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

Objectives To clarity ex-vivo polymorphonuclear leukocytes (PMNs) functions , we examined superoxide anion (O-2(-)) production and adhesion to a plasti c plate of isolated PMNs obtained from spontaneously hypertensive rats (SHR /Izm), N-G-nitro-L-arginine methyl ester (L-NAME)- and deoxycorticosterone acetate (DOCA)/salt-induced hypertensive rats. Design Sixteen week-old male SHR/lzm and Wistar-Kyoto rats (WKY/Izm) were u sed as a model of hypertension and its control. respectively. L-NAME-hypert ension was induced by oral administration of 100 mg/kg per day of L-NAME tw ice daily for 4 weeks using 4-week-old male Wistar rats. DOCA/salt-hyperten sion 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 hemi nephrectomy. Methods Heparinized whole blood was obtained from abdominal aorta. PMNs wer e isolated by density gradient following dextran sedimentation. A productio n of superoxide anion (O-2(-)) by PMNs stimulated with phorbol ester myrist ate 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. Results SHR/Izm showed a significant enhancement of O-2(-) production by is olated PMNs compared with WKY/Izm, Rats treated with L-NAME showed a lower O-2(-) production by PMNs compared to control animals. In DOCA/salt hyperte nsive rats, o(2)(-) production was not different from that in the control r ats. Adherent function of isolated PMNs did not differ significantly among these hypertensive animal models. Conclusions These results suggest that O-2(-) production by circulatory PMN s is augmented in SHR, but not in L-NAME and DOCA/salt hypertensive rats. T his enhanced function, which is also observed in human essential hypertensi on, might contribute to the development of cardiovascular damage in genetic ally determined hypertension. J Hypertens 2000, 18:703-707 (C) Lippincott W illiams & Wilkins.