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Biomedical subjects

N Frisina

Publications and source records attributed to N Frisina.

At least 91 records · Page 5Linked to original sources
PubMed1983

Evidence for dopaminergic control of aldosterone in man.

The effect of L-dopa (0.50 g, orally) on serum aldosterone, cortisol and potassium levels, plasma renin activity, and on urinary aldosterone excretion has been studied in normotensive subjects, before and after dexamethasone-induced ACTH suppression. L-dopa caused a further reduction in the levels of aldosterone but not cortisol, in the dexamethasone treated subjects. It is therefore suggested that the inhibitory action of L-dopa on aldosterone secretion is mediated by the dopaminergic system.

Adult↗
PubMed1983

[The lipocorticotropic system and prolactin secretion].

Administration of ACTH beta 1-24 (0.25 mg, i.m.) in six healthy subjects reduces blood prolactin response to sulpiride (100 mg, i.m.). Dexamethasone (2 mg, orally, given at 11.00 p.m. of preceding day) blocks blood prolactin response to insulin-induced hypoglycemia (0.20 U. kg of "Actrapid" Novo, i.v.) in six voluntary healthy subjects. Intravenous naloxone (0.4 mg/Kg of body weight) blocks in man blood prolactin response to insulin-induced hypoglycemia. On the basis of the above data we can hypothesize that ACTH and dexamethasone have influenced by a feed-back mechanism the lypocorticotropic system. Such system by beta-endorphin release can modulate the secretion of prolactin. Thus inhibition of the lipocorticotropic system may be responsible for the reduced response of the prolactin system to stimulation by sulpiride or hypoglycemic stress.

Adolescent↗
PubMed1981

[The vasoactive effects of captopril (SQ 14225). Preliminary research].

The Authors examined the behaviour of the humeral arterial pressure, of the heart frequency and of the muscular blood flow in inferior limbs. This study was performed before and after treatment with Captopril (SQ 14225), 100 mg per os, a selective inhibitor of the converting enzyme. Both resting blood flow (RBF) and maximal blood flow (NBF) were studied by Xenon 133 clearance. The A.A. observed that the drug induced a significant (P less than 0.01) increase of both RBF and MBF. Therefore, the Authors hypothesize that the Captopril is able to produce peripheral vasodilatation, without any significant variation of the cardiac index and frequency. Such an effect is considered to depend not only upon the inhibited angiotensin II production, but also upon stimulation of bradikinins and prostaglandins.

Adult↗
PubMed1980

[The dopaminergic system and aldosterone secretion. I. Suppressive effects of L-dopa on secondary hyperaldosteronism].

The authors studied the blood aldosterone, cortisol and kalium levels, the plasma renin activity and the aldosterone urinary excretion following L-DOPA (0.50 g per os) administration in seven patients affected by hypertension and secondary hyperaldosteronism. The results suggest that L-DOPA administration, by stimulating the dopaminergic biosynthesis. Nevertheless such a conclusion needs further investigations.

Adult↗
PubMed1980

[The dopaminergic system and aldosterone secretion. II. Effect of L-dopa and dexamethasone on aldosterone biosynthesis].

The authors studied the blood aldosterone, cortisol, and kalium levels, the plasma renin activity and the aldosterone urinary excretion following L-Dopa (0,50 g per os) administration in five patients affected by hypertension and six healthy control subjects, before and after the CRF-ACTH system suppression. The observed pattern shows that the aldosterone biosynthesis is inhibited also after the CRF-ACTH system has been suppressed. Therefore the authors conclude that the inhibiting action of L-Dopa on the aldosterone biosynthesis is mediated by the dopaminergic system stimulation.

Adult↗
PubMed1980

[Aldosterone production in vitro by angiotensin II: the role of Ca++].

In beef isolated and superfused adrenal glands, the Authors have studied the production of aldosteron and tissue concentration of cAMP during superfusion with angiotensin II alone or preceededby preincubation with indomethacin or verapamil. In such experimental conditions the Authors could evidence that th aldosterone-inductor effect of angiotensin II is not mediated by cAMP but by PGs and Ca++.

Adrenal Glands↗
PubMed1980

[Production of corticosterone in vitro: role of PGE2].

The Authors have studied corticosteron output and tissue levels of cAMP during superfusion with ACTH and/or PGE2 before and after preincubation with indometacin (2 microgram/ml) in beef adrenal glands isolated and superfused with Ringer solution. The Authors on the basis of Mieir studies, conclude that PGE2 can be considered as fixed intermediares of the corticosteroidogenetic action of ACTH.

Adrenal Glands↗
PubMed1980

[Saralasin in subjects with low renin arterial hypertension].

The Authors have studied, in a group of hypertensive subjects with low renin, the behavior of arterial blood pressure, PRA, plasma aldosterone, plasma K and Na, after intravenous load of Saralasin before and after treatment with Furosmide (40 mg orally given for 4 days). In such conditions we evidenced an agonist effect of Saralasin mainly on plasma aldosterone and less on arterial pressure. The Authors conclude that Saralasin, in given conditions (free receptor sites), can exhibit on agonist effect on aldosterone secretion; such agonist effect can be augmented by dopaminergic deficit, that sometimes in present is essential arterial hypertension.

Adult↗
PubMed1980

Increased aldosterone secretion induced by sulpiride.

Sulpiride induces an increase in plasma prolactin and a simultaneous increase of aldosterone release in man. In isolated and superfused bovine adrenal glands, prolactin does not increase aldosterone production even in high concentrations, whereas sulpiride induces a significant and long lasting increase in the production of this hormone and a concomitant increase in the tissue levels of cAMP. This suggests a direct effect on the biosynthesis of aldosterone.

Adrenal Glands↗
PubMed1979

[Inhibitory effects of indomethacin on prolactin liberation induced with peptides with opium-like activity].

Indomethacin inhibits prolactin liberating effects by MET-enkefalin-NH2, a synthetic analogue of MET-enkefalin, both in intact and in ovariectomized, estradiol benzoate treated rats. The introduction of PGE1 increases the intensity of this effect. It is therefore possible to suppose that the PGs are involved as intermediaries of the prolactin relasing effect induced by MET-ENH-NH2.

Animals↗
PubMed1979

[Adrenal cortex production of aldosterone "in vitro" caused by angiotensin II: effects of indomethacin].

Angiotensin II increases aldosterone production of isolated and superfused bovine adrenal glands. Indomethacin shows a bi-phasic effect on the production of the above-mentioned hormone, inhibitory at low doses (0,2 microgram/ml), stimulatory at high doses (5.0 microgram/ml). Preincubation with this drug impedes the increase of aldosterone production induced by angiotensin II. It is likely that the steroidogenetic effect of angiotnesin II is carried out through the PGs.

Adrenal Cortex↗
PubMed1979

[Circadian variations in glycemia and IRI in normal subjects, young and adult diabetics and in obese subjects].

Blood sugar and IRI were followed for 24 hr in healthy patients, young and adult diabetics, and in subjects with apparently primary obesity on a standard, normal calorie diet. Morning and nocturnal insulin positivity peaks were noted in the normal subjects, though circadians variations in these parameters were mainly related to meals. This periodicity was altered in young diabetics, for whom insulin responsivity was ruled out, and in the adult diabetics, who displayed deficient insulin secretion in the morning, and delayed secretion after the afternoon meal, and in the obese subjects, the quality of whose response was close to that of the previous group. The usefulness of this type on examination in the planning of diet and drug management, quite apart from diagnosis and prognosis, is stressed.

Blood Glucose↗