Effects of a calcium channel blocker, manidipine, on insulin sensitivity in essential hypertensives

• Published in: Journal of diabetes and its complications Vol. 9; no. 4; pp. 215 - 219
• Main Authors: Iimura, Osamu, Shimamoto, Kazuaki, Masuda, Atsushi, Higashiura, Katsuhiro, Miyazaki, Yoshinori, Hirata, Akifumi, Fukuoka, Masatada, Murakami, Hideyuki
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.10.1995
• Subjects: Blood Glucose - drug effects; Blood Glucose - metabolism; Blood Pressure - drug effects; Calcium Channel Blockers - pharmacology; Dihydropyridines - pharmacology; Glucose Clamp Technique; Humans; Hypertension - blood; Hypertension - physiopathology; Hypertension - urine; Infusions, Intravenous; Insulin - administration & dosage; Insulin - pharmacology; Middle Aged; Natriuresis - drug effects; Norepinephrine - blood; Renin - blood; Sodium - urine
• ISSN: 1056-8727; 1873-460X
• DOI: 10.1016/1056-8727(95)80005-Y

This study was designed to investigate the effects of the calcium channel blocker manidipine on insulin-dependent glucose uptake (insulin sensitivity) and insulin action to renal sodium handling and pressor systems in essential hypertensive (EHT). Seven EHT were hospitalized and a 2-h euglycemic hyperinsulinemic glucose clamp was performed in a fasting condition before and after 2 weeks administration of manidipine (20 mg/day). Insulin sensitivity was evaluated as M-value calculated from the infusion rate of glucose. Manidipine administration decreased mean blood pressure and increased M-value significantly in EHT. Before the manidipine treatment, hyperinsulinemia during the clamp induced a decrease of urinary sodium excretion and increases of plasma norepinephrine and plasma renin activity in EHT. After manidipine treatment, however, hyperinsulinemia induced natriuresis and did not augment the pressor systems activity. Thus, the calcium channel blocker improved insulin resistance as assessed by glucose clamp technique in EHT. Suppression of augmented renal sodium reabsorption and pressor system activities of insulin may be connected with the hypotensive mechanisms and the natriuresis caused by calcium channel blockers.