Effect of angiotensin converting enzyme (ACE) and angiotensins on human sperm functions.
The presence of components of the renin angiotensin system (RAS) and specific receptors of angiotensin II in the female and male reproductive tract supports the hypothesis that reproductive functions may be controlled by RAS. Therefore, the present study investigated the influence of ACE and angiotensins on sperm functions and the sperm-egg interaction. The experiments did not indicate direct effects of ACE on the capacitation process or acrosome reaction. Release of ACE from human spermatozoa during capacitation was not related to their ability to undergo acrosome reaction after stimulation with ionophore. Therefore, ACE release does not seem to be a useful clinical marker for human sperm capacitation. However, decreased binding of human spermatozoa to the oolemma of zonafree hamster oocytes after inhibition of ACE by captopril indicates that kininase II is involved in sperm-egg interactions. In contrast to other studies, incubation with captopril had no influence on sperm binding to the zona pellucida. Because effects of ACE on sperm-egg interactions but not on capacitation or acrosome reaction were observed, several experiments were performed to study the influence of substrates and products on the acrosome reaction. Angiotensin II induced the acrosome reaction dose-dependently, whereas angiotensin I had no effect on the acrosome reaction. The effect of angiotensin II on acrosome reaction seems to be calcium-dependent and mediated by protein kinases. Since a specific type 2 angiotensin II receptor inhibits the acrosome reaction induced by angiotensin II, this subtype of receptors may be present at the surface of sperm heads. Another clue for the presence of type 2 receptors on human spermatozoa is the finding that pertussis toxin did not inhibit the angiotensin II induced acrosome reaction. In contrast to type 1 angiotensin II receptors, type 2 receptors are known to be G-protein independent.
Köhn
F M
FM
Center of Dermatology and Andrology, Justus Liebig University, Giessen, Germany.
Müller
C
C
Drescher
D
D
Neukamm
C
C
el Mulla
K F
KF
Henkel
R
R
Hägele
W
W
Hinsch
E
E
Habenicht
U F
UF
Schill
W B
WB
D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000494:pharmacology; D000177:Acrosome / Q000187:drug effects; D000803:Angiotensin I / Q000494:pharmacology*; D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium; D002216:Captopril / Q000494:pharmacology; D006224:Cricetinae; D003470:Culture Media; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism*; D037342:Pertussis Toxin; D011725:Pyridines / Q000494:pharmacology; D013075:Sperm Capacitation; D013084:Sperm-Ovum Interactions; D013094:Spermatozoa / Q000187:drug effects / Q000502:physiology*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D000806:Angiotensin-Converting Enzyme Inhibitors; D003470:Culture Media; D004791:Enzyme Inhibitors; D007093:Imidazoles; D007476:Ionophores; D011725:Pyridines; D010566:Virulence Factors, Bordetella; D000804:Angiotensin II; C066253:PD 123177; D000001:Calcimycin; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D000803:Angiotensin I; D002216:Captopril; D037342:Pertussis Toxin; D007703:Peptidyl-Dipeptidase A; D002118:Calcium