Abstract
The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.
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