Protein-mediated elevations in renal hemodynamics: existence of a hepato-renal axis?

Unlike the intestinal hyperemia which occurs following ingestion of a mixed meal, postprandial renal hemodynamic responses to food appear to be specific to protein-rich meals. Several observations have led to the proposal that following ingestion of protein (meat), a blood-borne factor(s) is released into the systemic circulation which elicits the increases in renal hemodynamics. Glucagon was initially considered as a prime hormonal candidate since the polypeptide is preferentially secreted by the endocrine pancreas in response to protein-rich meals and because glucagon elevates renal hemodynamics by selectively dilating renal afferent arterioles. However, recent data indicate that at postprandial blood levels, glucagon fails to directly mediate protein-induced renal hyperemia and hyperfiltration thus questioning the physiologic importance of glucagon on the renal vasculature. Data have accumulated indicating the importance of the liver and hepatic metabolism during protein-mediated elevations in renal hemodynamics. A hypothesis is advanced suggesting the existence and physiologic importance of a "hepato-renal axis" in mediating the postprandial increases in renal hemodynamics following ingestion of protein-rich meals. The blood-borne factor(s) mediating this response remains to be further clarified and defined.