Atrial natriuretic peptide induces acrosomal exocytosis of human
spermatozoa.
Zamir, Nadav, Ronit Rotem, Nurit Keynan, Dalit Barkan, Haim Breitbart,
and Zvi Naor.
Department of Life Sciences, Bar-Ilan University, Ramat Gan 52900,
Israel. Department of Biochemistry, George S. Wise Faculty of Life
Sciences, Tel Aviv University, Ramat Aviv 69978, Israel.
APStracts 4:0233E, 1997.
Acrosomal exocytosis in mammalian spermatozoa is a process essential
for fertilization. Here we report that atrial natriuretic peptide
(ANP) markedly stimulates acrosomal exocytosis of capacitated human
spermatozoa. Typically, ANP exerts some of its actions via activation
of the ANP receptor (ANPR-A), a particulate guanylyl cyclase-linked
receptor, and subsequent formation of cyclic GMP (cGMP). We found
that ANP-stimulated acrosome reaction was inhibited by the
competitive ANPR-A receptor antagonist anantin, indicating a
receptor-mediated process. A linear fragment of ANP, ANP13-28, and
another ANP-like compound, brain natriuretic peptide (BNP), were
inactive. The stimulatory effect of ANP on acrosome reaction was
mimicked by the permeable cGMP analog, 8 bromo cyclic GMP (8-Br
-cGMP). Addition of the protein kinase C (PKC) inhibitors,
staurosporine and GF 109203X, resulted in a dose-related inhibition
of ANP-induced acrosome reaction. Also, down-regulation of
endogeneous PKC activity resulted in inhibition of ANP-, but not 8
-Br-cGMP-induced acrosome reaction. Removal of extracellular Ca2+
abolished ANP-induced acrosome reaction. Thus, ANP via Ca2+ influx,
PKC activation and stimulation of particulate guanylyl cyclase may
play a role in the induction of acrosome reaction of human
spermatozoa.
Received 9 June 1997; accepted in final form 25 August 1997.
APS Manuscript Number E263-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 29 October 1997