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To 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.Sixteen 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.Heparinized 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.SHR/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.These 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.