Chapter 25. Endogenous Natriuretic Agents

Abstract

Publisher Summary Expansion of the extracellular fluid volume leads to increased sodium ion excretion (natriuresis) by the kidney, independent of changes in glomerular filtrationrate (GFR), and of the reninangio-tensin-aldosterone system. Considerable evidence indicates that volume expansion (VE) in laboratory animals and in human causes the release of a humoral natriuretic factor that is excreted in the urine. One such agent that appears to be an endogenous inhibitor of the sodium transport system has been referred to as natriuretic hormone (NH). A humoral factor that causes natriuresis when cross circulated to recipient animals has been demonstrated in VE donor animals. An unknown pressor agent has been observed in the blood of animals and man with VE, low renin, and hypertension. Suppressed Na+,K+-ATPase activity in cardiovascular tissues of animals with either one-kidney renal, deoxycorticosterone acetate or reduced renal mass hypertension suggests that this pressor substance is an inhibitor of the Na+,Kt-ATPase. It has been proposed that the hypothalamus might secrete a substance that controls sodium excretion. The AV3V region of the brain is important for regulating blood pressure, since its destruction prevents several forms of hypertension. Furthermore, less Na+ is excreted, the blood level of Na+ is elevated, and NH is absent in animals with AV3V lesions. Atrial natriuretic factor is a recent discovery that yields readily to chemical characterization and synthesis.