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(Hypertension. 1996;28:1013-1017.)
© 1996 American Heart Association, Inc.

Articles

Chelerythrine Inhibits Na⁺-H⁺ Exchange in Platelets From Spontaneously Hypertensive Rats

Oscar A. Gende

Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata (Argentina).

Correspondence to Oscar A. Gende, Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 Y 120, 1900 La Plata, Argentina. E-mail cicme@isis.unlp.edu.ar.

Hypertension has been associated with increased activity of the Na⁺-H⁺ exchanger. To study the role played by protein kinase C in this process, we used chelerythrine, a potent and specific inhibitor of the kinase. After an acid load by ammonium chloride preincubation, platelets isolated from spontaneously hypertensive rats showed a faster and larger increase in intracellular pH than platelets from Wistar-Kyoto rats. The initial rate of intracellular pH recovery was 2.46±0.26 pH units per minute in spontaneously hypertensive rats and 1.74±0.19 in Wistar-Kyoto rats. For protein kinase C inhibition, platelets were incubated for 30 minutes with 10 µmol/L chelerythrine. This treatment induced a significant reduction in the recovery rate only in spontaneously hypertensive rat platelets, indicating that a pathway involving protein kinase C participates in the prestimulation of the exchanger in cells from this rat strain. Addition of chelerythrine reduced the baseline intracellular pH of platelets. No significant difference was found between the decrease of steady-state intracellular pH induced by chelerythrine in either rat strain. These findings indicate that this model of hypertension is characterized by increased Na⁺-H⁺ activity mediated by protein kinase C stimulation.

Key Words: hydrogen-ion concentration • blood platelets • ion exchange • sodium-hydrogen antiporter • protein kinases • chelerythrine • rats, inbred SHR

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