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Biomedical subjects

A Morganti

Publications and source records attributed to A Morganti.

At least 73 records · Page 4Linked to original sources
PubMed1986

Humoral and renal effects of ibopamine in normal subjects.

The acute effects of 50 mg of ibopamine (SB-7505), the 3,4-diisobutyryl ester of N-methyldopamine, were investigated after oral administration to 10 adult subjects without evidence of renal, hepatic or cardiovascular disease. Blood pressure and heart rate did not change while diuresis and urinary electrolyte excretion increased significantly during the 240 min of the study. Glomerular filtration rate (GFR) was also increased at 80 min after ibopamine, whereas plasma aldosterone and prolactin were slightly decreased. In contrast to dopamine, ibopamine did not stimulate plasma renin activity. These results are attributable to the ability of ibopamine to be rapidly deesterified to N-methyldopamine (epinine) which has been previously shown to exert peripheral effects similar to those of dopamine. Therefore, the increased GFR can be ascribed to an enhanced renal blood flow. On the contrary, taking into account the significant increase of the fractional excretion of sodium (FeNa) the rise in sodium excretion seems to be the consequence of a direct tubular effect of epinine, even though the slight decrease in peripheral aldosterone concentration would have been a contributing factor. Urinary flow rate might be enhanced by the high sodium delivery to the distal nephron, rather than by a postulated dopaminergic inhibition of arginine-vasopressin release.

Adult↗
PubMed1985

Participation of the renin-angiotensin system in the maintenance of blood pressure during changes in posture in patients with essential hypertension.

To assess whether and how the activation of the renin-angiotensin system that occurs in response to changes in posture contributes to the maintenance of blood pressure, we measured blood pressure, heart rate, plasma noradrenaline and plasma active and inactive renin in patients with essential hypertension in the supine, sitting and standing positions, (each sustained for 30 min), before and after administration of captopril. These studies were performed before and after a brief period of diuretic therapy. Both in the normal and in the sodium depleted state captopril reduced the normal adaptive response of blood pressure to changes in body position, whereas the responses of heart rate and plasma noradrenaline to these stimuli were unaffected by captopril. In contrast, the postural increases in active renin were magnified after captopril while inactive renin was unchanged throughout these acute studies. Our results indicate that during mild but rather prolonged postural stresses the generation of angiotensin by active renin supports blood pressure either through its direct vasoconstrictive effect and/or by potentiating the activity of the sympathetic nervous system. It is unlikely that the changes in active renin depend upon conversion from the inactive form.

Adult↗
PubMed1985

Acute and chronic converting enzyme inhibition reduces the vasomotor response to reflex sympathetic activation in man.

Several lines of evidence indicate that angiotensin II (ANG II) may potentiate the vascular response to sympathetic stimulation. However, there are no clear signs that this action of ANG II is physiologically relevant in man. To investigate this problem, we used the lower body negative pressure technique (LBNP, -15 mmHg) to deactivate cardiopulmonary receptors and reflexly stimulate the sympathetic nervous system. The haemodynamic (changes in blood pressure, heart rate, central venous pressure, forearm blood flow) and humoral effects [changes in plasma noradrenaline (PNA) and plasma renin activity (PRA)] of this manoeuvre were examined before and after blockade of angiotensin formation achieved by the administration of the converting enzyme inhibitor, captopril. Studies were performed in patients with essential hypertension in control conditions and after acute and chronic captopril treatment. We found that the reduction in forearm blood flow induced by LBNP was significantly diminished after acute and chronic captopril in spite of the fact that the fall in central venous pressure and the increases in PNA were similar to those observed in control conditions. In contrast, the response of renin to LBNP was enhanced, at least after acute captopril administration. These findings suggest that efficiency of the reflexes originating from the cardiopulmonary receptors is impaired after captopril. Angiotensin II contributes to the vasoconstrictive ability of the sympathetic nervous system, either through a direct vascular action or by enhancing the vascular responsiveness to noradrenaline stimulation. However, this sympathetic facilitatory action of ANG II does not appear to be extended on the adrenergic mechanisms which regulate renin release.

Adult↗
PubMed1985

The responses of adrenocorticotrophic hormone and cortisol to insulin-induced hypoglycaemic stress in man are unimpaired during chronic converting enzyme inhibition.

