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Biomedical subjects

E A Rosei

Publications and source records attributed to E A Rosei.

32 records · Page 2Linked to original sources
PubMed1986

Effect of captopril on left ventricular mass and function in hypertensive patients and in the rat.

Twenty-seven mild to moderate essential hypertensive patients were treated with captopril alone or combined with hydrochlorothiazide and left ventricular echocardiographic changes were evaluated after 1, 3 and 6 months. The left ventricular mass decreased slightly after 3 months, together with mean wall stress and total peripheral resistance, while the cardiac performance, as measured by fractional shortening and cardiac output, was unaffected. A high degree of individual variability was observed, and only 9 out of 20 patients examined after 3 months had a consistent reduction in left ventricular mass. The effect of captopril on the isomyosin composition was also evaluated in 4 normotensive rats after 12 weeks of drug administration. No interference with the physiological pattern was observed and no modifications of the biochemical and structural properties of the myocardium were detected.

Adult↗
PubMed1976

Effects of intravenous labetalol on blood pressure, angiotensin II and aldosterone in hypertension: comparison with propranolol.

1. Labetalol, a compound with both alpha- and beta-adrenoreceptor-blocking actions, was given intravenously (1-5-2-0 mg/kg) in twenty recumbent hypertensive patients. 2. There was a rapid reduction in systolic and diastolic pressures in all, maintained up to 24 h in some subjects. 3. Severe hypotension was not seen in recumbent subjects, but postural hypotension was common. 4. Labetalol caused significant lowering of heart rate. 5. Labetalol induced significant and related lowering of plasma angiotensin II and aldosterone concentrations, most obviously when these were initially high. 6. In a cross-over comparison in five patients against 10 mg of propranolol intravenously, labetalol was more effective in lowering blood pressure, but less effective in lowering pulse rate or plasma angiotensin II.

Aldosterone↗
PubMed1976

The effects of saralasin, an angiotensin II antagonist, on blood pressure and the renin-angiotensin-aldosterone system in normal and hypertensive subjects.

Blood pressure reduction with saralasin infusion was seen only in hypertensive patients with abnormally elevated basal plasma renin and angiotensin II levels, and after sodium depletion the reduction in blood pressure was more marked. In normal subjects, and in hypertensives with plasma renin and angiotensin II levels within the normal range, there was no marked fall in blood pressure across saralasin infusion regardless of the sodium status of the individual. Plasma aldosterone concentration fell during saralasin infusion in those subjects with high baseline renin and angiotensin II levels. This fall occurred in the sodium replete and deplete states. In the normal subjects, and those hypertensives with normal plasma renin levels, there was no fall in aldosterone in the sodium replete state. However, after sodium depletion the expected rise in aldosterone was abolished during saralasin infusion, the plasma aldosterone falling to within the normal sodium replete range, rising again after the saralasin infusion was stopped. This study supports the concept of a direct role for renin and angiotensin II in the maintenance of hypertension in those subjects with elevated basal plasma renin. Plasma aldosterone would appear to be controlled, at least in part, by the prevailing plasma angiotensin II level in those subjects with elevated basal levels of angiotensin II; that is in high renin hypertensives, and in normal subjects and normal renin hypertensives who are sodium deplete.

Adult↗
PubMed1976

Labetalol (AH5158), a competitive alpha- and beta-receptor blocking drug, in the management of hypertension.

The effects of intravenous labetalol, a drug with both alpha- and beta-adrenergic receptor blocking actions, have been studied in 20 severely hypertensive patients. There was a prompt and sustained fall in arterial pressure; severe hypotension did not occur in recumbent patients but postural hypotension was common. Pulse rate was consistently reduced, but bradycardia was not a problem. Significant and correlated falls in plasma angiotensin II and aldosterone were seen. In a direct comparison with intravenous propranolol, labetalol was less effective in lowering plasma angiotensin II, but more effective in reducing blood pressure. Oral labetalol provided good control of blood pressure and other features in two patients with phaeochromocytoma. Intravenous labetalol was similarly effective in controlling a hypertensive crisis following clonidine withdrawal.

Adrenergic alpha-Antagonists↗
PubMed1976

The effects of the angiotensin II antagonist saralasin on blood pressure and plasma aldosterone in man in relation to the prevailing plasma angiotensin II concentration.

