The effect of 17 beta-oestradiol on regional blood flow in anaesthetized pigs

1. The present study was designed to investigate the effects of 17 beta-oes tradiol on the mesenteric, renal, iliac and coronary circulations and to de termine the mechanisms involved. 2. In pigs anaesthetized with sodium pentobarbitone, changes in blood flow in the superior mesenteric, left renal, left external iliac and left circum flex coronary arteries caused by intravenous infusion of 17 beta-oestradiol at constant heart rate and arterial pressure were assessed using electroma gnetic flowmeters. 3. In eight pigs, infusion of 2 mu g h(-1) of the hormone caused an increas e in renal, iliac and coronary blood flow without affecting mesenteric bloo d flow, left ventricular dP/dt(max) (rate of change of left ventricular sys tolic pressure) and filling pressures of the heart. In four pigs, these vas odilator effects were enhanced by graded increases in the dose of the hormo ne between 1, 2 and 3 mu g h(-1); the highest dose also caused an increase in mesenteric blood flow. 4. In five pigs, blockade of muscarinic cholinoceptors and adrenoceptors wi th the intravenous administration of atropine, propranolol and phentolamine did not affect the vasodilator responses caused by infusion of 2 mu g h(-1 ) of 17 beta-oestradiol. 5. The increases in renal, iliac and coronary blood flow caused by infusion of 2 mu g h(-1) of 17 beta-oestradiol were prevented, respectively, by the injection of N-omega-nitro-L-arginine methyl ester (L-NAME) into the renal artery (five pigs), the iliac artery (five pigs) or the coronary artery (f ive pigs). In five pigs, all responses were prevented by injection of L-NAM E into all three arteries. In two pigs, injection of L-NAME into the mesent eric, renal, iliac and coronary arteries abolished the vasodilator response s to the infusion of 3 mu g h(-1) of 17 beta-oestradiol. 6. The present study shows that intravenous infusion of 2 mu g h-l of 17 be ta-oestradiol primarily dilated renal, iliac and coronary circulations and that a higher dose of the hormone also caused vasodilatation in the mesente ric vascular bed. The mechanism of these responses was shown to be nitric o xide dependent.