In vitro and animal studies indicate that circulating angiotensin II (ANG II) can stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion, but it is far from established that ANG II has a physiologically relevant influence on steroidogenesis. We studied the effects of hypoglycaemia induced with insulin injection (0.15 IU/kg) in patients with essential hypertension to answer this question. Hypoglycaemia was induced before and after a short term course of treatment with the converting enzyme inhibitor captopril to obtain a sustained blockade of ANG II formation. Alterations in serum glucose, plasma potassium, plasma ACTH, cortisol, renin activity and aldosterone were examined. In control studies there was a profound fall in serum glucose and plasma potassium after insulin, associated with increments in plasma renin activity, which correlated with those of aldosterone but not with those of ACTH and cortisol. Chronic captopril increased baseline plasma renin activity and lowered baseline aldosterone while leaving ACTH and cortisol unchanged. During converting enzyme inhibition the insulin-induced decrements in glucose and potassium, as well as the increments in ACTH, cortisol and aldosterone, were similar to those observed in control studies, whereas the increments in plasma renin activity were much greater. From these results it does not appear that ANG II has a relevant influence on ACTH and cortisol production, or on their responses to hypoglycaemic stress. Rather, these findings indicate that even under the present experimental conditions ANG II is the primary regulator of aldosterone secretion. However, this function can be taken over by ACTH when the generation of ANG II is blocked.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of haemodialysis on active and inactive renin in nephric and anephric patients.

To investigate the origin, the mechanisms of regulation and the possible biological significance of inactive renin we examined the effects of haemodialysis on plasma active and inactive (cryoactivatable) renin in four anephric and in 10 nephric patients. Before haemodialysis inactive renin was similar in anephric and in the majority of nephric patients; this suggests that the source of the inactive enzyme is predominantly extrarenal. In response to haemodialysis active renin rose significantly in nephric patients whereas inactive renin showed minor and inconsistent increments in both groups. These results indicate that the response of the inactive enzyme to haemodialysis is less than that of its active counterpart and is unaffected by the presence of the kidneys. Therefore, it appears unlikely that inactive renin represents a circulating precursor of active renin.

Adult↗
PubMed1982

Dissociation of the effects of alpha 1-adrenergic blockade on blood pressure and renin release in patients with essential hypertension.

Prazosin, a selective antagonist of postsynaptic alpha-adrenoreceptors, was used to investigate the influence mediated by the juxtaglomerular alpha-adrenoreceptors on renin release in man. We studied, in seven patients with essential hypertension, the acute effects of 0.25 mg prazosin, given intravenously, on blood pressure and plasma renin activity, the degree of alpha-blockade induced by the drug being assessed by comparing the increments in blood pressure following a test dose of phenylephrine before and after prazosin administration. We also measured the increments in plasma renin activity in response to beta-adrenergic stimulus consisting of an isoproterenol challenge, before and during the prazosin induced alpha blockade. Prazosin infusion caused, within 20 min, a marked reduction of the pressor response to phenylephrine, a significant increment in plasma renin activity, and no change in blood pressure. The increments in renin in response to isoproterenol were significantly greater, both in absolute and percent values, after rather than before prazosin. These results indicate that the increase in renin during systemic alpha 1-adrenoreceptor blockade may be independent of the fall in blood pressure and support the view that the juxtaglomerular alpha 1-adrenoreceptors participate in the regulation of renin release with an inhibitory action, which antagonizes the stimulating influence of the beta-adrenoreceptors.

Adolescent↗
PubMed1982

Plasma catecholamines and cardiovascular responses during converting enzyme inhibition in normotensive and hypertensive man.

The hemodynamic and plasma catecholamine responses to isometric exercise and head up tilt were investigated in normotensive and hypertensive subjects during normal and low sodium intake and before and during the administration of the converting enzyme inhibitors teprotide or captopril. Although teprotide and captopril decreased significantly the mean arterial pressure during both sodium intakes the normal pattern of hemodynamic response to hand grip and head up tilt was preserved. Moreover changes of plasma catecholamines during hand grip and head up tilt were not affected either by teprotide or captopril. When following the administration of teprotide or captopril fainting occurred either in the seated position or during head up tilt it was associated not only with a decrease in arterial pressure but also with a concurrent reduction in cardiac output and/or hypovolemia. It is concluded that converting enzyme inhibition does not impair significantly the cardiovascular responses which are mediated via the sympathetic nervous system either in normotensive or in hypertensive subjects.

