Mechanism of the response to captopril in glucocorticoid hypertension.
The effect of captopril was explored in salt-depleted methylprednisolone (MP)-hypertensive rats. MP treatment raised BP by 41+/-2 mmHg over 2 weeks. Controls (C) had no change in BP. Sodium balance and weight data indicated a greater salt depletion in MP than in C. On day 15, captopril reduced BP in both MP (20+/-4 mmHg) and C (31+/-4 mmHg). The effect was significantly smaller in MP than in C (p less than 0.05). Plasma renin activity (PRA) was similarly elevated in both groups, consistent with salt depletion. Serum (SCE) and lung-converting enzyme (LCE) activity were similar in MP and C. The diminished antihypertensive effect of captopril in MP is therefore not attributable to differences in PRA, SCE, or LCE. Our data suggest that depressor actions of captopril unrelated to the renin-angiotensin system are impaired in MP. Glucocorticoid-induced changes in vasodilator systems may explain these findings.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D005260:Female; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008168:Lung / Q000201:enzymology; D008775:Methylprednisolone / Q000494:pharmacology; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011392:Proline / Q000031:analogs & derivatives*; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism
D011392:Proline; D002216:Captopril; D012964:Sodium; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D008775:Methylprednisolone