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Renin-angiotensin system, renal physiology

Secondary hyperaldosteronism results from stimulation of the zona glomerulosa by an extra-adrenal factor, usually the renin-angiotensin system. Excessive potassium intake can create a physiologic increase in aldosterone, as can oral contraceptive use, pregnancy (10 times normal by the third trimester), and menses. Congestive heart failure, cirrhosis, renal artery stenosis, and Bartter s syndrome also can lead to elevated aldosterone concentrations. [Pg.1399]

Ritz, E. and Wagner, J. (2001) Effects of all-trans retinoic acid on renin-angiotensin system in rats with experimental nephritis. American Journal of Physiology. Renal Physiology, 281, F909-F919. [Pg.429]

Assuming the capsular pressures opposing the movement of water out of the blood and into the top of the nephron are constant, the net filtration pressure is due largely to the blood pressure. Any fall in blood pressure can have a dramatic effect on the efficiency of filtration and therefore clearance of waste materials. So important is the pressure within the renal vasculature that the kidney is critical in regulating systemic blood pressure via the renin-angiotensin-aldosterone (RAA) axis, a physiological process which relies on transport mechanisms within the renal tubules. [Pg.264]


See other pages where Renin-angiotensin system, renal physiology is mentioned: [Pg.451]    [Pg.16]    [Pg.483]    [Pg.485]    [Pg.327]    [Pg.329]    [Pg.518]    [Pg.331]    [Pg.338]    [Pg.141]    [Pg.421]    [Pg.28]    [Pg.19]    [Pg.372]   


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