Kupittayanant S, Kupittayanant P, Suwannachat C
School of Physiology, Institute of Science, Suranaree University of Technology, University Avenue, Nakhon Ratchasima 30000, Thailand.
Anim Reprod Sci. 2009 Oct;115(1-4):215-24. doi: 10.1016/j.anireprosci.2008.10.020. Epub 2008 Nov 5.
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 F(2alpha) (PGF(2alpha)) stimulation were therefore examined and the underlying mechanisms investigated. Uterine strips were isolated from laying hens 4h 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 microM PGF(2alpha) was applied to spontaneously contracting uterus, it significantly increased their amplitude and frequency of the contractions. As with spontaneous contractions, PGF(2alpha)-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 PGF(2alpha) which was not affected by wortmannin. Thus, extracellular Ca entry and MLCK phosphorylation are essential for uterine force production occurring spontaneously or by PGF(2alpha) stimulation. Our data supports the conclusion that the pathway dependent on extracellular Ca entry and MLCK phosphorylation predominates during PGF(2alpha) stimulation but suggests some involvement of an alternative force-producing pathway, presumably Ca-sensitization.
蛋鸡子宫收缩的生理基础尚未得到充分理解，但更好地理解这一点对于了解控制产蛋的机制很重要。因此，研究了自发产生或由前列腺素F(2α)（PGF(2α)）刺激引起的子宫收缩特性，并对其潜在机制进行了研究。在产卵前4小时从蛋鸡中分离出子宫条并测量张力。这些子宫条在体外保持健康并产生有规律的自发收缩。收缩是阶段性的，可以记录几个小时。暴露于特异性L型钙通道阻滞剂硝苯地平会导致张力消失。当应用L型钙通道激动剂Bay K8644或提高细胞外钙浓度时，收缩幅度和频率显著增加。自发收缩也被肌球蛋白轻链激酶（MLCK）的特异性抑制剂渥曼青霉素显著抑制。当向自发收缩的子宫施加1 microM PGF(2α)时，它会显著增加收缩的幅度和频率。与自发收缩一样，硝苯地平和渥曼青霉素可消除PGF(2α)诱导的张力产生。在没有细胞外钙的情况下，施加PGF(2α)会产生一个小的但持续的张力，该张力不受渥曼青霉素的影响。因此，细胞外钙内流和MLCK磷酸化对于自发或由PGF(2α)刺激产生的子宫张力至关重要。我们的数据支持这样的结论，即在PGF(2α)刺激期间，依赖于细胞外钙内流和MLCK磷酸化的途径占主导地位，但表明可能存在另一种产生张力的途径，推测是钙敏化。
