretion, an increase in muscle sodium concentration, and a decrease in muscle potassium concentration compared to the controls. Progesterone treatment significantly blunted the DOCA-induced changes in muscle electrolyte concentrations and increased the rate of sodium excretion. No hypotensive effect was observed when progesterone in doses similar to those of phase I was administered to spontaneously hypertensive rats. Thus, in experimental mineralocorticoid hypertension, the hypotensive effect of progesterone appears to correlate closely with its mineralocorticoid antagonistic properties.
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PMID:Antihypertensive effect of progesterone in rats with mineralocorticoid-induced hypertension. 43 99

A 10 mg bolus of the angiotensin blocker saralasin was injected 113 times in 68 subjects with essential or renovascular hypertension. Ninety percent of injections caused a transient increase in blood pressure, which correlated with plasma renin activity (PRA) (r = -0.54); Mean increase at 2 minutes was 21/13.4 mm Hg (P less than 0.001) and was independent of pre-injection control blood pressure, with a rapid decrease to or below control values thereafter. Thirty-seven subjects were studied on successive days before and after furosemide-induced sodium depletion (152 +/- 26 mEq [SE] sodium loss). In the low renin group, sodium depletion did not change PRA or the magnitude of the pressor response to saralasin, but significantly decreased control MAP by 13 mm Hg (P less than 0.01). In normal and high renin patients, MAP was unchanged after diuresis, but PRA increased significantly and the pressor response was attenuated. The net effect of sodium depletion was to reduce the pressor response to saralasin in all renin subgroups by 9 to 12 mm Hg. Saralasin bolus injection, unlike infusion, saturates available vascular receptors only briefly, eliminating prolonged pressor responses.
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PMID:Pressor response to saralasin (1-sar-8-ala-angiotensin II) bolus injection in hypertensive patients. 63 40

Oral contraceptives have been implicated as a causative factor of venous thrombosis and thromboembolism. Compounds containing over 50 mcg of estrogen have developed this complication most frequently. Steroid hormones have a marked influence on liver function. Large doses have caused cholestasis and hepatocellular damage. Disturbances in carbohydrate metabolism have been recorded. Lipid metabolism have also been shown to be disturbed with increased serum levels of triglycerides and low density lipoproteins. A rise in the cholesterol serum level seems to be correlated with the progestogen content of the compound. The ''minipill'' with a small dose of progestogen alone had been effective by alteration of the cervical mucus. The ''one-a-month pill'' is a combination of a long-acting estrogen, quinestrol, and a chorter acting progestogen, qunigestanol acetate. It has not been as acceptable or as effective as combined compounds. The ''morning-after'' pill consists of large doses of stilbestrol. The method has been effective but when de-ethylstilbestrol has been given to a patient already pregnant to prevent an early spontaneous abortion, adenocarcinoma of the cervix or vagina has been reported. Hypertension has been more common with increased duration of pill use. High dosage of progestogens and increasing age of patients have increased the incidence of hypertension. Cerebrovascular disease had also been more frequent among pill users. An increased incidence of gallbladder disease and of gallstones has been shown in pill users. Urinary tract and vaginal infections were reported more often in pill users. Increased sexual activity may have been a factor in this relationship. Resumption of ovualation after discontinuation of oral contraceptives usually follows within 4-6 weeks. In about 1% of patients amenorrhea and anovulation result for 6 months or more. This is often accopanied by galactorrhea. There is evidence that mestranol is demethylated to ethinyl estradiol in the liver. Progesterone seems to interfere with conversion. Therefore ethinyl estradiol is preferred as a compound of the pill. Also the different progestogens used are metabolized in the liver to norethisterone before they exert their biological effects. Several drugs, as ampicillin and barbiturates, have been shown to interfere with the efficacy of oral contraceptives. It is concluded that the overall results have shown oral contraceptives to be an excellent form of contraception with minimal and acceptable side effects and the least metabolic disturbance.
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PMID:Current status of oral contraceptive. 82 61

In an effort to help explain why it is often difficult to demonstrate hypotension with alpha-methyldopa on an acute basis in normotensive anesthetized animals, the drug was administered intravenously in single doses of either 50, 100, or 200 mg/kg to chloralose-anesthetized cats while monitoring mean arterial pressure; the systolic pressor response in arterial pressure to bilateral occlusion of the common carotid arteries; hind limb vascular resistance in a vascularly isolated, extracorporeally perfused but neurally intact hind limb; and the response of hind limb vascular resistance to CCO. Alpha-methyldopa failed to cause any significant hypotension and also failed to affect vasomotor tone to the hind limb vasculature, but the drug augmented the pressor response to CCO on MAP and hind limb vascular resistance. Alpha-methyldopa also had no effect on hind limb vascular resistance when added directly to the extracorporeally perfused hind limb vascular resistance when added directly to the extracorporeally perfused hind limb circuit, indicating a lack of direct vascular smooth muscle dilating properties in these preparations. It is postulated that the augmented baroreceptor demonstrated may help th explain why it is difficult to record hypotension on an acute experimental basis with this drug. Such actions of alphamethyldopa might also provide a basis for understanding the development of tolerance to the antihypertensive effects of the drug and instances of paradoxical hypertension with it when these occur in the hypertensive human.
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PMID:Some paradoxical aspects of the cardiovascular pharmacology of alpha-methyldopa. 83 45

