antiadrenergic/obesidade

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The neurobiology of human obesity.

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Earlier ideas that sympathetic nervous system activity is low in human obesity, contributing to weight gain through absence of sympathetically mediated thermogenesis, can now be discounted. The application of sympathetic nerve recording techniques and isotope dilution methodology quantifying

Essential hypertension. Matching pathophysiology and pharmacology.

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The underlying pathophysiologic mechanisms that elevate arterial pressure differ according to the patient's age, adipose body mass, and race. However, these mechanisms represent the extremes of a continuum, and overlap among them can be encountered in some patients. A few simple clinical clues allow

Sympathetic nerve activity and neurotransmitter release in humans: translation from pathophysiology into clinical practice.

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OBJECTIVE There has been a revolution in cardiovascular neuroscience in recent years with, in some cases, translation into clinical practice of the knowledge of pathophysiology gained through application of sympathetic nerve recording and catecholamine isotope dilution methodology. OBESITY-RELATED

Hemodynamic and cardiac adaptation in essential hypertension. Consequences for therapy.

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In so-called essential hypertension, at least three different subsets of pathophysiologic findings can be identified: mild hypertension in nonobese juvenile subjects characterized by elevated cardiac output, normal peripheral resistance, increased sympathetic activity as measured by norepinephrine

Cardiovascular pathophysiology of essential hypertension: a clue to therapy.

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Arterial hypertension is by definition a haemodynamic disorder. At least 3 different subsets of cardiovascular pathophysiological features can be identified in so-called essential hypertension: The young lean patient characterised by an elevated cardiac output and renal blood flow, elevated plasma

[Evaluation of lercanidipine in the general practice setting].

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OBJECTIVE To determine the efficacy and tolerability of a long-acting dihydropyridine in the clinical settings of general practice. METHODS 110 essential hypertensives were included (age 62.3 +/- 10.8 years, 51 men and 53 women, 38/ obese -IMC >30 kg/m2, ten diabetics). 104 patients ended the

Drug withdrawal and rebound hypertension: differential action of the central antihypertensive drugs moxonidine and clonidine.

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To examine the antihypertensive action of the centrally acting antiadrenergic drugs moxonidine and clonidine, systolic and diastolic blood pressure as well as heart rate were monitored by radio telemetry in spontaneously hypertensive rats (SHR) with established high blood pressure. Increasing doses

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