Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration

Abstract

Although the existence of postprandial renal hyperemia and hyperfiltration has been established, the precise mechanism governing protein-mediated increases in renal hemodynamics is not, as yet, clearly defined. Investigative effort over the past decade has provided at least two plausible mechanisms playing an important role in renal hyperemia and hyperfiltration associated with ingestion of a protein-rich meal: 1) blood-borne vasoactive agents (e.g., pancreatic glucagon and/or hepatic glomerulopressin); and 2) intrarenal mechanisms (e.g., the tubuloglomerular feedback system). Data supporting each of these two candidate mechanisms are reviewed as are data supporting the importance of other factors such as renal prostanoids, the renin-angiotensin system, and renal cyclic nucleotides. It is anticipated that future investigative effort will be stimulated by our present knowledge of postprandial renal hemodynamics so that one day we not only will know the precise mechanisms governing postprandial renal hyperemia and hyperfiltration but, in addition, may gain valuable insight into the pathogenesis of chronic renal disease.