Gene/Protein Disease Symptom Drug Enzyme Compound
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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

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

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

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

Hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting. This hypertension increases myocardial oxygen consumption and can be prevented by application of vasodilators. A possible cause is activation of the renin angiotensin system. Magnesium is a potent vasodilator and has a beneficial effect after myocardial ischaemia. The study was performed to analyse the influence of magnesium infusion on the haemodynamic status and plasma renin activity in patients undergoing aortocoronary bypass grafting. METHODS. Eighteen patients (NYHA classification II-III) undergoing bypass surgery were divided into two groups, a magnesium and a control group. The magnesium group (n = 9) received 0.8 mEq/kg per h magnesium aspartate as an infusion for 15 min while still awake. After induction of anaesthesia, the magnesium infusion was reduced to 0.2 mEq/kg per h and stopped after aortic cannulation was completed. Plasma magnesium levels and concentrations within erythrocytes were measured. Anaesthesia was induced by flunitrazepam (0.01 mg/kg), fentanyl (0.005 mg/kg) and pancuronium (0.1 mg/kg). After intubation, patients were normoventilated with N2O/O2 = 1:1 and isoflurane (0.5-1.0 vol%). Additional doses of fentanyl (0.0025 mg/kg) were injected before the incision and before sternotomy. Mean arterial pressure, heart rate, cardiac index, total peripheral resistance, pulmonary vascular resistance, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, left ventricular stroke work index, right ventricular stroke work index, intrapulmonary shunt and plasma renin activity were evaluated at five predefined points: (1) prior to magnesium infusion; (2) after magnesium infusion; (3) 10 min following induction of anaesthesia under steady-state conditions; (4) after sternotomy; (5) after aortic cannulation. RESULTS. Concerning the haemodynamic parameters (MAP, RAP, PAP, PCWP) no significant difference between the two groups could be demonstrated. In the control group peripheral resistance (TPR) was higher following sternotomy and aortic cannulation than in the magnesium group. Magnesium prevented decrease of the cardiac index (CI) under steady-state conditions, during sternotomy and following aortic cannulation. Left and right ventricular stroke work indexes (LVSWI and RVSWI) were higher in the magnesium group. Plasma renin levels were not significantly different between the two groups. CONCLUSION. Patients undergoing cardiac surgery benefit from magnesium administration in the pre-bypass phase. Due to its vasodilating effect, magnesium lowers the output impedance of the left ventricle and improves cardiac pumping function. It opposes detrimental cardiovascular responses to sternotomy and following aortic cannulation. Also of importance is the advantageous effect of magnesium on cardiac arrest elicited by cardioplegia and for reactivation of the ischaemic myocardium.
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PMID:[Hemodynamics of coronary surgery patients following magnesium aspartate infusion]. 148 73

Central obesity increases the risk for cardiovascular disease, but little is known about its hemodynamic effects. The aims were to investigate the influence of obesity (as defined by body mass index) and abdominal fat accumulation (as defined by the waist/hip ratio) on hemodynamics at rest and during mental stress. Invasive hemodynamic studies were performed in 20 healthy, normotensive young men (aged 18-22 years) recruited from an unbiased population sample. Their body mass index and waist/hip ratio ranged between 18.5 and 30.2 (mean 24.1) and 0.77 and 0.98 (mean 0.87), respectively. Hemodynamics were related to the two anthropometric indexes by bivariate regression analyses. Cardiac output and stroke volume were positively correlated to body mass index (p = 0.05 and p = 0.005), but inversely to waist/hip ratio (p = 0.01 and p = 0.01). Mental stress augmented the hemodynamic patterns. Total peripheral resistance during stress correlated inversely to body mass index (p = 0.02), whereas high waist/hip ratio was associated with higher systemic vascular resistance p = 0.002). The delta CO/delta MAP ratio, i.e., relative contribution of cardiac output for the stress-induced increase in mean arterial pressure, showed a strong positive association with body mass index (p = 0.004), but was inversely related to the waist/hip ratio (p = 0.002). Serum insulin correlated significantly to the stress-induced change in total peripheral resistance (r = 0.54; p = 0.02), whereas the increase in cardiac output was inversely related to insulin (r = -0.59; p = 0.007). Thus, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance, lower cardiac output, and a vasoconstrictor response to psychosocial stress.
Hypertension 1992 Jun
PMID:Relation of central hemodynamics to obesity and body fat distribution. 159 46

Thoracic aortic cross-clamping causes proximal aortic hypertension. Theoretically, the method used to treat hypertension can influence spinal cord perfusion pressure and neurologic outcome. Phlebotomy was compared to sodium nitroprusside/isoflurane in terms of ability to treat increased proximal mean aortic pressure (MAPp) after thoracic aortic cross-clamping in dogs. Dogs were assigned randomly to one of three groups depending on the method used to treat hypertension after cross clamping: 1) phlebotomy (n = 10); 2) sodium nitroprusside/isoflurane (n = 11); and 3) control (no treatment) (n = 8). In each dog, anesthesia was maintained with isoflurane in oxygen, 1.4% end-tidal. The thoracic aorta was occluded 2.5 cm distal to the left subclavian artery for 50 min and then was released. Hemodynamics, cerebrospinal fluid pressure (CSFP), and regional blood flows by the radioactive microsphere technique, were measured at 1) baseline; 2) 2 min after aortic cross-clamping; 3) after treatment of proximal aortic hypertension; 4) 5 min after aortic unclamping; and 5) 30 min after resuscitation. At 24 h, a neurologic assessment was performed. Thoracic aortic cross-clamping increased MAPp, decreased distal MAP (MAPd), and reduced lumbar spinal cord perfusion pressure (SCPPl), [SCPPl = MAPd - CSFP], in all three groups. Control of increased MAPp necessitated removal of 36 +/- 9 ml/kg of blood in the phlebotomy group. In the sodium nitroprusside/isoflurane group, sodium nitroprusside (16 micrograms.kg-1.min-1) was infused and end-tidal isoflurane concentration increased to 2.5 +/- 0.7%, restoring MAPp to baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of proximal aortic hypertension after thoracic aortic cross-clamping in dogs. Phlebotomy versus sodium nitroprusside/isoflurane. 164 54


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