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

The role of the renin angiotensin system was evaluated in 18 normotensive patients with chronic congestive heart failure and in 5 controls. No correlation was observed between plasma renin activity and cardiac index. There was a significant inverse correlation between renin and pulmonary capillary wedge pressure (r = -0.61, P less than 0.01). Renin values of the patients appeared to be increased when compared with controls with similar left ventricular filling pressure. Specific angiotensin II inhibition by saralasin decreased arterial pressure in 8 out of 14 patients: their renin was significantly higher than that of the remaining 6 patients (P less than 0.01). The 2 patients with the lowest renin levels responded to saralasin with a blood pressure increase. Left ventricular filling pressure decreased in all but these latter 2 patients with either little change or an increase in stroke volume. Thus, renin levels appear to be increased in normotensive patients with congestive heart failure when related to left ventricular filling pressure. Renin via angiotensin II plays a role in the blood pressure control of many patients with congestive heart failure. In some patients angiotensin II blockade appears to improve cardiac function by unloading the left ventricle.
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PMID:Congestive heart failure in normotensive man. Haemodynamics, renin, and angiotensin II blockade. 70 15

1. Haemodynamic and renin responses to dynamic exercise before and after intravenous beta-adrenoreceptor blockade with propranolol were compared in twenty-one patients with essential hypertension and either high (n = 7), normal (n = 7) or low plasma renin activity (n = 7). 2. Renin and heart-rate responses to exercise and beta-receptor blockade diminished from high-renin to normal and to low-renin patients, effects which were blunted with increasing age. 3. Among the renin groups cardiac output, stroke volume, diastolic pulmonary artery pressure, systemic pressure and peripheral vascular resistance as well as their changes produced by exercise and acute beta-receptor blockade were not significantly different. 4. Long-term anti-hypertensive propranolol effects correlated with pre-treatment renin status, renin stimulation and its suppression by acute beta-receptor blockade as well as with the exercise tachycardia and the patient's age. 5. The results suggest different adrenergic control mechanisms in renin sub-types of essential hypertension, age being a modulating factor.
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PMID:Haemodynamic responses to exercise and acute beta-receptor blockade in renin sub-types of essential hypertension. 107 70

Despite substantial progress in cardiovascular disease prevention, stroke and myocardial infarction remain the leading causes of death throughout the industrialized world. Treatment of high blood pressure, while contributing importantly to this progress, remains inefficient and less than optimally effective, particularly in regard to coronary artery disease events. Therapeutic intervention in the renin-angiotensin system offers promise of progress on both these fronts. Renin-sodium profiles have been shown to permit prognostic stratification of otherwise indistinguishable hypertensive patients. Indeed, low renin subjects, without other cardiovascular risk factors, have a particularly favorable prognosis. Now, the pharmacologic ability to mute the pathologic effects of angiotensin II also offers the genuine possibility that the cardioprotective value of antihypertensive therapy may be significantly improved.
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PMID:Prevention of myocardial infarction. 141 21

The haemodynamic and neurohumeral response to a novel vasodilator calcitonin gene-related peptide was assessed in 11 patients with severe chronic heart failure. To assess tolerance, a continuous 48-h infusion (n = 6) was compared with a regimen of two successive 8-h infusions (n = 5). Haemodynamic response profiles were similar for both regimens, though the continuous infusion was poorly tolerated. Reductions in afterload reflected by changes in systemic vascular resistance and systemic blood pressure led to increases in cardiac index of at least 24%. Increments in heart rate accounted for much of the increase in cardiac output, there being no significant change in stroke volume index. The response was maintained over the 48-h study period with no tachyphylaxis. Renin and angiotensin levels increased significantly after 24 h. Calcitonin gene-related peptide exerts a favourable haemodynamic response in patients with severe heart failure. The dose used in this study, however, caused troublesome side-effects, particularly when given by continuous infusion. Further studies are required to establish the therapeutic range of this new peptide.
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PMID:Calcitonin gene-related peptide: a haemodynamic study of a novel vasodilator in patients with severe chronic heart failure. 146 27

To compare the hemodynamic mode of action of captopril in patients with Congestive Heart Failure (CHF) with high- or low-plasma renin activity, we studied the systemic and renal hemodynamic changes induced by this drug in patients with refractory CHF (Group I) or untreated CHF (Group II). Plasma Renin Activity (PRA) was 7.46 +/- 3.7 ng/ml/hr in Group I and 1.15 +/- 0.45 ng/ml/hr in Group II. After the administration of captopril, these values increased to 14.35 +/- 6.19 and to 1.99 +/- 0.76 ng/ml/hr respectively (p less than 0.05). We observed that patients of Group I responded with increases in cardiac index and stroke volume and diminutions in total peripheral resistance, but Group II did not show any significant change in these variables. In contrast to this difference in responses between the refractory and untreated patients, both groups showed similar decreases in pulmonary artery and wedge pressures. Both groups also showed similar increases in plasma volume and effective renal plasma flow, and decreases in renal vascular resistance. These results show that captopril has predominantly venodilator effects in patients with CHF with low PRA levels, and it acts as a mixed vasodilator in patients refractory to conventional therapy, receiving high doses of diuretics, and in whom PRA is elevated. Our results also suggest that the venodilator action of captopril is not mediated by the Renin-Angiotensin System.
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PMID:Acute hemodynamic action of captopril in congestive heart failure: contrasts between refractory and untreated patients. 333 Sep 91