Progesterone (2.5 mg per kilogram) caused sustained hypertension in rabbits. When the same dose of progesterone was administered together with prolactin (1.25 mg. per kilogram), there was no increase in the blood pressure. In rabbits with progesterone-induced hypertension, the addition of prolactin caused a sharp drop in blood pressure. It is suggested that prolactin acts by reducing the sensitivity of the blood vessels to circulating pressor substances and further that a reduced prolactin response may be the cause of heightened sensitivity to pressor substances observed in pre-eclampsia.
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PMID:Prolactin and hypertension. 84 88

The antihypertensive effect of minoxidil was studied in 6 patients with varying degrees of hypertension. Their baseline mean arterial pressure (MAP bi) ranged from 122 to 197 mm Hg. Single oral doses between 2.5 and 25 mg were administered in sequence and the time-course of hypotensive action was followed. We have reported previously that when the peak lowering of MAP is linearly regressed against log dose, both the dose-response slope (M) and threshold dose (Dt) are positively correlated with the MAP bi of individual patients. This investigation focuses on the temporal pattern of effect. It was found that the hypotensive effect of minoxidil declined linearly with time at a rate consistent with an average effective biologic half-life of about one day. The rate of decline of effect was apparently independent of dose but was dependent on MAP bi. Since both response to and duration of effect of minoxidil are functions of MAP bi, there is an abvious need to individualize dosage regimens based on the severity of disease. Using pharmacodynamic parameters, guidelines for loading dose, maintenance dose, and dosing frequency as a function of the degree of hypertension are suggested. Loading dose requirements were found to increase with MAP bi while maintenance doses were largely independent of the severity of the disease. Frequently of dosing was found to range from 3 times a day in very severe hypertension to once a day in moderate hypertension.
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PMID:Pharmacodynamics of minoxidil as a guide for individualizing dosage regimens in hypertension. 112 15

The purpose of this study was to determine if alpha 1-adrenergic receptor blockade alters the hemodynamic response to exercise in young (less than 25 yr) male borderline hypertensives differently than in young normotensives. Five hypertensive (HTN, MAP greater than 105 mmHg) and 7 normotensive (NTN, MAP less than 95 mmHg) college-age males underwent two 30 min bouts of cycle ergometry exercise at 50% VO2pk in a warm (25 degrees C, 50% rh) environment; one following alpha 1-receptor blockade with prazosin (PRAZ) and the other following placebo administration (PLAC). During resting PLAC and compared to NTN, HTN exhibited an elevated cardiac index (CI, p = .002), similar HR and elevated total peripheral resistance index (TPRI, p = .015). During resting PRAZ, CI and TPRI were similar but HR was higher (p = .013) in HTN than NTN. While reduced during PRAZ, resting MAP was higher in HTN than NTN (p = .007) for both trials. With exercise and PLAC, CI was higher (p = .029) while HR and TPRI were similar for HTN compared to NTN. With PRAZ, the exercise CI, TPRI and HR responses were similar for both groups. Exercise MAP was blunted in both groups with PRAZ. While not differing significantly between groups for each treatment, MAP was stable for NTN while it declined after 10 min of exercise in HTN. The elevated CI seen in exercising HTN with PLAC was removed with PRAZ; the exercise response was otherwise unaltered by alpha 1-blockade. Consequently, these data suggest that young male hypertensives have an elevated blood pressure due to an elevated CI incompletely offset by a reduced TPRI. While alpha 1-blockade lowers MAP by lowering CI, the MAP response to exercise remains unaltered.
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PMID:Effects of alpha 1-receptor blockade on the hemodynamic responses to exercise in young hypertensives. 135 66

Hemodynamic parameters were studied in 80 cases of pregnancy induced hypertension (PIH) using noninvasive cardiovascular detector (TP-CBS). Women were categorized into 3 kinds of hemodynamic patterns: (1) normal cardiac output, 45 cases, cardiac index (CI) = 2.5-4 L.min-1/m2; (2) high cardiac output, 10 cases, CI greater than 4 L.min-1/m2; (3) low cardiac output, CI less than 4 L.min-1/m2, 25 cases (31.5%). Ten cases in each category were selected for test after volume expansion therapy. MAP decreased in varying degrees. CI showed marked increase in the low cardiac output group, but decreased to normal in the high output group. The monitoring criteria for protecting against pulmonary edema during volume expansion therapy were discussed.
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PMID:[Hemodynamic surveillance in pregnancy induced hypertension during volume expansion therapy]. 138 Apr 22


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