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

1. The present study was designed to investigate the effects of 17β-oestradiol on the mesenteric, renal, iliac and coronary circulations and to determine 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 circumflex coronary arteries caused by intravenous infusion of 17β-oestradiol at constant heart rate and arterial pressure were assessed using electromagnetic flowmeters. 3. In eight pigs, infusion of 2 μg h^-1 of the hormone caused an increase in renal, iliac and coronary blood flow without affecting mesenteric blood flow, left ventricular dP/dt(max) (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In four pigs, these vasodilator effects were enhanced by graded increases in the dose of the hormone between 1, 2 and 3 μg h^-1; the highest dose also caused an increase in mesenteric blood flow. 4. In five pigs, blockade of muscarinic cholinoceptors and adrenoceptors with the intravenous administration of atropine, propranolol and phentolamine did not affect the vasodilator responses caused by infusion of 2 μg h^-1 of 17β-oestradiol. 5. The increases in renal, iliac and coronary blood flow caused by infusion of 2 μg h^-1 of 17β-oestradiol were prevented, respectively, by the injection of N(ω)-nitro-L-arginine methyl ester (L-NAME) into the renal artery (five pigs), the iliac artery (five pigs) or the coronary artery (five pigs). In five pigs, all responses were prevented by injection of L-NAME into all three arteries. In two pigs, injection of L-NAME into the mesenteric, renal, iliac and coronary arteries abolished the vasodilator responses to the infusion of 3 μg h^-1 of 17β-oestradiol. 6. The present study shows that intravenous infusion of 2 μg h^-1 of 17β-oestradiol primarily dilated renal, iliac and coronary circulations and that a higher dose of the hormone also caused vasodilatation in the mesenteric vascular bed. The mechanism of these responses was shown to be nitric oxide dependent.