Petkov G V, Boev K K
Institute of Biophysics, Bulgarian Academy of Sciences, Sofia.
Eur J Pharmacol. 1999 Feb 19;367(2-3):335-41. doi: 10.1016/s0014-2999(98)00875-9.
In some smooth muscle cells, the rise in intracellular Ca2+ as a result of a Ca2+ influx via plasma membrane Ca2+ channels can activate a further increase in intracellular Ca2+ as a result of Ca2+ release from intracellular stores. This study examined the role of the Ca2+-induced Ca2+ release from the ryanodine-sensitive intracellular Ca2+ stores in shaping the smooth muscle contractions of guinea pig stomach. The contractile activity of isolated muscle strips of the fundus, corpus and antrum region of the stomach was recorded under isometric conditions. Ryanodine, an activator of Ca2+-induced Ca2+ release, concentration dependently (10(-7)-3x10(-5) M) increased the tone of fundus and corpus strips. Ryanodine had a dual action on the phasic contractions of the antrum and corpus: increase by the low concentrations (up to 10(-6) M) and inhibition by the high concentrations (10(-6)-3x10(-5) M). Nifedipine (10(-5) M) completely inhibited the ryanodine (10(-6) M)-induced phasic contractions and only partly the ryanodine (3x10(-5) M)-induced tonic contractions. In the presence of 10(-5) M cyclopiazonic acid, a specific inhibitor of sarcoplasmic reticulum Ca2+-ATPase, ryanodine (3x10(-5) M) further increased the tone of the corpus and fundus strips. Ryanodine (3x10(-5) M) induced tonic contractions in the fundus and corpus precontracted by acetylcholine (10(-5) M), and inhibited the acetylcholine (10(-6) M)-induced phasic contractions in the antrum and corpus. Ruthenium red, an inhibitor of Ca2+-induced Ca2+ release, concentration dependently (10(-6)-10(-4) M) decreased the tone and amplitude of the phasic contractions. The data obtained provide evidence for the participation of a sarcoplasmic reticulum Ca2+-induced Ca2+ release mechanism in shaping the tonic and phasic contractions of guinea pig stomach, and highlight important tissue differences.
在一些平滑肌细胞中，通过质膜钙通道的钙内流导致细胞内钙离子浓度升高，进而可激活细胞内钙库释放钙离子，使细胞内钙离子浓度进一步升高。本研究探讨了兰尼碱敏感的细胞内钙库中钙诱导的钙释放（CICR）在豚鼠胃平滑肌收缩形成过程中的作用。在等长条件下记录胃底、胃体和胃窦区域离体肌条的收缩活性。兰尼碱作为钙诱导的钙释放的激活剂，浓度依赖性地（10⁻⁷ - 3×10⁻⁵ M）增加胃底和胃体肌条的张力。兰尼碱对胃窦和胃体的相性收缩有双重作用：低浓度（高达10⁻⁶ M）时增加，高浓度（10⁻⁶ - 3×10⁻⁵ M）时抑制。硝苯地平（10⁻⁵ M）完全抑制兰尼碱（10⁻⁶ M）诱导的相性收缩，仅部分抑制兰尼碱（3×10⁻⁵ M）诱导的强直性收缩。在存在10⁻⁵ M环匹阿尼酸（肌浆网钙 - ATP酶的特异性抑制剂）的情况下，兰尼碱（3×10⁻⁵ M）进一步增加胃体和胃底肌条的张力。兰尼碱（3×10⁻⁵ M）在乙酰胆碱（10⁻⁵ M）预收缩的胃底和胃体中诱导强直性收缩，并抑制乙酰胆碱（10⁻⁶ M）诱导的胃窦和胃体相性收缩。钌红作为钙诱导钙释放的抑制剂，浓度依赖性地（10⁻⁶ - 10⁻⁴ M）降低相性收缩的张力和幅度。所获得的数据为肌浆网钙诱导的钙释放机制参与豚鼠胃的强直性和相性收缩形成提供了证据，并突出了重要的组织差异。
