title: Effects of diabetes mellitus and acute hypertension on plasma nitric oxide and endothelin concentrations in rats.
abstract: OBJECTIVE
  To examine the plasma nitrate/nitrite (NOx-two end products of the nitric oxide metabolism) and endothelin (ET) concentrations, and response to acute adrenaline induced hypertension in diabetic rats.
  
  
  METHODS
  Four groups of 4-month-old rats were used: control rats (C, n=10) rats received adrenaline (A, 40 microg/kg i.v., n=10), rats received streptozotocin (S, 50 mg/kg i.v., n=8), and rats received STZ and adrenaline (SA, n=9). The experiments were performed 4 weeks after the STZ administration. Plasma NOx, ET, glucose, and mean arterial blood pressure (MAP) were measured.
  
  
  RESULTS
  Plasma ET concentrations were significantly increased in diabetic rats (S and SA) in comparison with the controls and adrenaline-only administered rats. NOx concentrations in diabetic groups (S and SA) were significantly decreased in comparison with the controls. Acute adrenaline induced hypertension in diabetes leads to a significant decrease of NOx concentrations in comparison with the controls, adrenaline-only administered and STZ-only administered rats. There was no difference between the MAP in diabetic and control rats. Adrenaline injection caused a significant increase of MAP in A and SA groups. Plasma glucose concentrations in diabetic rats (S and SA) were significantly increased in comparison with the nondiabetic groups (C and A). There was a weak but significant correlation between the NOx and ET concentrations in the controls, which probably reveal the balance between these vasoactive factors. In A, S, and SA groups, no significant correlation between the NOx/ET was found.
  
  
  CONCLUSIONS
  An impairment of the NOx and ET formation could be involved in the pathogenesis of diabetes mellitus and especially acute hypertension and diabetes. A lack of correlation between the NOx and ET probably indicated that in diabetes and acute hypertension, a primary mechanism of compensatory nitric oxide might be lost.
authors: Department of Biochemistry, Istanbul Medical Faculty, Capa 34390, Istanbul, Turkey. pervinvural@dostmail.com
authors: Pervin
authors: P
authors: Vural
authors: Aydin
authors: A
authors: Cevik
authors: Asli
authors: A
authors: Curgunlu
authors: Mukaddes
authors: M
authors: Canbaz
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D003920:Diabetes Mellitus / Q000097:blood* / Q000139:chemically induced; D016232:Endothelins / Q000097:blood*; D004837:Epinephrine / Q000494:pharmacology; D006029:Glycosuria / Q000503:physiopathology; D006973:Hypertension / Q000097:blood* / Q000139:chemically induced; D008297:Male; D009569:Nitric Oxide / Q000097:blood*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D016232:Endothelins; D009569:Nitric Oxide; D013311:Streptozocin; D004837:Epinephrine