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首页> 外文期刊>American Journal of Physiology >KCa+ channels contribute to exercise-induced coronary vasodilation in swine.
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KCa+ channels contribute to exercise-induced coronary vasodilation in swine.

机译：KCa +通道有助于运动引起的猪冠状血管舒张。

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Coronary blood flow is controlled via several vasoactive mediators that exert their effect on coronary resistance vessel tone through activation of K(+) channels in vascular smooth muscle. Because Ca(2+)-activated K(+) (K(Ca)(+)) channels are the predominant K(+) channels in the coronary vasculature, we hypothesized that K(Ca)(+) channel activation contributes to exercise-induced coronary vasodilation. In view of previous observations that ATP-sensitive K(+) (K(ATP)(+)) channels contribute, in particular, to resting coronary resistance vessel tone, we additionally investigated the integrated control of coronary tone by K(Ca)(+) and K(ATP)(+) channels. For this purpose, the effect of K(Ca)(+) blockade with tetraethylammonium (TEA, 20 mg/kg iv) on coronary vasomotor tone was assessed in the absence and presence of K(ATP)(+) channel blockade with glibenclamide (3 mg/kg iv) in chronically instrumented swine at rest and during treadmill exercise. During exercise, myocardial O(2) delivery increased commensurately with the increase in myocardial O(2) consumption, so that myocardial O(2) extraction and coronary venous Po(2) (Pcv(O(2))) were maintained constant. TEA (in a dose that had no effect on K(ATP)(+) channels) had a small effect on the myocardial O(2) balance at rest and blunted the exercise-induced increase in myocardial O(2) delivery, resulting in a progressive decrease of Pcv(O(2)) with increasing exercise intensity. Conversely, at rest glibenclamide caused a marked decrease in Pcv(O(2)) that waned at higher exercise levels. Combined K(Ca)(+) and K(ATP)(+) channel blockade resulted in coronary vasoconstriction at rest that was similar to that caused by glibenclamide alone and that was maintained during exercise, suggesting that K(Ca)(+) and K(ATP)(+) channels act in a linear additive fashion. In conclusion, K(Ca)(+) channel activation contributes to the metabolic coronary vasodilation that occurs during exercise. Furthermore, in swine K(Ca)(+) and K(ATP)(+) channels contribute to coronary resistance vessel control in a linear additive fashion.
机译：冠状动脉血流通过几种血管活性介质来控制，这些介质通过激活血管平滑肌中的K（+）通道对冠状动脉阻力血管张力发挥作用。因为Ca（2+）激活的K（+）（K（Ca）（+））通道是冠状血管中的主要K（+）通道，所以我们假设K（Ca）（+）通道的激活有助于运动引起的冠状血管扩张。鉴于先前的观察结果，即ATP敏感的K（+）（K（ATP）（+））通道特别有助于静息的冠状动脉阻力血管张力，我们另外研究了K（Ca）（ +）和K（ATP）（+）频道。为此，在不存在和存在格列本脲的K（ATP）（+）通道阻断剂的情况下，评估了四乙基铵（TEA，20 mg / kg iv）对K（Ca）（+）的阻断对冠脉血管舒缩的影响。 iv）在休息时和在跑步机锻炼期间长期用仪器检测的猪静脉注射3 mg / kg。在运动过程中，心肌O（2）的输送与心肌O（2）的消耗量相应增加，因此心肌O（2）的提取和冠状静脉Po（2）（Pcv（O（2）））保持恒定。 TEA（对K（ATP）（+）通道无影响的剂量）对静止时心肌O（2）平衡的影响很小，并削弱了运动引起的心肌O（2）传递的增加，导致随着运动强度的增加，Pcv（O（2））逐渐降低。相反，在静止状态下格列本脲导致Pcv（O（2））的显着下降，而Pcv（O（2））在较高的运动水平上会下降。联合的K（Ca）（+）和K（ATP）（+）通道阻滞导致静息时的冠状动脉血管收缩，类似于单独使用格列本脲引起的收缩，并且在运动过程中得以维持，这表明K（Ca）（+）和K（ATP）（+）通道以线性加性方式起作用。总之，K（Ca）（+）通道激活有助于运动过程中发生的代谢性冠状动脉舒张。此外，在猪中，K（Ca）（+）和K（ATP）（+）通道以线性累加方式有助于控制冠状动脉阻力血管。

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