Biomedical subjects

F Veglio

Publications and source records attributed to F Veglio.

80 records · Page 5Linked to original sources

PubMedDate not supplied

Baroreflex sensitivity in secondary hypertension.

A deranged baroreceptor control of the cardiovascular functions has been reported in essential hypertension. Studies performed in experimental animals and in humans using different approaches have documented an impairment of both baroreflex heart rate modulation (resetting and loss of sensitivity) and baroreceptor control of peripheral vasomotor tone (only resetting). Baroreflex alterations have been reported also in secondary forms of hypertension, but data are controversial. This paper reviews recent works concerning baroreflex function in secondary hypertension. Either structural changes of arterial wall (decrease of vascular distensibility) or functional processes (involving angiotensin II, aldosterone, catecholamines, nitric oxide) have been proposed as potential mechanisms responsible for baroreflex readjustments in secondary hypertension. It remains unclear, and it is difficult to define exactly, if baroreflex changes associated with secondary form of hypertension are primarily due to factors specific for different hypertensive conditions, or merely follow blood pressure elevation.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

Antihypertensive drugs and sympathetic nervous system.

Several studies have demonstrated that essential hypertension is accompanied by sympathetic activation, which contributes to blood pressure elevation. Sympathetic activation also has adverse consequences in hypertensive patients beyond initiating blood pressure elevation. There is evidence that neural vasoconstriction has metabolic effects in skeletal muscle, impairing glucose delivery to muscles. In the liver, retarding of post prandial clearance of lipids contributes to hyperlipidemia. Cardiac sympathetic activation is a probable cause of sudden death in hearth failure. A trophic effect of sympathetic activation on cardiovascular growth is also likely, contributing to the development of left ventricular hypertrophy. Consequently, one of the major aims of antihypertensive therapy should be to attenuate sympathetic tone. It is possible that, among the antihypertensive drugs available, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Dopaminergic regulation of aldosterone secretion: assessment in different subtypes of primary aldosteronism and in essential hypertension.

The inhibitory effect of dopamine on aldosterone secretion was investigated in patients with different types of primary aldosteronism, six with idiopathic hyperaldosteronism (IHA) and four with dexamethasone-suppressible hyperaldosteronism (DSH), and in 10 patients with essential hypertension. The effects of 10 mg metoclopramide given intravenously, 10 mg bromocriptine given orally and 100 micrograms adrenocorticotrophic hormone given intravenously on plasma aldosterone and renin activities were investigated in all patients. Metoclopramide induced a rise in plasma aldosterone activity only in patients with IHA and not in those with DSH and essential hypertension. After bromocriptine plasma aldosterone concentrations decreased in patients with IHA only, and after adrenocorticotrophic hormone plasma aldosterone concentrations increased in patients with DSH only. Plasma renin activity was unaffected in all cases. These results provide evidence of increased endogenous dopaminergic inhibition of aldosterone secretion in IHA and of a blunted aldosterone response in both DSH and essential hypertension.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

[Primary dexamethasone-suppressible hyperaldosteronism and hyperprolactinemia].

This report describes a clinical case with rare association: dexamethasone-suppressible hyperaldosteronism (DSH) and hyperprolactinemia. Previous studies reported that endogenous dopaminergic activity would be increased in both primary aldosteronism and in hyperprolactinemic syndromes. By manipulating dopamine tone with metoclopramide, bromocriptine, ACTH and amineptine, the aldosterone and prolactin responsiveness was evaluated. Our results showed a lack of dopamine inhibiting aldosterone secretion, despite dopaminergic tone is known to be increased in hyperprolactinemia. Thus it seems unlikely that dopaminergic control of aldosterone secretion could be account for this type of hyperaldosteronism associated to hyperprolactinemia, where the suggestion is that ACTH represents the principal regulator of aldosterone secretion.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

[Role of aldosterone in the metabolic syndrome].

The purpose of this review is to summarize the current knowledge regarding metabolic syndrome prevalence and features in primary aldosteronism. We will also discuss the link between aldosterone and the different metabolic changes typical of the metabolic syndrome. Hypertensive patients have a high prevalence of obesity, dyslipidemia and hyperglycaemia. These are risk factors for the metabolic syndrome, and are associated with an increased cardiovascular risk profile. In particular, insulin resistance seems to be the major alteration in patients affected by primary aldosteronism. We will then describe the experimental and clinical evidences of the role of aldosterone in the pathogenesis of insulin resistance. Higher rates of cardiovascular events have been recently reported in primary aldosteronism: they could be partly due to the increased prevalence of the metabolic syndrome in this disorder.

Aldosterone↗

PubMedDate not supplied

Circadian rhythm of the angiotensin converting enzyme (ACE) activity in serum of healthy adult subjects.

Angiotensin converting enzyme (ACE) activity was measured in the peripheral serum of 10 healthy, diurnally-active and nocturnally-resting adult subjects (5 women and 5 men). Blood was drawn serially at 4-h intervals throughout a 24-h cycle with the subjects hospitalized and synchronized. They were not kept in recumbency. Data were evaluated by conventional statistical analysis and by single- and population mean- cosinor procedures. A low-amplitude circadian rhythm was statistically validated for the group. Acrophase was located in the afternoon, at about 1630. The recognition that ACE activity oscillates physiologically in the peripheral blood according to a circadian rhythm may serve to amplify the clinical use of ACE measurements.

Adult↗

PubMedDate not supplied

Acute effects of alpha-1 adrenoceptor antagonist, doxazosin on circulating vasoactive hormones.

The acute effects of doxazosin, a new selective alpha-1 adrenergic blocking agent, on blood pressure, heart rate, and on some circulating vasoactive hormones, such as plasma renin activity, catecholamines, serotonin and endothelin-1 in ten healthy normotensive volunteers and eight moderate-severe essential hypertensives were studied. Two milligrams doxazosin was administered orally in randomised fashion as compared to placebo and the acute effects were evaluated one half to four hours later. Doxazosin did not reduce blood pressure and did not increase heart rate in normotensive subjects as compared to placebo. A significant decrease in blood pressure was found in hypertensives after doxazosin (p < 0.01), without change in heart rate. Simultaneously, doxazosin did not modify plasma renin activity, catecholamines, serotonin and endothelin-1 concentrations both in normotensive and hypertensive subjects when compared with placebo administration. Thus, it appears that doxazosin does not influence local and systemic vasopressor hormones involving in the regulation of blood pressure. In conclusion, the lack of effects on plasma vasoactive factors confirms the selective alpha-1 postsynaptic antagonism of doxazosin and an effective antihypertensive action in the treatment of essential hypertension.

Adrenergic alpha-1 Receptor Antagonists↗

PubMedDate not supplied

[The L-arginine/nitric oxide metabolic pathway. Its physiopathology and clinical implications].

The L-arginine/nitric oxide (NO) pathway plays a key role in a number of biological processes within most organs and systems. Increasing attention has been addressed to its involvement in the pathogenesis of various human diseases. In this review we examine the enzymology of different NO-synthase isoforms, the major NO detection techniques as well as the possible clinical and pharmacological implications of this new metabolic pathway.

Arginine↗