Gunst S J, al-Hassani M H, Adam L P
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202.
Am J Physiol. 1994 Mar;266(3 Pt 1):C684-91. doi: 10.1152/ajpcell.1994.266.3.C684.
Evidence suggests that the mechanical behavior of smooth muscle tissues is regulated by Ca(2+)-dependent changes in the phosphorylation of the 20,000-Da light chain of myosin (MLC). However, alternative mechanisms activated by specific kinases may be involved in regulating the shortening velocity in some smooth muscle tissues. To determine how the activation of protein kinases A or C affects the regulation of the shortening velocity in canine tracheal smooth muscle, we evaluated the effects of forskolin (10(-5) M) and phorbol 12,13-dibutyrate (PDBu, 3 x 10(-6) M) on active stress, intracellular Ca2+ ([Ca2+]i), MLC phosphorylation, and isotonic shortening velocity during contractions elicited by 60 mM KCl. Forskolin depressed and PDBu increased active stress, [Ca2+]i, MLC phosphorylation, and shortening velocity; thus the effects of these agents on the shortening velocity may result from changes in Ca(2+)-dependent MLC phosphorylation. In contrast, the decline in velocity that occurred with time during tonic contractions elicited by K+ depolarization was not associated with significant changes in MLC phosphorylation; thus the time-dependent changes in shortening velocity may be regulated by a mechanism other than MLC phosphorylation.
有证据表明，平滑肌组织的力学行为受肌球蛋白20,000道尔顿轻链（MLC）磷酸化的钙（Ca2+）依赖性变化调节。然而，由特定激酶激活的其他机制可能参与调节某些平滑肌组织的缩短速度。为了确定蛋白激酶A或C的激活如何影响犬气管平滑肌缩短速度的调节，我们评估了福斯高林（10-5 M）和佛波醇12,13 - 二丁酸酯（PDBu，3×10-6 M）对60 mM KCl诱发收缩期间的主动张力、细胞内钙（[Ca2+]i）、MLC磷酸化和等张缩短速度的影响。福斯高林降低而PDBu增加主动张力、[Ca2+]i、MLC磷酸化和缩短速度；因此，这些药物对缩短速度的影响可能源于钙（Ca2+）依赖性MLC磷酸化的变化。相比之下，K+去极化诱发的强直收缩期间速度随时间的下降与MLC磷酸化的显著变化无关；因此，缩短速度的时间依赖性变化可能由MLC磷酸化以外的机制调节。
