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首页> 外文期刊>American Journal of Physiology >Contractile effects of adenosine A1 and A2A receptors in isolated murine hearts.
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Contractile effects of adenosine A1 and A2A receptors in isolated murine hearts.

机译：腺苷A1和A2A受体在离体小鼠心脏中的收缩作用。

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The adenosine A1 receptor (A1R) inhibits beta-adrenergic-induced contractile effects (antiadrenergic action), and the adenosine A2A receptor (A2AR) both opposes the A1R action and enhances contractility in the heart. This study investigated the A1R and A2AR function in beta-adrenergic-stimulated, isolated wild-type and A2AR knockout murine hearts. Constant flow and pressure perfused preparations were employed, and the maximal rate of left ventricular pressure (LVP) development (+dp/dt(max)) was used as an index of cardiac function. A1R activation with 2-chloro-N6-cyclopentyladenosine (CCPA) resulted in a 27% reduction in contractile response to the beta-adrenergic agonist isoproterenol (ISO). Stimulation of A2AR with 2-P(2-carboxyethyl)phenethyl-amino-5'-N-ethylcarboxyamidoadenosine (CGS-21680) attenuated this antiadrenergic effect, resulting in a partial (constant flow preparation) or complete (constant pressure preparation) restoration of the ISO contractile response. These effects of A2AR were absent in knockout hearts. Up to 63% of the A2AR influence was estimated to be mediated through its inhibition of the A1R antiadrenergic effect, with the remainder being the direct contractile effect. Further experiments examined the effects of A2AR activation and associated vasodilation with low-flow ischemia in the absence of beta-adrenergic stimulation. A2AR activation reduced by 5% the depression of contractile function caused by the flow reduction and also increased contractile performance over a wide range of perfusion flows. This effect was prevented by the A2AR antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]et hyl)phenol (ZM-241385). It is concluded that in the murine heart, A1R and A2AR modulate the response to beta-adrenergic stimulation with A2AR, attenuating the effects of A1R and also increasing contractility directly. In addition, A2AR supports myocardial contractility in a setting of low-flow ischemia.
机译：腺苷A1受体（A1R）抑制β-肾上腺素引起的收缩作用（抗肾上腺素作用），而腺苷A2A受体（A2AR）既反对A1R的作用，又增强了心脏的收缩性。这项研究调查了β-肾上腺素刺激的，分离的野生型和A2AR基因敲除小鼠心脏中的A1R和A2AR功能。采用恒定流量和压力灌注制剂，将左心室压力（LVP）的最大发展速度（+ dp / dt（max））用作心脏功能的指标。用2-氯-N6-环戊基腺苷（CCPA）激活A1R可使对β-肾上腺素能激动剂异丙肾上腺素（ISO）的收缩反应降低27％。用2-P（2-羧乙基）苯乙基-氨基-5'-N-乙基羧酰胺基腺苷（CGS-21680）刺激A2AR减弱了这种抗肾上腺素的作用，导致部分（恒流制备）或完全（恒压制备）恢复。 ISO压缩响应。在敲除心脏中不存在A2AR的这些作用。据估计，高达63％的A2AR影响是通过抑制A1R抗肾上腺素能来介导的，其余的是直接的收缩作用。进一步的实验研究了在没有β-肾上腺素刺激的情况下，A2AR激活和相关的血管舒张与低血流缺血的关系。 A2AR激活将流量减少导致的收缩功能下降降低了5％，并且在较大范围的灌注流量中也提高了收缩性能。 A2AR拮抗剂4-（2- [7-氨基-2-（2-呋喃基）[1,2,4] triazolo [2,3-a] [1,3,5] triazin-5阻止了该作用-基氨基]叔）苯酚（ZM-241385）。结论是，在鼠心脏中，A1R和A2AR调节A2AR对β-肾上腺素能刺激的反应，从而减弱A1R的作用并直接增加收缩力。此外，A2AR支持在低流量缺血情况下的心肌收缩力。

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