M. Ohmori et al., Polymorphonuclear leukocytes (PMNs) functions in SHR, L-NAME- and DOCA/salt-induced hypertensive rats, J HYPERTENS, 18(6), 2000, pp. 703-707
Citations number
25
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
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.