Bertalan Varga

Effect of local gaba administration on rat ovarian blood flow, and on progesterone and estradiol secretion

The effect of gamma-aminobutyric acid (GABA)--superfused onto the surface of the ovary--on ovarian blood flow and on estradiol-17-beta (E2) and progesterone (P) secretion was studied in anaesthesized, pseudopregnant rats. GABA, 0.5 mumol per 50 microliter per animal, significantly reduced the blood pressure in the femoral artery, increased ovarian blood flow, enhanced the rate of E2 release and markedly decreased P secretion. The present findings indicate that local GABAergic mechanisms may be involved in the regulation of ovarian blood flow and hormone secretion.

Stimulation of the Alpha- and Beta-Adrenergic Receptors in Human Ovarian Vasculature in vitro

The effect of fenoterol and norepinephrine was studied on the vascular resistance of in vitro perfused human ovary. It was found that the beta-adrenergic stimulant fenoterol causes vasodilatation, whereas the alpha-adrenergic stimulant norepinephrine elicits vasoconstriction in the arterial vascular bed of the ovary showing the role of adrenergic mechanism in the regulation of ovarian blood flow. It was supposed that therapeutical administration of beta-mimetic drugs leads to the elevation of ovarian blood flow, which may have special importance in the case of corpus luteum insufficiency.

Alteration in the reactivity of hamster cheek pouch arterioles to prostaglandin E2 and noradrenaline during pregnancy or sex steroid treatment

Dioestrous and pregnant, or ovariectomized hamsters treated with sunflower oil, oestradiol or progesterone were anesthetized with pentobarbital and the arterioles of the cheek pouch membrane were prepared for microcirculatory study. Prostaglandin E2 (PGE2) or noradrenaline (NA) were topically applied and changes of the arteriolar diameter were measured on the screen of a closed-circuit television. PGE2 induced arteriolar dilatation in dioestrous or ovariectomized hamsters, but induced vasoconstriction in pregnant or in oestrogen-treated animals. Vasoconstriction induced by PGE2 in oestrogen-treated animals disappeared after administration of alpha-adrenergic blockers. In this situation, PGE2 induced vasodilatation once again. NA elicited arteriolar constriction in each experimental group. In ovariectomized hamsters treated with oestrogen the constriction was more pronounced than in progesterone treated animals. In pregnant animals it was significantly greater on day 14 than in dioestrous animals. Progesterone treatment blunted the vascular effect of both PGE2 and NA. It was concluded that the reverse effect of PGE2 and the increased sensitivity to NA induced by high oestradiol levels may have roles in the regulation of local blood flow during the ovarian cycle and pregnancy.

Antagonism by PGE2 of the Vasoconstriction Induced by PGF2α in Human Ovary in vitro

Human ovaries from adnexectomy were perfused via the ovarian artery with constant volume of Thyrode’s solution. Perfusion pressure was recorded while doses of PGF2Α or PGE2

Increase of Progesterone Production in Human and Rat Luteal Cells by Beta-Adrenergic Stimulation

The effects of the beta 2-adrenergic agonist hexoprenaline were studied on the progesterone production of rat and human corpora lutea and compared to hCG-induced hormone production. Human corpora lutea were obtained from healthy patients, rat corpora lutea were harvested on day 6 of pseudopregnancy. Corpora lutea were digested by trypsin and homogeneous luteal cell suspension (6 X 10(5) cells/ml) was incubated for 2 h. Hexoprenaline and hCG were added to the medium and progesterone production was measured by RIA. Hexoprenaline or hCG dose-dependently increased the progesterone production of rat luteal cells and of human cells in mid- and late luteal phase. Moreover, hexoprenaline further increased the hCG-induced hormone production. The stimulatory effect of hexoprenaline could be prevented by propranolol. It is supposed that beta 2-adrenergic stimulation induces an increase in progesterone production of luteal cells and potentiates the effects of gonadotropic hormones.