Adrenoceptor mechanisms in the extrinsic uterine arteries from late pregnant guinea-pigs were characterized pharmacologically and compared with contractile responses of uterine arteries from non-pregnant and oophorectomized control, progesterone and oestrogen treated animals. Pregnancy caused an increase in diameter of the arteries, more pronounced the more distal they were. There was no change in potassium-evoked maximum contractions during pregnancy.Noradrenaline (10 nM to 1 mM), in the presence of cocaine (1 pM) and propranolol (0.1 pM), induced concentrationdependent contractions of the arterial segments, with approximately similar pD2 values. The maximum responses (Emax) were significantly increased during pregnancy and hormone supplementation. Prazosin (10 nM to 1 pM), but not rauwolscine (10 nM to 1 pM), antagonized noradrenaline-evoked contractions of the arteries. Isoprenaline (10 nM to 1 pM), in the presence of prazosin (0.1 pM) and cocaine (1 pM), had no relaxant effect on arteries contracted submaximally by prostaglandin Fz. ( 5 pM). Neither cocaine nor normetanephrine modified noradrenalhe-evoked contractions of the uterine artery. The results indicate that guinea-pig uterine vasoconstriction is mediated by a]-adrenoceptors while relaxant P-adrenoceptor effects, neuronal and extraneuronal uptake mechanisms are of minor importance. The observed increase in Em,, may be due either to an increase in the number of a]-adrenoceptors or to an enhanced pharmaco-mechanical coupling, which conceivably is regulated by sex steroids since this response was reproduced in castrated animals by hormone supplementation.
The effects of low doses (0.05 to 20 micrograms./kg.) of estradiol-17 beta (E2) and estriol (E3) on blood perfusion in the genitourinary tissues were examined two and 24 hours after an intra-arterial injection into rabbits. Whereas 0.05 microgram./kg. E2 or E3 caused no detectable change, 0.5 microgram./kg. of either E2 or E3 markedly increased blood flow measured after two hours in urethra, vagina and uterus. No significant increase in the blood flow in the urinary bladder or the ureters was observed. With 20 micrograms./kg. E2 or E3 a much greater increase (10 to 25-fold) in the blood flow in the urethra, vagina and uterus was observed after two hours. At this time a small increase (about two-fold) could also be measured in urinary bladder and ureters. Twenty-four hours after this treatment (20 micrograms./kg. E2 or E3), the blood flow in the urinary organs was not significantly different from the pretreatment values but it was still significantly elevated in uterus and vagina. These data show that the blood flow in the female urethra is just as sensitive to low doses of estrogens as uterus and vagina. Both E2 and E3 seem to be equally effective in increasing blood perfusion in the urogenital tissues.
The effects of oestrogen and of oestrogen combined with progesterone were examined on the fractional distribution of cardiac output (blood flow) in the genitourinary tissues of the female rabbit. Oestradiol treatment significantly increased blood perfusion in the uterus, vagina and urethra but caused no change in the perfusion of the urinary bladder or the kidneys. The wet weight of the uterus and vagina increased significantly and in the urethra there was a tendency to weight gain following oestradiol treatment. Progesterone treatment following oestrogen appeared to reduce the effect of oestrogen on both perfusion and weight gain.
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