The effect of 17beta-oestradiol on regional blood flow in anaesthetized pigs.
1. The present study was designed to investigate the effects of 17beta-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 17beta-oestradiol at constant heart rate and arterial pressure were assessed using electromagnetic flowmeters. 3. In eight pigs, infusion of 2 microg h-1 of the hormone caused an increase in renal, iliac and coronary blood flow without affecting mesenteric blood flow, left ventricular dP/dtmax (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 microg 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 microg h-1 of 17beta-oestradiol. 5. The increases in renal, iliac and coronary blood flow caused by infusion of 2 microg h-1 of 17beta-oestradiol were prevented, respectively, by the injection of Nomega-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 microg h-1 of 17beta-oestradiol. 6. The present study shows that intravenous infusion of 2 microg h-1 of 17beta-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.
Vacca
G
G
Laboratorio di Fisiologia, Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia di Novara, Università del Piemonte Orientale A. Avogadro, Italy. Vacca@scimed1.med.no.unipmn.it
Battaglia
A
A
Grossini
E
E
Mary
D A
DA
Molinari
C
C
Surico
N
N
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D018680:Cholinergic Antagonists / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D007083:Iliac Artery / Q000187:drug effects; D066298:In Vitro Techniques; D018727:Muscarinic Antagonists / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III; D012039:Regional Blood Flow / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects; D013152:Splanchnic Circulation / Q000187:drug effects; D013552:Swine; D014664:Vasodilation / Q000187:drug effects; D016277:Ventricular Function, Left / Q000187:drug effects
D018680:Cholinergic Antagonists; D004791:Enzyme Inhibitors; D018727:Muscarinic Antagonists; D004958:Estradiol; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D019331:NG-Nitroarginine Methyl Ester