The Signal Transduction System of α2-Adrenoceptor Arteriole Constriction

本研究旨在阐明百日咳毒素敏感的三磷酸腺苷结合蛋白(G&lt；Ptx&gt；)和三磷酸腺苷敏感钾通道(K&lt；ATP&gt；)在α_2-肾上腺素受体小动脉收缩中的信号转导。从WKY大鼠的发育器上分离出一条微动脉(φ10 0μm)，两端插入玻璃微导管，在组织浴中用Krebs液灌流。在第一个方案中，我们评估了α-2激动剂(UK-10,304：UK)和K~+通道拮抗剂(格列本脲：GLb)对腺苷环化酶拮抗剂(SQ：SQ)和硝普钠(NP)治疗前后小动脉的反应。在这两种情况下，GLB均使小动脉收缩，但在未经处理的小动脉中完全观察到的UK收缩，在SQ和NP给药后完全消失。在第二种方法中，用NP或腺苷环化酶激动剂NKH477(NKH)检测UK或GLB型小动脉收缩。两种情况下均可观察到GLB微动脉收缩。微动脉仅在NP给药后被UK收缩，而在NKH给药后未见收缩。这些结果表明，G&lt；PTX&gt；与K&lt；ATP&gt；之间的信号转导依赖于腺苷环化酶抑制。

The aim of this study was to clarify the signal transduction between pertussis toxin sensitive GTP binding protein (G_<PTX>, and ATP sensitive potassium channel (K_<ATP>) on α2-adrenoceptor arteriole constriction. An arteriole (φ100μm) was dissected out from the WKY rat cremaster and was inserted glass micropipettes from both ends, and was perfused by Krebs solution in tissue bath. We evaluated response in the arterioles to α 2-agonists (UK-10,304 : UK) and ATP-sensitive K^+ channel (K_<ATP>) antagonist (glibenclamide : GLB) in untreated and after adenylate cyclase antagosist (SQ22536 : SQ) and nitroprusside (NP) administration in the first protocol. Arterioles were constricted by GLB in both conditions, but UK contractions, completely were observed in untreated arterioles, were completely abolished after SQ and NP administration. In the second protocol, UK or GLB arteriole constrictions were tested after NP or adenylate cyclase agonist, NKH 477 (NKH), administration. GLB arteriole constriction were observed in both conditions. Arterioles were constricted by UK only after NP administration, but not after NKH administration. These results indicated that the signal transduction between G_<PTX> and K_<ATP> depend on adenylate cyclase inhibition.