Biomedical subjects

F Rabbia

Publications and source records attributed to F Rabbia.

43 records · Page 3Linked to original sources

PubMedDate not supplied

Peripheral adrenergic system and hypertension.

Hypertension is a condition where adrenergic responsiveness, sympathetic activity and adrenoceptors are somewhat altered. Many techniques are available to assess human sympathetic nervous system activity. They each present limitations and disadvantages. Characterization and subdivision of the alpha and beta-adrenoceptors, according to their localization and answer to different agonists, was facilitated in recent years by the extensive use of pharmacological and molecular biology techniques. Some adrenoceptor studies were conducted on animal models, human tissues and peripheral blood cells to assess their changes in various forms and stages of hypertension. Our group has pointed out that alpha1-adrenergic receptors expressed by human peripheral blood lymphocytes underwent changes of density in essential hypertensives, compared to normotensive control subjects. The importance of these findings could provide an assessment of alpha1-peripheral receptors with possible future clinical implications in the pathophysiology and treatment of hypertension.

Animals↗

PubMedDate not supplied

Obesity and autonomic function in adolescence.

Hypertension and obesity are risk factors for coronary heart diseases in adults. In turn, childhood overweight and high blood pressure increase the risk of subsequent obesity and hypertension in adulthood. Human obesity is characterized by profound alterations of hemodynamic and metabolic states. Whether these alterations involve sympathetic nervous system control on cardiac function is controversial. We report the results of our study, conducted in a sample of obese adolescents by using power spectral analysis of heart rate variability. An increase in sympathetic tone coupled with a reduction in vagal tone was found. This allowed us to hypothesize that autonomic nervous system changes depend on the time course of obesity development. It is still unclear if treatment of obesity in adolescence prevents subsequent autonomic imbalance and hypertension.

Adolescent↗

PubMedDate not supplied

Heart rate variability and left ventricular diastolic function in patients with borderline hypertension with and without left ventricular hypertrophy.

The relationships between heart rate variability (HRV), left ventricular mass and diastolic function in borderline hypertensive patients (BHT) were evaluated. 24 h Holter electrocardiogram (ECG) and blood pressure (BP) monitoring, M and 2 D echocardiogram and Doppler analysis in 42 BHT with and without left ventricular hypertrophy (LVH) and in 20 normotensive controls were assessed. From 24-h ECG, time domain indexes of HRV were calculated. Standard Deviation of all Cycles (SDNN) and Standard Deviation of the means of heart periods over five-minute intervals (SDANN) were significantly reduced in BHT with LVH but not in BHT without LVH. No significant differences of short-term variability measures were detectable, although a progressive decrease among control subjects and BHT with and without LVH was observed. Diastolic left ventricular compliance evaluated by early to late transmitral flow velocity ratio (E/A ratio) significantly declined from normotensive subjects to BHT with LVH. There was a significant positive correlation between E/A and SDNN and SDANN throughout all studied groups. This indicates that BHT with LVH has a reduced HRV compared to other groups. This impairment is probably related to left ventricular mass and left ventricular filling abnormalities.

Adult↗

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↗