Zhang L
Department of Pharmacology, Loma Linda University School of Medicine, California 92350, USA.
Comp Biochem Physiol A Mol Integr Physiol. 1998 Mar;119(3):661-7. doi: 10.1016/s1095-6433(98)01002-2.
Hypoxia is one of the most common stresses that affect an organism's homeostasis. Although much is known of the mechanisms of the cellular and biochemical responses to acute hypoxia, relatively little is known of the mechanisms of the responses to prolonged or chronic hypoxia. Chronic hypoxia suppresses vascular smooth muscle contractility in many vascular beds. While the endothelium is likely to play a role, part of the mechanisms underlying chronic hypoxic-induced changes in vascular responses resides in the changes in receptor-mediated excitation-contraction coupling and/or signal transduction in the vascular smooth muscle. Recent studies have demonstrated that chronic hypoxia attenuates both receptor-second messenger and second messenger-contraction coupling efficiencies in the vascular smooth muscle. This suppression of pharmacomechanical coupling is likely to represent one of the adaptive mechanisms of vascular smooth muscle and to play an important role in an adjustment of vascular tone and blood flow under the stress of moderate chronic hypoxia.
缺氧是影响机体稳态的最常见应激之一。尽管对细胞和生化反应应对急性缺氧的机制已有很多了解,但对机体应对长期或慢性缺氧的机制却知之甚少。慢性缺氧会抑制许多血管床的血管平滑肌收缩性。虽然内皮细胞可能发挥作用,但慢性缺氧诱导血管反应变化的部分机制在于血管平滑肌中受体介导的兴奋 - 收缩偶联和/或信号转导的改变。最近的研究表明,慢性缺氧会减弱血管平滑肌中受体 - 第二信使以及第二信使 - 收缩偶联效率。这种对药物机械偶联的抑制可能是血管平滑肌的适应性机制之一,并在中度慢性缺氧应激下调节血管张力和血流方面发挥重要作用。