Mineralocorticoid activity in patients in the early benign phase of essential hypertension.
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Biomedical subjects
Publications and source records attributed to W Nowaczynski.
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Splanchnic blood flow (SBF) was measured simultaneously with cardiac output (dye dilution) and intrarterial blood pressure by constant infusion of indocyanine green in 11 control subjects, 13 patients with essential hypertension (EH) and seven hypertensive patients with renal artery stenosis (RAS). The cardiac index (CI) was lower (P less than 0.05) in patients with EH (3.17 plus or minus 0.07 L/min/m-2) (mean plus or minus SEM) than in control subjects (3.43 plus or minus 0.09). Associated with the lower CI was a significantly (P less than 0.01) lower SBF (0.797 plus or minus 0.02 L/min/m-2 vs 0.889 plus or minus 0.04). Patients with RAS presented with higher (P less than 0.01 vs EH, nonsignificant vs control subjects) cardiac index (3.66 plus or minus 0.17) and even lower SBF (0.749 PLUS OR MINUS 0.02). Furthermore, there was a negative correlation (r = - 0.652) between the mean arterial pressure and the SBF when results for all patients were considered. The correlation remained (r = - 0.568) in the EH group and the slope of regression line was not different from that for all subjects. The CI and SBF were weakly correlated (r = 0.423) in control subjects and patients with EH, whereas in patients with RAS, a negative correlation was found (r = - 0.778). This study indicates that the SBF, although significantly decreased in patients with EH, remains proportional to the CI in control subjects and in essential hypertensive patients. No redistribution of CI in regard to the splanchnic circulation occurs in EH. In contrast, in patients with RAS a dissociation of CI and SBF occurs and the fraction of the CI which passes through the splanchnic vascular bed is markedly reduced. The close correlation between mean arterial pressure and SBF suggests that both parameters are influenced by a common pathophysiological factor.
Plasma arginine vasopressin (PAV) concentration was determined by radioimmunoassay during the diurnal cycle in 8 recombent healthy male subjects. Two subjects were studied again 3 weeks later while receiving 1 mycles. In 8 out of 10 cycles, a nocturnal increase in PAV was found; there was a progressive rise during the night in 5 subjects and a peak occurred at 2400 or 3400 h. In 1 subject no variation was detected and in another, the pattern was compleetly different. The mean PAV in the 10 cycles was significantly (P less than 0.001) higher during the night than during the day. Dexamethasone did not modify the pattern of variation, but induced a significant (P less than 0.001) decrease in PAV. Hematocrit remained stable throughout the study as did osmolality, except at 2000 h, when a significant (P less than 0.001) increase (5 mOsm) on average occurred in every subject. Blood sugar, sodium or chloride did not account for the observed rise in osmolality and no simultaneous change in PAV occurred. A rise in PAV explains, to some extent, the known nocturnal decrease in urine output. Diurnal variations in PAV must be taken into account in clinical investigations involving vasopressin.
Propranolol administration to rats was studied for its effects on plasma renin activity, renal renin content, and adrenal and brain isorenins. Propranolol was given intraperitoneally at 6 and 30 mg/kg/day for a 15-day period. Pulse rate was significantly decreased. There were no effects on the isorenin content of adrenal or brain tissue or on renal renin content. Rats responded in two completely different ways with respect to plasma renin activity. Two-fifths had a total suppression of plasma renin activity; the rest had concentrations similar to those in controls. These observations are consistent with those seen during chronic administration of propranolol to hypertensive patients and suggest that its antihypertensive effect may in some patients be through the suppression of renin release. Its mechanism of action in most patients remains at present unclear.
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MAJOR SCREENING PROGRAMS FOR HYPERTENSION ARE NECESSARY FOR THE FOLLOWING REASONS: (a) the 12 to 15% prevalence of hypertension in the North American population; (b) the high proportion of hypertensive patients who are inadequately treated or whose disease is not even recognized; (c) the fact that in too many medical centres hypertension is poorly investigated or considered an insignificant finding; (d) the demonstration by many groups, especially the Framingham study, of hypertension as the major factor in the occurrence of severe cardiovascular disease; and (e) the achievement of a marked decrease in severe cardiovascular complications following adequate treatment. But such screening programs are of little value if unaccompanied by a major educational effort directed not only to the public but also to the medical profession, and a parallel increase in the funding of biomedical research into the basic physiopathological mechanisms of hypertension.
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An analysis of the plasma renin levels in relation to the incidence of severe cardiovascular complications (coronary thrombosis, stroke, ruptured aortic aneurysm) was made in 325 patients with various types of hypertension. These patients had one to four measurements of plasma renin activity taken under standard conditions of sodium intake and posture in the period 1963-68. The follow-up was 5 to 10 years in the four groups of hypertensive patients (essential hypertension, malignant hypertension, hypertension secondary to renal parenchymatous disease and hypertension caused by, or associated with, renal artery obstruction). For all 325 patients, the incidence of such complications was 23.6, 20.4 and 44.7% in the low, normal and high renin groups. These findings are at variance with the claim that renin constitutes a serious risk factor in hypertensive patients, especially if it is isolated from other parameters such as the level of diastolic pressure, the adequacy of kidney function, the effectiveness of dietary and drug management of hypertension, and especially the presence or absence of atherosclerotic lesions of the large vessels at the time of the renin determination.
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