The impact of subchronic lead poisoning on the vascular effect of nitric oxide in rats.

Lead-induced arterial hypertension is suggested to have resulted mainly from a reduction in nitric oxide (NO) bioactivity in vessel walls. The aim of this study was to evaluate the impact of poisoning by lead in so-called hypertensive doses on the basal and stimulated released NO effect in the rat mesenteric bed. Male Buffalo rats were given lead in a dose of 50 or 100ppm in drinking water for three months. The isolated mesenteric bed preconstricted by norepinephrine (0.5μg/ml) was used to determine the changes in vascular resistance induced by N-ω-nitro-l-arginine injected in increasing doses from 1.0 to 200.0μg or by acetylcholine administered in doses from 0.05 × 10(-10) to 5.0 × 10(-10)mol. These changes were measured as an increase or decrease in perfusion pressure in the constant flow system. In comparison with controls rats given 50ppm of lead, an increase in maximal response to N-ω-nitro-l-arginine (P < 0.01) and acetylcholine (P < 0.05) and a shift to the left of the dose-response curve for acetylcholine were demonstrated. Vascular responses in rats, who were given 100ppm of lead, were similar to those observed in the control group. It is concluded that lead induces NO-mediated changes of vascular tone and vascular reactivity only in the small range of doses known as hypertensive.