Effect of Hormone Pretreatment on Contractility of Rabbit Oviductal Isthmus PDF Download

Author: Dorianne E. Rheaume
Publisher:
ISBN:
Category : Oviduct
Languages : en
Pages : 0

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Book Description
The exact mechanism for the hormonal modification of ovum transport is not known. The effects of transmural stimulation and of adrenergic agonists on the contractility of isthmic circular muscle of the oviduct were investigated in rabbits in estrus and after hormone treatments which disrupt normal ovum transport. We studied certain oviductal adrenergic mechanisms to define their possible role in mediating hormonal control over oviduct function. Stimulation at 24 Hz was maximal in all tissues but the tension developed was greater in the Estrous group than in the HCG-treated groups. Also, the frequency required to produce a 50% of maximum response was less in Estrous tissues. Cocaine, hydrocortisone and propranolol did not eliminate these differences. Both a- and g-adrenoceptors were present in all tissues. The a-receptors were predominant in all cases; transmural stimulation, adrenaline and noradrenaline always caused contractions that were blocked by phenoxybenzamine. (-)-Adrenaline was more potent than (-)-noradrenaline or (-)-phenylephrine in all tissues. Agonist potency between groups did not vary but for one notable exception: in HCG + Progesterone tissues, noradrenaline was significantly less potent than in the Estrous or HCG + Estrogen groups. Modifications in catecholamine reuptake processes and a- and g-adreno- ceptor sensitivity changes were investigated as possible explanations for these observations. Neither cocaine (3 x 10~^M) nor cocaine + hydrocortisone (10 _/[pipe] M) eliminated the between-group noradrenaline potency differences. a-Adrenoceptor sensitivity did not vary between groups, since the potencies of phenylephrine in the presence of propranolol and of adrenaline in the presence of cocaine + hydrocortisone + propranolol were not affected by hormone treatment. Propranolol (3.8 x 10 _ ^M) potentiated noradrenaline only in the HCG + Progesterone group and abolished between-group noradrenaline potency differences. Therefore, the possibility of increased 3-activity in HCG + Progesterone tissues was further investigated. We studied 3-activity by measuring the ability of adrenergic agonists to inhibit contractile responses to acetylcholine in the presence of cocaine + hydrocortisone + pre-exposure to phenoxybenzamine. (±)-Iso- prenaline inhibited the acetylcholine response by 90% in HCG + Progesterone tissues but by only 30% in Estrous tissues. Papaverine, however, a nonspecific smooth muscle relaxant, produced identical dose-response curves in both hormone groups. ID^q values for (±)-isoprenaline, calculated from normalized curves, were not significantly different, however. The order of agonist potency on 3-adrenoceptors ((±)-isoprenaline > ( )-noradrenaline >(-)-adrenaline ”(±)-salbutamol), as well as pA 2 values for 3-antagonists, propranolol (8.3) and practolol (5.3) were similar to those quoted by Furchgott (1972) for 3i~receptors. These results indicate that HCG + Progesterone-pretreatment causes increased 3-activity possibly by increasing numbers of 3-receptors, and also suggest that the 3-receptor is largely 3j_ in nature. Increased 3-activity may be responsible for the reduced responsiveness to noradrenaline following progesterone treatment; this adrenergic phenomenon might decrease the isthmic barrier to transport and result in accelerated ovum transport.