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(Hypertension. 1995;25:731-734.)
© 1995 American Heart Association, Inc.

Articles

Decreased Dihydropyridine Receptor Number in Hypertensive Rat Vascular Muscle Cells

Kent Hermsmeyer; Anita C. White; David J. Triggle

From the Oregon Regional Primate Research Center, Beaverton.

Correspondence to Dr Kent Hermsmeyer, Oregon Regional Primate Research Center, 505 NW 185th Ave, Beaverton, OR 97006.

Abstract To further investigate the altered function of Ca²⁺ channels in vascular muscle cells in hypertension, a novel fluorescently labeled dihydropyridine was used with ultrahigh-sensitivity photometry to study dihydropyridine binding sites on the surface membrane of living vascular muscle cells from stroke-prone spontaneously hypertensive rats and their normotensive controls. Fluorescent nitrobenzoxadiazol-6-dihydropyridine in concentrations of 1 to 100 nmol/L bound specifically to vascular muscle cells' Ca²⁺ channels, and was displaced by the unlabeled dihydropyridine analogue or nisoldipine (10 µmol/L). Stroke-prone spontaneously hypertensive rat vascular muscle cells showed significantly decreased binding of nitrobenzoxadiazol-6-dihydropyridine compared with normotensive National Institutes of Health rats. Decreased binding of dihydropyridine by vascular muscle cells from stroke-prone spontaneously hypertensive rats (cells that in other studies show increased Ca²⁺ channel function) indicates a change in channel regulation that is possibly due to a deficiency in the inactivation mechanism, consistent with our earlier electrophysiological studies reporting deficiencies in Ca²⁺-dependent inactivation in genetic hypertension. These data demonstrate decreased numbers of localized sites of dihydropyridine binding on the sarcolemma of living vascular muscle cells, and support the hypothesis that Ca²⁺ channel alterations may significantly contribute to the molecular etiology of genetic hypertension.

Key Words: Calcium channels • rats, inbred SHR • sarcolemma • binding sites • hypertension, genetic

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