Role of NO in cyclosporin nephrotoxicity: effects of chronic NO inhibition and NO synthases gene expression.

The role of nitric oxide (NO) during cyclosporin renal vasoconstriction was evaluated by glomerular hemodynamic and histological changes produced by chronic NO synthesis inhibition and neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) NO syntheses mRNA expression in renal cortex and medulla. Uninephrectomized rats treated during 7 days with vehicle (Veh), cyclosporin A (CsA) 30 mg/kg, CsA + nitro-L-arginine methyl ester (L-NAME), and Veh + L-NAME (10 mg/dl) in the drinking water were studied. Increase in arterial pressure and afferent and efferent resistances, as well as decrease in glomerular plasma flow, ultrafiltration coefficient, and single-nephron glomerular filtration rate were significantly greater with CsA + L-NAME than with CsA alone.

A vasoactive serum component and reactivity of isolated rat aorta after chronic alcohol administration.

Norepinephrine-induced contractility and relaxation to acetylcholine of isolated aortas taken from normal and chronic alcoholic rats were measured. Similar experiments were performed adding serum from normal (NS) or alcoholic rats (AS), with or without norepinephrine and acetylcholine. Responses of normal and alcoholic aortas to agonists were comparable.

Effect of circulating factors on vascular smooth muscle contraction and its calcium uptake in uremia.

Uremia is often associated with alterations in calcium metabolism and vascular smooth muscle function in hypertension and atherosclerosis. The ways in which these conditions inter-relate are not clearly understood. In order to study the possibility that circulating factors might influence smooth muscle function, experiments were performed on rat aortic strips.