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Biology of Reproduction, Vol 22, 211-216, Copyright © 1980 by Society for the Study of Reproduction

Further Evidence Suggesting the Hormonal Stimulation of Hamster Sperm Acrosome Reactions by Catecholamines in vitro

STANLEY MEIZEL 1, and PETER K. WORKING 1

1 Department of Human Anatomy, University of California, Davis, California 95616


A previous report from this laboratory has shown that catecholamines can stimulate activation (motility characteristic of capacitation) and the acrosome reaction in hamster sperm in vitro and has suggested that agr- and beta-adrenergic mechanisms are involved in this stimulation. The present work was undertaken to provide further evidence to support or modify the previous conclusion that catecholamines can stimulate these events in hamster sperm in vitro through hormonal mechanisms.

In the present experiments the (-)-isomers of epinephrine, norepinephrine and the beta-adrenergic agonist isoproterenol (all at 50 µM) stimulated significantly greater numbers of acrosome reactions than did the (+)-isomers. Sperm incubated with the (+)-isomers gave significantly greater numbers of acrosome reactions than did the control sperm incubated in the absence of the (-) and (+)-isomers. These results support the earlier suggestion that (-)-isomers stimulated acrosome reactions through interaction with adrenergic receptors. However, in all cases both the (-) and (+)-isomers stimulated activation to the same extent over control levels.

In another series of experiments, physiological levels (0.5 nM) of (-)-epinephrine significantly stimulated acrosome reactions, but only in the presence of the chelator D-penicillamine (20 µM). The latter alone also increased acrosome reactions as compared to the control, but to a significantly lower level than when in the presence of (-)-epinephrine (0.5 nM). (+)-Epinephrine (0.5 nM) did not increase acrosome reactions over the control level, either in the presence or absence of D-penicillamine. (-)-Epinephrine or D-penicillamine alone or (+)-epinephrine (0.5 nM) plus D-pencillamine stimulated activation to the same extent over control levels. The beta-adrenergic antagonist oxprenolol (2.5 nM) inhibited the stimulation of acrosome reactions by (-)-epinephrine plus D-penicillamine to the level obtained with D-penicillamine alone. Oxprenolol did not inhibit activation. The results of experiments with 3 other chelators, chromotropic acid, catechol-3,5-disulfonic acid and EDTA, were identical to those obtained with D-penicillamine.

All of these results strongly support the previous suggestion by this laboratory that (-)-isomers of catecholamines do stimulate acrosome reactions primarily by interaction with adrenergic receptors. However, the (+)-isomers appear to stimulate primarly through nonhormonal mechanisms.

Note:
ACKNOWLEDMENTS This work was supported by NIH grant HD06698.

Submitted on August 2, 1979
Accepted on October 12, 1979




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