Fig. 5. Proposed regulatory pathways to explain the effect of CaM antagonists on sperm capacitation, sperm motility and protein tyrosine phosphorylation. All antagonists used inhibited/prevented capacitation, as evident by the poor response of spermatozoa to undergo agonist-induced AR (Table 1). Three antagonists (W7, OA and CZ) inhibited sperm motility before protein tyrosine phosphorylation (A) or vice versa (B), and capacitation. The second set of antagonists (i.e. compound 48/80, W13 and CBD) adversely affected capacitation without altering sperm motility or protein tyrosine phosphorylation. Inclusion of purified CaM in the capacitation medium significantly enhanced tyrosine phosphorylation of the 95 kDa and 82 kDa proteins (A).