Hypertension, Vol 22, 735-742, Copyright © 1993 by American Heart Association
AM Kahn, CL Seidel, JC Allen, RG O'Neil, H Shelat and T Song
Resistance to insulin-induced glucose disposal is associated with
hypertension, in accord with recent reports that insulin-induced
vasodilation is impaired in men with resistance to insulin-induced glucose
disposal. Nevertheless, the mechanism of insulin-induced vasodilation is
not known. We wished to determine whether a physiological concentration of
insulin inhibits agonist-induced contraction at the level of the individual
vascular smooth muscle cell, and if so, how. Dispersed vascular smooth
muscle cells from dog femoral artery were grown on collagen gels for 4 to 8
days. Contraction and intracellular Ca2+ concentration of individual cells
were measured by photomicroscopy and fura 2 epifluorescence microscopy,
respectively. Serotonin and angiotensin II contracted cells in a
dose-dependent manner. Preincubation of cells for 20 minutes (short-term)
or 7 days (long-term) with insulin (40 microU/mL) inhibited serotonin- and
angiotensin II-induced contractions by approximately 50%. Insulin (10
microU/mL) acutely inhibited serotonin-induced contraction by 34%. The
maximal effect of high extracellular K(+)-induced contraction was not
affected by short-term insulin exposure, but the ED50 for extracellular
K(+)-induced contraction was increased from 7.6 +/- 2.5 to 16.0 +/- 3.9
mmol/L (P < .05). Short-term insulin exposure also attenuated the peak
rise of the serotonin-induced intracellular Ca2+ transient and increased
the rate constant for intracellular Ca2+ decline. Verapamil and ouabain
completely blocked the attenuation of agonist-induced contraction by
short-term insulin exposure, indicating the importance of voltage-operated
Ca2+ channels and the Na(+)-K+ pump for this effect.(ABSTRACT TRUNCATED AT
250 WORDS)
ARTICLES
Insulin reduces contraction and intracellular calcium concentration in vascular smooth muscle
Department of Medicine, University of Texas Medical School, Houston.
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