Polymorphonuclear leukocytes (PMNs) functions in SHR, l-NAME- and DOCA/salt-induced hypertensive rats


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Abstract

ObjectivesTo clarify ex-vivo polymorphonuclear leukocytes (PMNs) functions, we examined superoxide anion (O2) production and adhesion to a plastic plate of isolated PMNs obtained from spontaneously hypertensive rats (SHR/Izm), NG-nitro-L-arginine methyl ester (L-NAME)- and deoxycorticosterone acetate (DOCA)/salt-induced hypertensive rats.DesignSixteen week-old male SHR/Izm and Wistar-Kyoto rats (WKY/Izm) were used as a model of hypertension and its control, respectively. L-NAME-hypertension was induced by oral administration of 100 mg/kg per day of L-NAME twice daily for 4 weeks using 4-week-old male Wistar rats. DOCA/salthypertension was induced by once daily subcutaneous injection of 1 mg DOCA with 1% NaCl drinking water for 2 weeks using 8-week-old male Wistar rats with heminephrectomy.MethodsHeparinized whole blood was obtained from abdominal aorta. PMNs were isolated by density gradient following dextran sedimentation. A production of superoxide anion (O2) by PMNs stimulated with phorbol ester myristate acetate (PMA, 100 ng/ml) was determined by a superoxide dismutase (SOD)-inhibitable cytochrome-C reduction method. Adhesion of PMNs was evaluated by their protein content on a plastic plate measured by Lowry method.ResultsSHR/Izm showed a significant enhancement of O2 production by isolated PMNs compared with WKY/Izm. Rats treated with L-NAME showed a lower O2 production by PMNs compared to control animals. In DOCA/salt hypertensive rats, O2 production was not different from that in the control rats. Adherent function of isolated PMNs did not differ significantly among these hypertensive animal models.ConclusionsThese results suggest that O2 production by circulatory PMNs is augmented in SHR, but not in L-NAME and DOCA/salt hypertensive rats. This enhanced function, which is also observed in human essential hypertension, might contribute to the development of cardiovascular damage in genetically determined hypertension.

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