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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of submaximal exercise upon haemodynamic and biochemical variables was investigated in healthy male subjects, aged 17-27 years, before and at the end of 2 weeks treatment with propranolol (40 mg p.o., q.i.d.). Propranolol reduced the resting blood pressure in normal subjects significantly. This effect was due to reduction of cardiac output and of systemic vascular resistance. No effect of propranolol on BP was seen during maximal exercise, since a reduced cardiac output was accompanied by an increased peripheral resistance. The reduction of cardiac output during exercise can be compensated in part by an increase in stroke volume. The sympathetic activity induced by physical exercise in normotensives increased plasma renin concentration (PRC) and plasma aldosterone (PA), and suppressed urinary excretion of c-AMP. PRC returned to basal levels after 45 min. No increase of PRC was observed after exercise in subjects treated with propranolol. Yet the increase of PA was not completely suppressed. No direct relation was demonstrated between PRC and the haemodynamic variables before or during the administration of propranolol.
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PMID:Effect of exercise and of prolonged oral administration of propranolol on haemodynamic variables, plasma renin concentration, plasma aldosterone and c-AMP. 20 Apr 33

1. The effects of long-term treatment with the angiotensin I converting-enzyme inhibitor YS 980 were examined in stroke-prone spontaneously hypertensive (sp-SH) rats. Development of hypertension was markedly blunted in the YS 980-treated animals. 2. Effective converting-enzyme inhibition was confirmed by significant increases in plasma angiotensin I (ANG I) and plasma renin concentration, inhibition of the pressor responses to intravenous ANG I and potentiation of the depressor responses to intravenous bradykinin. 3. Urinary free aldosterone excretion was decreased but no changes in urinary sodium and potassium excretion were observed. 4. The pressor responses to intravenous leucine-enkephalin were reduced. 5. The pressor responses to injection of ANG I and bradykinin into the lateral brain ventricle were unaltered. 6. We conclude that the antihypertensive action of YS 980 in sp-SH rats cannot be explained by the inhibition of the plasma renin-angiotensin system alone. Effects on other peptide systems must be considered.
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PMID:A novel orally active converting-enzyme inhibitor YS 980: effects on blood pressure in spontaneously hypertensive rats. 23 20

Correlates of plasma renin activity and plasma aldosterone levels with hemodynamic functions were studied in 47 male patients with untreated, permanent essential hypertension. All subjects had a normal creatinine clearance and received a diet of 110 mEq/day of sodium. Supine plasma renin activity was directly correlated with cardiac index (P less than.01) and cardiopulmonary blood volume (P=.01). Percentage changes in plasma renin activity and total peripheral resistance in response to upright position were positively correlated (P less than.001). Supine plasma aldosterone level was directly correlated with stroke index (P less than .001) and negatively correlated with hear rate (P less than .05). No significant correlation of aldosterone level was observed with the other measurements, including plasma renin activity. The study points to the neural sympathetic control of plasma renin activity in essential hypertension and suggests the existence of some interrelationships between aldosterone level and cardiac performance.
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PMID:Relationship of plasma renin activity and aldosterone levels with hemodynamic functions in essential hypertension. 32 63

1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P less than 0.001) and mean brachial artery pressure (MBAP) by 18.7 mmHg (P less than 0.001) within 75 min in 26 hypertensive patients. After 2 months (on 150-600 mg/day) MBAP had decreased by 27.1 mmHg (n = 18) with no further change of plasma ANG II. delta MBAP was significantly related to control log plasm renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11.2 mmHg greater (P less than 0.001) than delta MBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+3.3 beats/min; P less than 0.005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P less than 0.01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P less than 0.01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P less than 0.001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.
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PMID:Haemodynamic effects of captopril in hypertensive patients: comparison with saralasin. 39 66

