Angiotensin in the hemodynamic response to chronic nephron obstruction.
Microsphere techniques were employed to investigate the role of intrarenal angiotensin generation in producing the arteriolar constriction associated with 24-h tubular obstruction in rats. In each animal, glomerular blood flow (GBF) and nephron vascular resistance were determined for normal and oil-blocked superficial cortical nephrons. In 17 control rats, GBF of normal and blocked nephrons averaged 226 +/- 12 and 130 +/- 9 nl/min, respectively (P less than 0.001). Captopril treatment in five rats (10 mg/kg orally) improved GBF to blocked nephrons to 252 +/- 31 nl/min. Saralasin treatment in six rats (10 micrograms . kg-1 . min-1 i.v.) lessened the difference between GBF of normal and obstructed nephrons. In six rats subjected to a high salt intake and deoxycorticosterone injections, GBF to obstructed nephrons was improved to 181 +/- 21 nl/min. Since both pharmacologic interruption of angiotensin activity and renin suppression were associated with improved GBF of blocked nephrons, these observations support a role for angiotensin as a local factor controlling glomerular hemodynamics of chronically obstructed nephrons.
D000803:Angiotensin I / Q000494:pharmacology*; D000809:Angiotensins / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure; D002216:Captopril / Q000494:pharmacology; D003900:Desoxycorticosterone / Q000494:pharmacology; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007678:Kidney Glomerulus / Q000098:blood supply*; D008297:Male; D008863:Microspheres; D009399:Nephrons / Q000187:drug effects / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation / Q000187:drug effects
D000809:Angiotensins; D003900:Desoxycorticosterone; D000803:Angiotensin I; D002216:Captopril