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抑制劑描述：

產(chǎn)品名稱：Clonidine hydrochloride

產(chǎn)品別名：鹽酸可樂定

英文別名：Clonidine hydrochloride

靶點(diǎn)：Adrenergic Receptor

CAS：4205-91-8

純度：>98%

外觀：白色結(jié)晶性粉末

保存方法：-20°C

描述：

Clonidine hydrochloride (Catapres) is a direct-acting α2 adrenergic agonist with an ED50 of 0.02±0.01 mg/kg. It treats high blood pressure by stimulating α2 receptors in the brain, which decreases cardiac output and peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem. This binding decreases presynaptic calcium levels, and inhibits the release of norepinephrine (NE). The net effect is a decrease in sympathetic tone.

溶解性：DMSO ：20 mg/mL (75 mM)
Water ：26.7 mg/mL (100 mM)

體外研究：

Clonidine (0.01, 0.1 or 1 μM) significantly induces CGRP (α and β) mRNA expression in a dose-dependent manner in endothelial cells. Clonidine treatment (1 μM) for 24 h significantly increases the NO level in endothelial cells. NO pathway modulates CGRP production induced by clonidine.

體內(nèi)研究：

Clonidine (50 μg/kg, i.p.) induces a significant decrease in body temperature of rat lasting 3 hr, with the maximum at 1 hr after administration. An intracerebroventricular pretreatment of rats with neutral doses of phentolamine 15 min before clonidine considerably antagonizes the clonidine-induced hypothermia. Clonidine (0.003-0.05 mg/kg, i.p.) potently suppresses dopamine efflux in the prefrontal cortex induced by PCP. Pretreatment with the alpha-2A receptor antagonist (BRL-44408) prevents clonidine from suppressing PCP-induced dopamine overflow in the prefrontal cortex. In DMSO-pretreated SO rats, clonidine (0.6 μg i.c.) has no effect on blood pressure. However, after central adenosine A1R blockade (DPCPX) in SO rats, clonidine significantly (P < 0.05, one-way ANOVA) reduces blood pressure. In contrast, in DMSO-pretreated ABD rats, clonidine (0.6 μg i.c.) causes significant reduction in blood pressure; importantly, central A1R blockade (DPCPX pretreatment) does not influence (P > 0.05, one-way ANOVA) clonidine-evoked reduction in blood pressure in ABD rats. In DPCPX-pretreated SO rats and along with the appearance of the hypotensive response, clonidine causes a significant (P < 0.05) increase in the RVLM pERK1/2 level compared with basal or clonidine treatment in DMSO-pretreated SO rats. In vehicle (DMSO)-pretreated ABD rats, clonidine significantly (P < 0.05) enhances RVLM pERK1/2, and this response is not affected by DPCPX pretreatment.

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