Some authors usually described an enhanced vascular reactivity to vasodilatoragents during pregancy. We would like toverifythis hypothesis with acetylcholin which is the vasodilator agent habitually used in animal experimentation. Young adult Wistar rats, pregnant and nonpregnant, were used. Rats received either a control diet, or this control diet supplemented with nitroargininin (0.063 % i.e. 30 mg/kg for7 days [treated group], from day 13th to day 20th for pregnants. Relaxation of rings thoracic aorta, with or without endothelium, in the presence of acetylcholin in cumulative was studied after contraction induced by depolarisation with KCl or after noradrenalin addition. The results show that relaxation in the presence of acetylcholin needs functional endothelial cells and that the nitric oxide plays a key role in this relaxation. So, there is no difference in vascular reactivity in late pregnant rats compared to nonpregnant rats. In addition, chronic inhibition of nitric oxide synthesis in pregnant rats do not modify pregnancy reactivity to nitric oxide because relaxation to S-nitroso-N acetyl penicillamin, which is a nitric oxide donor, is not different in control pregnant rats compared to treated pregnant rats. A judicious observation of work conditions with a particular attention with calcium concentration in organ bath solutions would certainly explain contradictory results obtained by different authors on vascular reactivity in vitro during gestation.
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Eur J Clin Invest
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