Depressor and pressor actions of purine nucleosides and nucleotides in the anaesthetized rat

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Abstract
Depressor and pressor actions of purine nucleosides and nucleotides in the anaesthetized rat.Acta Physiol Scand130, 373–380. Received 12 May 1986, accepted 28 January 1986. ISSN 0001–6772. Departments of Physiology, University of Goteborg, Sweden and Anatomy & Embryology and Centre for Neuroscience, University College, London, UK.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 β,γ‐methyleneATP (β,γ‐meATP) and α,β‐methyleneATP (α,β‐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 β,γ‐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 α,β‐meATP was more potent than β,γ‐meATP. The latter compound also produced delayed (probably P1‐purinoceptormediated) depressor actions, presumably via slow degradation to AD.

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