Y. Harano et al., IMPROVEMENT OF INSULIN SENSITIVITY FOR GLUCOSE-METABOLISM WITH THE LONG-ACTING CA-CHANNEL BLOCKER AMLODIPINE IN ESSENTIAL HYPERTENSIVE SUBJECTS, Metabolism, clinical and experimental, 44(3), 1995, pp. 315-319
To clarify whether the long-acting calcium-channel blocker amlodipine
restores insulin insensitivity in essential hypertension, insulin sens
itivity tests were performed at the physiological steady-state insulin
level (45 to 55 mu U/mL) before and after amlodipine (2.5 to 7.5 mg/d
) administration for 2 to 4 months in borderline and mild essential hy
pertensive subjects. Instead of somatostatin, Sandostatin (Sandoz, Bas
el, Switzerland) was used for the determination of steady state plasma
glucose (SSPG) in the same way as previously described. SSPG, which w
as initially high (212.9 +/- 18.0 mg/dL, mean +/- SE), was significant
ly reduced to 169.8 +/- 14.7 after amlodipine treatment. Responses of
ketone bodies during the test at 30 minutes, which reflect the insulin
effect on lipolysis in adipose tissue and hepatic fatty acid oxidatio
n, also improved after amlodipine treatment. Norepinephrine, noted to
be mildly elevated after amlodipine treatment, decreased during the se
nsitivity test at 2 hours probably due to the sedative effect, without
any change in the fractional extraction of Na. This indicates that th
e physiological level of insulin does not activate sympathetic nerve a
ctivity or stimulate Na reabsorption. The long-acting calcium-channel
blocker amlodipine has significantly improved the initially decreased
insulin sensitivity for glucose metabolism at least partially in borde
rline or mild essential hypertension. Copyright (C) 1995 by W.B. Saund
ers Company