The effect of saralasin in lowering blood pressure and plasma aldosterone concentration in normal subjects, both sodium-replete and sodium-deplete, and in patients with various forms of hypertension, is closely related to the basal plasma angiotensin II concentration. These findings confirm and extend earlier studies of angiotensin II/arterial pressure and angiotensin II/aldosterone dose-response curves. They also emphasize the importance of the renin-angiotensin system in the control of aldosterone in sodium depletion and in renal hypertension.

Aldosterone↗
PubMed1976

Effect of blood pressure angiotensin II and aldosterone concentrations during treatment of severe hypertension with intravenous labetalol: comparison with propranolol.

1 The actions of labetalol 1.0-2.0 mg/kg intravenously on blood pressure, heart rate, plasma angiotensin II and aldosterone concentrations have been studied in 20 recumbent hypertensive patients. 2 In all subjects there was a reduction in systolic and diastolic blood pressures within 5 min of completion of injection. 3 Severe hypotension was not seen but three patients who had a marked fall in blood pressure experienced side-effects. Postural hypotension was common at the end of the study. 4 Labetalol caused significant reduction in heart rate. 5 Labetalol induced significant lowering of plasma angiotensin II and in plasma aldosterone concentrations, which were most obvious when these were increased initially; overall there was a close correlation between concurrent measurements of angiotensin II and aldosterone concentrations. 6 In five patients a comparison was made against propranolol 10 mg intravenously. Labetalol was more effective in lowering blood pressure but less effective in reducing pulse rate of plasma angiotensin II concentration.

Aldosterone↗
PubMed1976

Treatment of phaeochromocytoma and of clonidine withdrawal hypertension with labetalol.

1 Labetalol has been used as medical treatment in five patients with phaeochromocytoma. 2 In four of the five patients, blood pressure was satisfactorily controlled, and symptoms and signs were relieved. 3 Labetalol also provided satisfactory cover across surgery for the removal of tumours in two cases. 4 In one instance, it was not possible to give sufficient labetalol orally to suppress the attacks of phaeochromocytoma. This patient was not effectively controlled at operation with a combination of propranolol and phenoxybenzamine. 5 Intravenous labetalol rapidly lowered blood pressure and relieved symptoms in a patient experienced hypertensive crisis after clonidine withdrawal. 6 Labetalol is a useful addition to the medical treatment of phaeochromocytoma.

Administration, Oral↗
PubMed1975

Effect of oxprenolol on catecholamines and plasma renin activity: acute response to frusemide in hypertensive patients.

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge. 2. The same procedure was repeated in the same subjects 3--4 days later after pretreatment with oxprenolol. 3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged. 4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values. 5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.

Adult↗
PubMedDate not supplied

High-dose, not low-dose insulin increases the vasoconstrictor effect of norepinephrine in spontaneously hypertensive rats: effects of antihypertensive treatment.

The effect of insulin on the vasoconstriction induced by norepinephrine is presently controversial. Therefore, the aims of our study were: (1) to evaluate the effect of low- and high-dose insulin on the concentration-response curve to norepinephrine in small resistance arteries of spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) before and after the development of hypertension, and (2) to evaluate the effects of antihypertensive treatment on vascular response to insulin and norepinephrine. Fifty-six rats were included in the study. Six SHR were treated with enalapril and 6 with candesartan cilexetil from the 4th to the 12th week of age, while 10 WKY and 14 SHR were kept untreated. Two additional groups of 10 untreated SHR and 10 WKY were killed at 4 weeks of age, in a prehypertensive phase. Mesenteric small arteries were dissected and mounted on a micromyograph. A dose-response curve to norepinephrine was performed at cumulative concentrations in the presence or absence of low- and high-dose insulin. We found that only high-dose insulin increased the vascular response to norepinephrine in 12-week-old SHR, but not in 4-week-old SHR or in age-matched WKY. The increased responsiveness to norepinephrine disappeared after preincubation of the vessels with a selective inhibitor of endothelin-1 type A receptors. After antihypertensive treatment with enalapril or candesartan cilexetil, the potentiation of the vasoconstrictor response to norepinephrine was abolished. In conclusion, insulin at high, nonphysiological doses seems to induce an increase in the reactivity to norepinephrine in mesenteric small arteries of SHR, possibly mediated by a local production of endothelin-1. Antihypertensive treatment with an ACE inhibitor or an angiotensin II receptor blocker may normalize this altered response. This mechanism may be relevant in the development of hypertension in SHR.

Angiotensin Receptor Antagonists↗