β-Adrenergic receptor blockade impairs NO-dependent dilation of large coronary arteries during exercise
β-Adrenergic receptor blockade impairs NO-dependent dilation of large coronary arteries during exercise
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DOI：
10.1152/ajpheart.00419.2002
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发表时间：
2003-02-01
影响因子：
4.8
通讯作者：
Lavallée, M
中科院分区：
文献类型：
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作者：
Okajima, M;Takamura, M;Lavallée, M
剪切应力依赖性一氧化氮（NO）的形成可防止血管过度收缩。我们研究了剪切应力依赖性NO的形成是否限制了β -肾上腺素能受体阻断后狗运动诱导的冠状动脉收缩。对照组运动导致冠状动脉血流量（CBF）从41 +/- 5 ml/min增加38 +/- 5 ml/min，心外膜冠状动脉外径（CD）从3.33 +/- 0.20 mm增加0.24 +/- 0.03 mm （P < 0.01）。CD与剪应力呈线性相关。心得安后，运动时CD由3.23 +/- 0.19 mm下降至0.08 +/- 0.03 mm (P < 0.01)， CD与剪应力关系斜率减小（P < 0.01）。这个斜坡没有被NO形成的额外封锁进一步改变。在服用心得安的静息犬中，冠状动脉内腺苷的血流依赖效应模拟运动诱导的剪切应力增加（心得安后）导致CD增加（P < 0.01）（从3.68 +/- 0.27 mm增加0.09 +/- 0.02）。因此，在运动过程中，需要剪切应力依赖的NO形成和β -肾上腺素能受体激活来引起CD扩张。抑制β -肾上腺素能受体激活导致剪切应力依赖性NO形成受损，并使α -肾上腺素能收缩成为主导。
Shear stress-dependent nitric oxide (NO) formation prevents immoderate vascular constriction. We examined whether shear stress-dependent NO formation limits exercise-induced coronary artery constriction after beta-adrenergic receptor blockade in dogs. Control exercise led to increases (P < 0.01) in coronary blood flow (CBF) by 38 +/- 5 ml/min from 41 +/- 5 ml/min and in the external diameter of epicardial coronary arteries (CD) by 0.24 +/- 0.03 mm from 3.33 +/- 0.20 mm. CD and shear stress were linearly related. After propranolol, CD fell (P < 0.01) during exercise (0.08 +/- 0.03 from 3.23 +/- 0.19 mm), and the slope of the relationship between CD and shear stress was reduced (P < 0.01). This slope was not further altered by the additional blockade of NO formation. In propranolol-treated resting dogs, flow-dependent effects of intracoronary adenosine to mimic exercise-induced increases in shear stress (after propranolol) led to increases (P < 0.01) in CD (0.09 +/- 0.02 from 3.68 +/- 0.27 mm). Thus both shear stress-dependent NO formation and beta-adrenergic receptor activation are required to cause CD dilation during exercise. Suppression of beta-adrenergic receptor activation leads to impaired shear stress-dependent NO formation and allows alpha-adrenergic constriction to become dominant.