Adult↗
PubMed1982

Time course of the changes in active and cryoactivatable renin in response to acute stimuli before and after diuretic therapy in man.

In order to elucidate whether inactive renin may represent a precursor of the active enzyme we examined the short-term effects of ambulation and of Captopril administration on active and cryoactivatable renin in patients with essential hypertension before and after 5 days of diuretic therapy. We have found that in the large majority of patients before diuretic the increments in active renin in response to these stimuli were moderate and associated with unchanged levels of cryoactivatable renin; significant decrements in cryoactivatable renin were observed only in a small group of patients in whom the increments in active renin induced by ambulation were unusually rapid and marked. Diuretic therapy caused parallel increments in baseline values of active and of cryoactivatable renin and potentiated the response of the active enzyme to ambulation and to Captopril; however, cryoactivatable renin was still unmodified during both the acute stimuli. Thus, it appears that, normally, the rise in active renin induced by ambulation and Captopril administration is associated, both before and after diuretic therapy, with unchanged levels of the inactive enzyme; however, before diuretic, abrupt increments in the demand for active renin can determine changes in opposite direction of inactive renin as if the latter were a precursor of the former.

Adolescent↗
PubMed1982

[Immunological parameters in subjects with essential arterial hypertension. I. Lymphocyte subpopulations].

Peripheral venous blood lymphocytes were defined, in 21 subjects with essential hypertension and 20 controls, on the basis of reactivity with monoclonal antibodies OKT3, OKT4, OKT8, OK1Ia. Total lymphocyte count, OKT3+ and OKT4+ cells percentage were similar in normal and hypertensive. OKT8+ cells percentage was significantly lower only in hypertensive stage II and III patients (WHO classification).

Adult↗
PubMed1982

[Immunological parameters in subjects with essential arterial hypertension. II. Serological observations].

M, G, and A immunoglobulins as well as C3 and C4 complement fractions were determined in 20 patients with essential hypertension: all the values were in the normal range. Nearly half of the patients had an abnormally high value of circulating immune complexes as determined with Clq binding assay and/or with CIC test. The rise of circulating immune complexes is not related to the stage of arterial hypertension.

Adult↗
PubMed1981

Alpha 1-Adrenoceptor blockade: dissociation of its effects on renin release and arterial blood pressure in man.

1. The possibility that the juxtaglomerular alpha 1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective alpha 1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of alpha-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced alpha-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the beta-adrenoceptor stimulus suggest that, in man, the juxtaglomerular alpha 1-adrenoceptors exert a direct, suppressive action on renin release.

Adolescent↗
PubMed1979

Contrasting effects of acute beta blockade with propranolol on plasma catecholamines and renin in essential hypertension: a possible basis for the delayed antihypertensive response.

Blood pressure, heart rate, plasma renin activity, plasma norepinephrine and plasma epinephrine were determined in 11 patients with essential hypertension at rest before and 15, 30, 45, and 60 minutes after an intravenous infusion of 0.12 mg./Kg. propranolol given over five minutes. After propranolol mean blood pressure was unchanged; heart rate decreased by 14 per cent within 15 minutes and showed no further changes. Plasma renin activity decreased progressively by 48 per cent 60 minutes after propranolol, whereas plasma norepinephrine and epinephrine were always higher after propranolol than control values. Increases in norepinephrine were statistically significant at 30, 45, and 60 minutes (respectively 49, 39, and 45 per cent, P less than 0.005 at least) and those of epinephrine even at 15 minutes (respectively 60, 82, 62, and 94 per cent P less than 0.01 for all). These results indicate that acute beta blockade with propranolol incudes increases in circulating plasma norepinephrine and epinephrine which might be consequent to rapidly induced hemodynamic changes. This augmented sympathetic activity might explain why propranolol, when acutely infused, does not decrease blood pressure despite effective cardiac and renin blockade.

Adrenergic beta-Antagonists↗