Angiotensin in the hemodynamic response to chronic nephron obstruction

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Abstract
Microsphere techniques were used 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 < 0.001). Captopril treatment in 5 rats (10 mg/kg orally) improved GBF to blocked nephrons to 252 .+-. 31 nl/min. Saralasin treatment in 6 rats (10 .mu.g/kg per min i.v.) lessened the difference between GBF of normal and obstructed nephrons. In 6 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, a role for angiotensin as a local factor controlling glomerular hemodynamics of chronically obstructed nephrons was supported.