title: Polymorphonuclear leukocytes (PMNs) functions in SHR, L-NAME- and DOCA/salt-induced hypertensive rats.
abstract: OBJECTIVE
  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/lzm), NG-nitro-L-arginine methyl ester (L-NAME)- and deoxycorticosterone acetate (DOCA)/salt-induced hypertensive rats.
  
  
  METHODS
  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/salt-hypertension 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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Clinical Pharmacology, Jichi Medical School, Tochigi, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ohmori
authors.forename: Y
authors.initials: Y
authors.lastname: Kitoh
authors.forename: K
authors.initials: K
authors.lastname: Harada
authors.forename: K
authors.initials: K
authors.lastname: Sugimoto
authors.forename: A
authors.initials: A
authors.lastname: Fujimura
mesh_terms: D000818:Animals; D001772:Blood Cell Count; D001794:Blood Pressure; D002448:Cell Adhesion; D003900:Desoxycorticosterone; D006973:Hypertension / Q000097:blood / Q000139:chemically induced / Q000235:genetics / Q000503:physiopathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009504:Neutrophils / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017208:Rats, Wistar; D012965:Sodium Chloride; D013481:Superoxides / Q000378:metabolism
chemical_list: D013481:Superoxides; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D019331:NG-Nitroarginine Methyl Ester