Delbro D, Burnstock G
Acta Physiol Scand. 1987 Jul;130(3):373-80. doi: 10.1111/j.1748-1716.1987.tb08151.x.
In pentobarbitone-chloralose anaesthetized rats, the effects of aortic administration of various purine compounds on systemic arterial pressure were investigated. All animals were pretreated with atropine and guanethidine to (largely) eliminate reflex neurogenic cardiovascular adjustments, and drugs influencing purine receptors, prostaglandin synthesis, etc. were used for analytical purposes. The compounds used were adenosine (AD) and its slowly degradable analogue, 2-chloroadenosine (2-chloro), adenosine-5'-triphosphate (ATP) and its slowly degradable analogues beta, gamma-methyleneATP (beta,gamma-meATP) and alpha,beta-methyleneATP (alpha,beta-meATP). Control cardiac output measurements before, at and after the peak pressure changes in some experiments revealed that they were at least 80% due to changes in systemic resistance, i.e. dominated by shifts in resistance vascular tone. Adenosine, 2-chloro, ATP and beta,gamma-meATP all elicited depressor (vasodilator) responses. 2-chloro was more potent than AD. Furthermore, the results suggest that the depressor action of ATP involves P1-purinoceptors, following the rapid degradation of ATP to AD, and probably also other mechanisms. The stable ATP analogues caused prompt pressor (vasoconstrictor) responses, where alpha,beta-meATP was more potent than beta,gamma-meATP. The latter compound also produced delayed (probably P1-purinoceptormediated) depressor actions, presumably via slow degradation to AD.
在戊巴比妥-氯醛糖麻醉的大鼠中，研究了经主动脉给予各种嘌呤化合物对体循环动脉压的影响。所有动物均预先用阿托品和胍乙啶处理以（在很大程度上）消除反射性神经源性心血管调节，并使用影响嘌呤受体、前列腺素合成等的药物进行分析。所用化合物为腺苷（AD）及其缓慢降解类似物2-氯腺苷（2-氯）、腺苷-5'-三磷酸（ATP）及其缓慢降解类似物β,γ-亚甲基ATP（β,γ-meATP）和α,β-亚甲基ATP（α,β-meATP）。在一些实验中，在压力变化峰值之前、之时和之后进行的心输出量对照测量显示，至少80%的变化是由于体循环阻力的改变，即主要由阻力血管张力的变化所主导。腺苷、2-氯、ATP和β,γ-meATP均引起降压（血管舒张）反应。2-氯比AD更有效。此外，结果表明，ATP的降压作用在ATP迅速降解为AD后涉及P1嘌呤受体，可能还涉及其他机制。稳定的ATP类似物引起迅速的升压（血管收缩）反应，其中α,β-meATP比β,γ-meATP更有效。后一种化合物还产生延迟的（可能由P1嘌呤受体介导的）降压作用，推测是通过缓慢降解为AD。
