Merkus Daphne, de Beer Vincent J, Houweling Birgit, Duncker Dirk J
Experimental Cardiology, Thoraxcenter, Cardiovascular Research Institute COEUR, Erasmus MC, University Medical Center Rotterdam, The Netherlands.
Pharmacol Ther. 2008 Sep;119(3):242-63. doi: 10.1016/j.pharmthera.2008.04.003. Epub 2008 May 14.
Despite the importance of the pulmonary circulation as a determinant of exercise capacity in health and disease, studies into the regulation of pulmonary vascular tone in the healthy lung during exercise are scarce. This review describes the current knowledge of the role of various endogenous vasoactive mechanisms in the control of pulmonary vascular tone at rest and during exercise. Recent studies demonstrate an important role for endothelial factors (NO and endothelin) and neurohumoral factors (noradrenaline, acetylcholine). Moreover, there is evidence that natriuretic peptides, reactive oxygen species and phosphodiesterase activity can influence resting pulmonary vascular tone, but their role in the control of pulmonary vascular tone during exercise remains to be determined. K-channels are purported end-effectors in control of pulmonary vascular tone. However, K(ATP) channels do not contribute to regulation of pulmonary vascular tone, while the role of K(V) and K(Ca) channels at rest and during exercise remains to be determined. Pulmonary hypertension is associated with alterations in pulmonary vascular function and structure, resulting in blunted pulmonary vasodilatation during exercise and impaired exercise capacity. Although there is a paucity of studies pertaining to the regulation of pulmonary vascular tone during exercise in idiopathic pulmonary hypertension, the few studies that have been performed in models of pulmonary hypertension secondary to left ventricular dysfunction suggest altered control of pulmonary vascular tone during exercise. Since the increased pulmonary vascular tone during exercise limits exercise capacity, future studies are needed to investigate the vasomotor mechanisms that are responsible for the blunted exercise-induced pulmonary vasodilatation in pulmonary hypertension.
尽管肺循环作为健康和疾病中运动能力的决定因素具有重要意义，但关于运动期间健康肺脏中肺血管张力调节的研究却很少。本综述描述了目前关于各种内源性血管活性机制在静息和运动期间控制肺血管张力中作用的知识。最近的研究表明内皮因子（一氧化氮和内皮素）和神经体液因子（去甲肾上腺素、乙酰胆碱）发挥重要作用。此外，有证据表明利钠肽、活性氧和磷酸二酯酶活性可影响静息肺血管张力，但其在运动期间控制肺血管张力中的作用仍有待确定。钾通道被认为是控制肺血管张力的最终效应器。然而，ATP敏感性钾通道对肺血管张力调节无作用，而电压门控钾通道和钙激活钾通道在静息和运动期间的作用仍有待确定。肺动脉高压与肺血管功能和结构改变有关，导致运动期间肺血管扩张减弱和运动能力受损。尽管关于特发性肺动脉高压运动期间肺血管张力调节的研究很少，但在左心室功能障碍继发的肺动脉高压模型中进行的少数研究表明运动期间肺血管张力控制发生改变。由于运动期间肺血管张力增加限制了运动能力，未来需要研究负责肺动脉高压中运动诱导的肺血管扩张减弱的血管运动机制。
