Brain development and evolution from the aspect of cerebrovascular reactivity and drug distribution of receptor subtypes

1.α受体和5-HTi受体亚型可能在蛇基底动脉收缩中起重要作用。内皮细胞可能在蛇基底动脉对响尾蛇BK的反应性中起重要作用，但可能不参与对ACh、BK和静息血管张力的反应性. NO可抑制考克斯或TXA_2合成酶，因此抑制NOS可解除考克斯或TXA_2合成酶的抑制，从而诱导猪基底动脉内皮细胞产生TXA_2。另一方面，由于TXA_2和其他收缩相关的前列腺素可抑制NOS，因此抑制考克斯或TXA_2合成酶可解除NOS的抑制，从而增加NO.3的自发产生。Ang Ⅱ的收缩作用可能是通过激活猪基底动脉平滑肌细胞上的AT_1受体介导的，并通过激活血管内皮细胞上的AT_2受体，进而产生NO来调节.内毒素增强NO生产镁缺乏大鼠睾丸直接，内毒素受体可能，至少部分，有助于这种增强。

1. Adrenoceptor a and 5-HTi receptor subtypes might be important in arterial contraction in snake basilar artery. Endothelial cells might play an important role in the responsiveness of snake basilar arteries to rattlesnake BK, but they might not be involved in the responsiveness to ACh, BK and resting vascular tone.2. NO may inhibit COX or TXA_2 synthetase, and that therefore inhibition of NOS might disinhibit COX or TXA_2 synthetase, subsequently inducing TXA_2 production in porcine basilar arterial endothelial cells. On the other hand, as TXA_2 and other contractility-related prostaglandin(s) may inhibit NOS, therefore the inhibition of COX or TXA_2 synthetase might disinhibit NOS, and then increase the spontaneous production of NO.3. The contraction induced by Ang II might be mediated via the activation of ATi receptors on the porcine basilar arterial smooth muscle cells and be modulated via the activation of AT_2 receptors on the endothelial cells, followed by NO production.4. Endotoxin enhances NO production in Mg-deficient rat aortas directly, and that endotoxin receptors might, at least in part, contribute to this enhancement.