Cardiorespiratory, thermal, and renal responses to a 30-min head-out immersion in 15 degree C water were studied at 1-ATA air and 11-ATA helium-oxygne environments in four male subjects wearing dry suits. Cardiorespiratory responses to immersion (reductions in heart rate, expiratory reserve volume, vital capacity, and thoracic impedance; and increases in stroke volume, cardiac output, and inspiratory capacity) were comparable at both pressures. However, thermal responses to immersion (a reduction in mean skin temperature and increases in skin heat flux and suit conductance) were significantly greater at 11 ATA compared to those at 1 ATA. The rate of urinary excretion of norepinephrine increased significantly during and after immersion at 11 ATA but not at 1 ATA. In contrast, the urinary excretion of epinephrine was not altered by pressure or immersion. The immersion diuresis was greater and lasted longer at 11 ATA than at 1 ATA although there was no difference in the endogenous creatinine excretion . This diuresis was accompanied by a significant natriuresis which was more marked at 1 ATA than at 11 ATA. At 1 ATA, the urinary excretion of both aldosterone and antidiuretic hormone (ADH) decreased during immersion. At 11 ATA, the rate of excretion of these hormones before immersion was lower compared to that at 1 ATA and did not change significantly during immersion. These results indicate that immersion in a hyperbaric helium-oxygen environment presents a greater cold stress than at 1-ATA air, and also that immersion diuresis and natriuresis at high pressure may be induced by a factor other than inhibition of aldosterone and ADH.
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PMID:Physiological responses to head-out immersion in water at 11 ATA. 63 73

In 12 patients with mitral stenosis of a severity that surgery was required, some hemodynamic parameters after intravenous injection of 400 mg Kaliumcanrenoat were studied. The hemodynamic changes were noted after 15 min and reached maximal values after 60 min. The increased values of pulmonary wedge, pulmonary artery and right atrial pressures were significantly reduced and the cardiac index and stroke volume index augmented, with unchanged systemic arterial pressure. Thus, a remarkable relief from pulmonary congestion followed, accompanied by an increase of the left-ventricular working index.--These results encourage the use of aldosterone antagonists in certain cases suffering from severe mitral stenosis.
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PMID:[Hemodynamic effects of aldosterone antagonists in patients with mitral stenosis (author's transl)]. 68 76

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.
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PMID:What makes the renin-angiotensin system a pathogenic factor? 69 4

1. The changes in plasma volume, haemodynamic variables, plasma renin activity and plasma aldosterone were studied in forty-one hypertensive patients after administration of adrenergic-blocking agents. Four drugs were used: alpha-methyldopa (fourteen patients), guanethidine (ten patients), clonidine (nine patients) and reserpine (eight patients). Drugs were administered orally during 7 days' hospitalization on a normal sodium diet (110 mmol/day). 2. The four drugs had similar effects: a significant decrease in blood pressure, a significant increase in plasma volume and no change in stroke volume. 3. With alpha-methyldopa and guanethidine, heart rate, plasma renin activity and plasma aldosterone were unchanged. 4. With reserpine and clonidine, heart rate and plasma renin activity were significantly decreased, whereas plasma aldosterone did not change significantly. 5. This study suggests that the decrease in plasma renin activity was related to the lowering of the heart rate rather than to sodium retention and that adrenergic-blocking agents can impair the normal relationship between stroke index and plasma volume, between plasma volume and plasma renin activity, and between plasma renin activity and plasma aldosterone.
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PMID:Anti-hypertensive adrenergic-blocking agents: effects on sodium balance, the renin-angiotensin system and haemodynamics. 80 49

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.
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PMID:Effect of sotalol on haemodynamics and renin-angiotensin-aldosterone system in hypertensive patients. 93 70

Two hundred one patients with essential hypertension, who had studies of their renin-aldosterone system performed between April 1967 and December 1972, were surveyed for myocardial infraction or cerebrovascular accident. Of the patients, 42% had low plasma renin activity. Myocardial infractions or cerebrovascular accidents were documented in 15% of those with low plasms renin activity and in 5% of those with normal plasma renin activity. When adjustments were made for differences in afe and blood pressure , a protective effect in low-renin hypertension was evident. When black patients were considered separately,there was no difference in diastolic blood pressure; however, vascular complications were not less frequent in low-renin hypertensives. The results suggest that low plasma renin activity does not protect against the development of vascular complications in essential hypertension.
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PMID:Low-renin hypertension. Occurrence in vascular complications. 114 29


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