Renal hyperemia in portal hypertension is not mediated by gastrointestinal peptides.
The objectives of this study were to characterize the time course of development of the renal hyperemia induced by chronic portal vein stenosis (PVS) in the rat, and to assess the possibility that vasoactive blood-borne gastrointestinal peptides mediate the renal hyperemia in established portal hypertension. Blood flow to the kidneys was measured with radioactive microspheres over a ten day time course. On day 2, no difference in renal blood flow (RBF) was observed in PVS rats as compared with controls. However, by day 4, RBF significantly increased by 35% in PVS vs. control animals. On day 6, the renal hyperemia in PVS rats reached a maximal value that was 42% higher than controls. A steady state hyperemia (approximately 40%) was maintained thereafter. Radioimmunoassay of plasma from control and established portal hypertensive rats (10 days samples) revealed that vasoactive intestinal polypeptide, substance P, cholecystokinin, gastrin, neurotensin, pancreatic polypeptide, beta-endorphin and peptide histidine-isoleucine amide are not elevated in arterial plasma of portal hypertensive rats. These data suggest that the renal hyperemia induced by chronic portal vein stenosis is apparent within 4 days of the onset of a hypertensive state and attains a steady state by day 8. Furthermore, at least eight blood-borne gastrointestinal peptides are not directly involved in the renal hyperemia associated with chronic portal hypertension.
D000818:Animals; D005768:Gastrointestinal Hormones / Q000502:physiology*; D006940:Hyperemia / Q000209:etiology* / Q000503:physiopathology; D006975:Hypertension, Portal / Q000150:complications* / Q000503:physiopathology; D007674:Kidney Diseases / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014664:Vasodilation
D005768:Gastrointestinal Hormones