The rest and exercise hemodynamic-inotropic response to administration of the beta-blocker pindolol was evaluated in 10 patients with congestive cardiomyopathy to determine whether the intrinsic sympathomimetic activity (ISA) of this agent may preserve ventricular function in the setting of beta-blockade. A significant (p less than .05) rise in systemic and pulmonary vascular resistance and a decline in stroke volume and cardiac index was observed after a single 10 mg dose. The change in cardiac index was negatively correlated with free drug concentration (r = -.59, p less than .01); the change in pulmonary and systemic vascular resistance showed a positive correlation with plasma concentration (r = .67, r = .57, respectively; all p less than .05). The response to exercise reflected a predominant beta-blocking effect, with a significant decrease in peak heart rate and cardiac index and an increase in pulmonary vascular resistance. There were no significant changes in variables of right or left ventricular inotropy after administration of the drug. The mean baseline plasma norepinephrine concentration for the population was 609 +/- 172 pg/ml (normal = 196 +/- 7 pg/ml) and was markedly elevated in two patients (931 and 2053 pg/ml) who developed severe pindolol-induced hypotension. Renin increased markedly in these two patients, but decreased in each of the remaining eight patients. These data indicate that although inotropy is not adversely affected by pindolol, increased afterload, which appears to be mediated by peripheral beta-blockade, results in a reduction in ventricular performance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic-inotropic response to beta-blocker with intrinsic sympathomimetic activity in patients with congestive cardiomyopathy. 353 53

Plasma renin levels, measured in 39 untreated patients in 1967, under conditions of sodium loading and sodium depletion have been related to the incidence of stroke and myocardial infarction. Renin levels were not significantly different in patients with or without vascular complications. Out of 13 patients with persistently low renin levels 6 had suffered either a stroke or a myocardial infarction and 7 had not. Plasma renin levels were also measured in 116 treated hypertensive patients. There was no relation between plasma renin level and vascular complications. It is concluded that levels of plasma renin are not a reliable index of the probability of hypertensive patients suffering a stroke or myocardial infarction.
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PMID:Plasma renin levels and vascular complications in hypertension. 470 8

Renin is stored in synaptosomes of rat brain, separately from cathepsin D and intraneuronal angiotensin II (ANG II) has been demonstrated with the electron-microscope. Although the subcellular localization of other components of the renin-angiotensin system (RAS) have still to be investigated, these data suggest possible intracellular synthesis of ANG II in the brain. Brain ANG II is biochemically identical to the plasma peptide and corresponds to (IIe) 5-ANG II. The peptide level is unchanged after bilateral nephrectomy, and angiotensin I (ANG I) accumulation is observed in nephrectomized animals following brain angiotensin converting enzyme blockade. The significantly greater accumulation of ANG I and reduction of ANG II in stroke prone spontaneously hypertensive Wistar-Kyoto rats (WKY) indicates a higher synthesis and turnover rate of ANG II in SHR. Most converting enzyme inhibitors (CEI) penetrate the brain after chronic oral treatment. Part of their blood pressure lowering action may therefore be explained by an inhibition of the brain RAS.
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PMID:The brain angiotensin system: subcellular localization and interferences with converting enzyme inhibitors. 610 Jun 13

Acute hemodynamic changes induced by Betaxolol (B.) were studied in 10 patients (7 men, 3 women, mean age: 36 years), with uncomplicated essential hypertension. The brachial artery was cannulated with a short Teflon catheter and Swan-Ganz catheter was introduced into the pulmonary artery. Brachial (BAP) and Pulmonary arterial pressures (PAP), cardiac output (dye dilution) were recorded before (To) and after intravenous infusion of B. (0.2 mg/kg) during 5 minutes (T1), followed by the infusion of B. at a rate of 0.4 mg/kg during 15 minutes (T2). Cardiac index (C.I.), Stroke index (S.I.), Systemic Vascular (SVR) and Pulmonary Vascular Resistances (PVR), Left Ventricular Stroke Work Index (LVSWI) were calculated. C.I. declined significantly. This resulted from a significant decrease of heart rate, since S.I. was unsignificantly changed. BAP (systolic and mean) decreased significantly, since unsignificant changes of PAP were noted. SVR and PVR were significantly increased and LVSWI was significantly decreased. Plasmatic Renin Activity was unsignificantly decreased.
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PMID:[Acute hemodynamic effects of betaxolol in uncomplicated arterial hypertension in young persons]. 681 Aug 22

Blood pressure, cardiac output, plasma volume, renin, and aldosterone were measured in 13 patients with essential hypertension on placebo and after 1, 4, and 12 wk on hydrochlorothiazide 100 mg daily. In 9 patients the same variables were also measured after 24 and 36 wk. Hydrochlorothiazide lowered mean arterial pressure (p less than 0.01). Cardiac output was reduced after 4 and 12 wk of treatment, followed by a return to placebo levels. Stroke volume changed in the same way but heart rate and total peripheral resistance did not differ from placebo values. Plasma volume was reduced after 1 and 24 wk. Renin was permanently elevated (p less than 0.01), but aldosterone rose only during the first 12 wk of treatment. A comparison between responders (greater than 10% fall in mean arterial pressure) and nonresponders (less than 10% fall) revealed different hemodynamic patterns. In responders the initial fall in cardiac output was followed by a return to pretreatment levels, whereas in nonresponders it was permanently reduced. Consequently, total peripheral resistance was lowered only in responders. Nonresponders tended to show a greater degree of plasma volume depletion and greater stimulation of renin and aldosterone, which probably contributed to elevated peripheral resistance. It is concluded that changes in cardiac output are unlikely to be of decisive importance in the ultimate reduction of peripheral resistance in responders to thiazide therapy.
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PMID:Hemodynamic changes during long-term thiazide treatment of essential hypertension in responders and nonresponders. 698 24


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