Mechanisms of uterine contractility in laying hens

The physiological basis of uterine contractility in laying hens is not well understood, but a better understanding is important for understanding the mechanisms governing egg laying. The characteristics of uterine contractility arising spontaneously or by prostaglandin F2α (PGF2α) stimulation were therefore examined and the underlying mechanisms investigated. Uterine strips were isolated from laying hens 4 h before oviposition and force measured. These strips remained healthy in vitro and produced regular spontaneous contractions. The contractions were phasic and could be recorded for several hours. Exposure to nifedipine, the specific L-type Ca channel blocker, led to the abolition of force. The contraction amplitude and frequency were significantly increased when Bay K8644, an agonist of L-type Ca channels, was applied or when the concentration of extracellular Ca was elevated. Spontaneous contractions were also significantly inhibited by wortmannin, the specific inhibitor of myosin light chain kinase (MLCK). When 1 μM PGF2α was applied to spontaneously contracting uterus, it significantly increased their amplitude and frequency of the contractions. As with spontaneous contractions, PGF2α-induced force production was abolished by nifedipine and wortmannin. In the absence of extracellular Ca, a small but tonic force was generated upon application of PGF2α which was not affected by wortmannin. Thus, extracellular Ca entry and MLCK phosphorylation are essential for uterine force production occurring spontaneously or by PGF2α stimulation. Our data supports the conclusion that the pathway dependent on extracellular Ca entry and MLCK phosphorylation predominates during PGF2α stimulation but suggests some involvement of an alternative force-producing pathway, presumably Ca-sensitization.