BISOPROLOL AND CAPTOPRIL EFFECTS ON INSULIN-RECEPTOR TYROSINE KINASE-ACTIVITY IN ESSENTIAL-HYPERTENSION

Angiotension converting enzyme (ACE) inhibitors and beta-blockers have been reported to possess disparate effects on insulin sensitivity. Th e aim of this study was to study the effects of the selective beta-1 b locker bisoprolol and of the ACE inhibitor captopril on cellular insul in action in hypertensive individuals. After washout, 12 mild to moder ate essential hypertensives were randomized in a double-blind manner t o 5 mg bisoprolol daily or 25 mg captopril twice daily for 8 weeks. Er ythrocyte insulin binding and insulin-stimulated tyrosine kinase (TK) activity were measured before and after therapy. Both agents decreased diastolic blood pressure significantly (bisoprolol 96.5 +/- 0.9 to 87 .8 +/- 3.1 mm Hg; captopril 96.5 +/- 0.9 to 91.5 +/- 1.8 mm Hg; P < .0 5). Easting plasma glucose, insulin, and insulin/glucose indices remai ned unchanged after both therapies, as did lipid profiles. Maximal ins ulin-stimulated TK activity, assessed by phosphorylation of the exogen ous substrate poly-Glu(80)Tyr(20), was significantly higher (P < .05) after bisoprolol treatment but not after captopril treatment, when com pared to placebo (bisoprolol 8.5 +/- 1.8; captopril 7.3 +/- 1.5; place bo: 6.4 +/- 3..3 pmol P-32-ATP/fmol bound insulin). However, captopril , but not bisoprolol, increased the sensitivity of the receptor TK act ivity, as measured by the half-maximal activity concentration (ED50). Specific insulin binding was not affected by these two agents. Thus, b oth captopril and bisoprolol may have favorable but different effects on TK activity and insulin action at the cellular level. (C) 1997 Amer ican Journal of Hypertension, Ltd.