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Effects of a Circulating Factor in Patients with Essential Hypertension on Intracellular Free Calcium in Normal Platelets

List of authors.
  • Armando Lindner, M.D.,
  • Margaret Kenny, Ph.D.,
  • and Alice J. Meacham, R.N.

Abstract

Intracellular free (cytosolic) calcium has been reported to be increased in the platelets of patients with essential hypertension. We investigated the possibility that the high cytosolic calcium concentration may be caused by a circulating plasma factor, by incubating platelets from normotensive subjects with plasma ultrafiltrates from patients with essential hypertension. The cytosolic calcium concentration in normal platelets increased after incubation with plasma from patients with untreated hypertension (80±15 percent [±SEM]) or from patients in whom hypertension was well controlled by calcium-influx blockers (129±33 percent). In contrast, the cytosolic calcium concentration was unchanged after incubation with plasma from normotensive subjects. When platelets from the patients were incubated with plasma from the controls, cytosolic calcium in platelets decreased by more than 30 percent, into the normal range (P<0.01).

These data demonstrate that plasma from patients with essential hypertension contains a substance that increases the cytosolic calcium concentration in platelets. Cytosolic calcium is a trigger for vascular smooth-muscle-cell contraction, and if the plasma factor acts on these cells as it acts on platelets, it may be responsible for the increased peripheral vascular resistance associated with hypertension. (N Engl J Med 1987; 316:509–13.)

Funding and Disclosures

Supported by core research funds from the Veterans Administration and a research award from the American Heart Association, Washington Affiliate.

We are indebted to Thomas R. Hinds, Ph.D. (Department of Pharmacology, University of Washington), for technical collaboration in measuring intracellular QUIN 2 concentrations and QUIN 2 leakage from platelets, which was invaluable in completing our studies.

Author Affiliations

From the Departments of Medicine and Laboratory Medicine, The Veterans Administration Medical Center, and the University of Washington, Seattle. Address reprint requests to Dr. Lindner at the Veterans Administration Medical Center, 1660 S. Columbian Way, Seattle, WA 98108.

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