Gwirtz P A
Department of Physiology, University of North Texas Health Science Center at Fort Worth 79107-2690, USA.
Circulation. 1995 Sep 15;92(6):1576-81. doi: 10.1161/01.cir.92.6.1576.
A coronary alpha 1-adrenergic constrictor tone exists under conditions associated with increased sympathetic stimulation but not during resting conditions in the normal heart. During renovascular hypertension, elevated circulating angiotensin II may enhance sympathetic stimulation of the heart, even at rest. This study tested the hypothesis that an alpha 1-adrenergic constrictor tone imposes limitations on coronary blood flow in resting dogs after development of renovascular hypertension, exacerbates coronary alpha-constrictor tone during exercise, and increases coronary vascular adrenergic responsiveness.
Left circumflex blood flow velocity (CFV), aortic pressure (AoP), and heart rate (HR) were examined in five quietly resting dogs during control conditions and after selective alpha 1-adrenergic blockade using an intracoronary injection of 0.5 mg prazosin. In the normotensive state, AoP was 87 +/- 7 mm Hg (mean +/- SD), HR was 105 +/- 25 beats per minute, and CFV was 28 +/- 6 cm/s. These parameters were not affected by alpha 1-adrenergic blockade. During submaximal exercise, removal of an alpha 1-adrenergic constrictor resulted in a 14 +/- 4% increase in CFV (P < .05). Two weeks after development of renovascular hypertension induced by stenosis of the left renal artery, mean AoP was 114 +/- 7 mm Hg (P < .05 versus normotensive state), HR was 111 +/- 28 beats per minute, and CFV was 21 +/- 8 cm/s. In contrast to the normotensive state, alpha 1-adrenergic blockade caused a 28 +/- 6% increase in CFV at rest (P < .05) and a 27 +/- 13% increase in CFV during exercise in the hypertensive state (P < .05 versus exercise before blockade and versus normotensive state). This resting coronary constrictor tone was associated with enhanced vasoconstrictor responsiveness to norepinephrine and phenylephrine.
It appears that renovascular hypertension results in a significant coronary alpha 1-adrenergic constrictor tone in the resting dog and an enhanced constrictor tone during exercise.
在与交感神经刺激增加相关的情况下，冠状动脉存在α1 - 肾上腺素能收缩张力，但在正常心脏的静息状态下不存在。在肾血管性高血压期间，即使在静息状态下，循环中升高的血管紧张素II也可能增强心脏的交感神经刺激。本研究检验了以下假设：α1 - 肾上腺素能收缩张力对肾血管性高血压发展后静息犬的冠状动脉血流施加限制，在运动期间加剧冠状动脉α - 收缩张力，并增加冠状动脉血管的肾上腺素能反应性。
在五只安静休息的犬处于对照状态时以及使用0.5毫克哌唑嗪冠状动脉内注射进行选择性α1 - 肾上腺素能阻滞之后，检测左旋支血流速度（CFV）、主动脉压（AoP）和心率（HR）。在正常血压状态下，AoP为87±7毫米汞柱（平均值±标准差），HR为每分钟105±25次搏动，CFV为28±6厘米/秒。这些参数不受α1 - 肾上腺素能阻滞的影响。在次最大运动期间，去除α1 - 肾上腺素能收缩作用导致CFV增加14±4%（P<.05）。在左肾动脉狭窄诱导肾血管性高血压两周后，平均AoP为114±7毫米汞柱（与正常血压状态相比，P<.05），HR为每分钟111±28次搏动，CFV为21±8厘米/秒。与正常血压状态相反，α1 - 肾上腺素能阻滞在静息时使CFV增加28±6%（P<.05），在高血压状态下运动期间使CFV增加27±13%（与阻滞前运动相比以及与正常血压状态相比，P<.05）。这种静息冠状动脉收缩张力与对去甲肾上腺素和苯肾上腺素的血管收缩反应性增强相关。
肾血管性高血压似乎导致静息犬冠状动脉出现显著的α1 - 肾上腺素能收缩张力，并在运动期间增强收缩张力。
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