Date of Award:

5-1973

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Biology

Committee Chair(s)

Raymond T. Sanders

Committee

Raymond T. Sanders

Committee

R. P. Sharma

Committee

LeGrande C. Ellis

Committee

Warren Foote

Committee

Thomas L. Bahler

Abstract

Smooth-muscle active compounds were extracted from rat and rabbit testicular homogenates, and from bathing media of rabbit testicular capsular preparations and were tentatively characterized as prostaglandins. The endogenous prostaglandins were responsible for spontaneous testicular capsular contractions in vitro, but were not solely responsible for spontaneous testicular capsular motility in vivo. In this respect, significantly greater concentrations of prostaglandins were extracted from bathing media from spontaneously contracting capsules in vitro than from inactive capsules in vitro or spontaneously contracting capsules in vivo. No significant difference was observed in the amount of prostaglandin extracted from the bathing media of inactive in vitro and spontaneously active in vivo preparations.

Various sex steroids (progesterone, testosterone, androstenedione, 17 α-hydroxyprogesterone, 5α-androstan-17 β-ol-3-one, and pregnenolone) inhibited spontaneous or prostaglandin-induced contractions in vitro and contractions potentiated by serotonin or acetylcholine, but the steroids did not inhibit spontaneous in vivo capsular motility or capsular motility generated by epinephrine in vitro. In this respect, α - and β-adrenergic receptors were present in rabbit testicular capsules, and α-adrenergic blocking agents inhibited spontaneously contracting in vivo capsules suggesting that sympathetic nervous innervation may regulate testicular motility.

Log dose-response curves for the effect of prostaglandin E1, E2, F1α, F and epinephrine on in vitro rabbit testicular capsules were determined, log dose-response curves for prostaglandin E1, F, and epinephrine indicate that they are equivalent for both in vivo and in vitro preparations. All of these compounds generated stimulatory responses, but prostaglandin E1 and E2 were inhibitory at higher concentrations. The data suggested that the inhibitory response of the capsule to higher concentrations of prostaglandin E1 and E2 were mediated by cyclic AMP. Theophylline (a phosphodiesterase inhibitor), isoproterenol (a β-adrenergic agonist), and cyclic AMP inhibited testicular capsular motility. Moreover, subthreshold concentrations of cyclic AMP potentiated the inhibitory response to PGE.

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Biology Commons

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