Titlebook: Kidney in Essential Hypertension; Proceedings of the C Franz H. Messerli (Director Associate Professor of Conference proceedings 1984 Marti

評(píng)論者

Prostaglandins and Hypertensions renal function from excessive effects of angiotensins and catecholamines. Prostaglandins not only antagonize the actions of pressor hormones and the adrenergic nervous system, they also contribute to the renal effects of kinins by augmenting their vasodilator and diuretic-natriuretic actions. Rena

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Kallikrein and Kinins in Epithelial Ion Transport in any form of experimental or human hypertension. Nevertheless, such participation continues to be reasonable because of findings which established that: 1) changes in endogenous renal kallikrein-kinin activity are correlated with changes in renal excretory or hemodynamic behavior (1,2); 2) correl

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LAIR

Renal Blood Flow and Function in Essential Hypertensionan abnormality of the renal blood supply also participates in the pathogenesis of essential hypertension, as a factor initiating or sustaining the rise in blood pressure, has been the subject of recurring interest for many decades. There is clearly a functional abnormality, reflected in increased re

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Wallow

Atmosphere

Renal Hemodynamics in Obese and Lean Essential Hypertensive Patientsterial pressure. The obese hypertensive patients had a greater cardiac output, renal blood flow and total blood volume. In contrast total peripheral and renal vascular resistances were less in the obese patients than in their lean counterparts. Therefore, we postulate that the high blood flow state

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Sodium and Water Excretion in Patients with Congestive Heart Failure and Cirrhosis retention in cirrhosis seems to be mediated by a decreased central blood volume (afferent mechanism) and increased sympathetic activity, as well as stimulation of the renin aldosterone system (efferent mechanism). An increase in renal sympathetic activity appears to 1) diminish renal hemodynamics,

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