Peptide hormones and the regulation of sodium excretion.

TWENTY years ago, intensive research led to the delineation of the role played by alterations in blood composition in mediating the natriuresis that resulted from the infusion of colloidfree isotonic saline solutions into humans and experimental animals. Results of this research indicated that changes in renal hemodynamics (glomerular filtration rate [GFR], renal blood flow, renal vascular resistance, filtration fraction) and hematocrit and plasma protein concentration occurring in response to saline infusion led to inhibition of tubular sodium reabsorption through changes in hydrostatic and oncotic pressures in the peritubular capillary circulation, the socalled physical factor effects. Because of these findings, the view emerged that, regardless of the extrarenal consequences of saline expansion, the natriuresis resulted from strictly intrarenal mechanisms.' This viewpoint was later strengthened by in vitro studies on isolated perfused rabbit proximal convoluted tubule segments that demonstrated a direct effect of bath protein concentration on fluid transport.