Clonidine hydrochloride 是一种α2-adrenoceptor激动剂，是一种抗高血压药。

Clonidine is a centrally active alpha-adrenergic agonist used predominantly as an antihypertensive agent, usually in combination with other agents. Despite wide scale use for many years, clonidine has not been linked definitively to either serum aminotransferase elevations or clinically apparent liver injury.

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 clonidine-induced CGRP production[2].

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[1]. 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[3]. 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. On the contrary, in DMSO-pretreated ABD rats, clonidine (0.6 μg i.c.) results in a 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[4].

4205-91-8

C9H10Cl3N3

266.55

Clonidine HCl;盐酸可乐定;Catapres

DMSO:20 mg/mL (75 mM)
H2O:26.7 mg/mL (100 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years