EFECTO DE LA DEXAMETASONA EN LA LIBERACIÓN DE OXIDO NITRICO EN TEJIDO RENAL

MARAÑÓN R,; JOO TURONI C,; COVIELLO A; PERAL DE BRUNO M.

Tafi del Valle, Tucumán

Jornada; Poster XVIII JORNADAS DE LA SOCIEDAD DE BIOLOGÍA DE TUCUMÁN; 2001

Asociación de Biología de Tucumán

Nitric oxide (NO) is a vasodilator that regulates arterial pressure in an antagonistic form to angiotensin II (Ang II). Its release would be controlled by local tissue leves of Ang II. It has been demonstrated that one of the enzymes that produce NO, inducible-NO-synthase (iNOS) would be constitutible expressed in the kidney. Our objective was to study the rol of iNOS in basal and stimulated NO in renal cortex (C) and medulla (M). Fractions (158±30 mg, n=14) of total renal tissue (T), of M and C of rats were obtained. NO contents were measured by Griess reaction in presence and absence of Ang II (10-8-10-6M) and/or L-NAME (NO synthesis inhibitor) and dexamethasone: DEXA (10-4M). Basal NO content after equilibration period was 15.3±1.8 (nmoles/mg, n=20). In M and C significant differences were find between NO contents (16.8±3.7 vs 3.4±1.1 nmoles/mg, p<0.05, M and C respectively). After washing a diminution (p<0.01) was observed of NO in all cases. In M DEXA inhibited a 20% NO levels and did not modify NO levels in C. In T the response to Ang II was variable (all doses). L-NAME did not modify basal or Ang II levels of NO. CONCLUSIONS: NO contents are very high in comparition with vascular tissues. Lack of action of DEXA in C and the low effect of M suggest that iNOS induced by inflamatory reaction is not involved in renal NO content regulation. However, an iNOS constitutively expressed can not be discarded.