Renin-angiotensin system in phlorhizin compared with alloxan diabetes in the rat.
In alloxan-treated diabetic rats, plasma renin activity (PRA) is decreased. One possible mechanism that may explain the decreased PRA is an increased delivery of sodium to the macula densa produced by the glucose osmotic diuresis, resulting in decreased renin release. To evaluate this possible mechanism, rats with phlorhizin diabetes, which produces a glucose osmotic diuresis without hyperglycemia, were studied and compared with rats with alloxan-induced diabetes. Whereas phlorhizin-treated rats had low blood glucose and alloxan-treated rats had elevated glucose, the glucose osmotic diuresis was similar in the two groups. PRA and plasma renin concentration (PRC) were significantly increased in the phlorhizin group. In the alloxan group, PRA was decreased and angiotensin II sensitivity increased, both significantly. Plasma renin substrate (PRS) remained adequate in each group. These results suggest that the decreased PRA in alloxan-induced diabetes is due neither to factors associated with the glucose osmotic diuresis including changes in renal tubular sodium not to decreased PRS.
D000496:Alloxan / Q000494:pharmacology; D000804:Angiotensin II / Q000097:blood*; D000808:Angiotensinogen / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000097:blood* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D008297:Male; D010695:Phlorhizin / Q000494:pharmacology; D051381:Rats; D012083:Renin / Q000097:blood*; D014882:Water-Electrolyte Balance
D001786:Blood Glucose; D000808:Angiotensinogen; D000804:Angiotensin II; D000496:Alloxan; D010695:Phlorhizin; D012083:Renin