ALPHA ADRENERGIC-RECEPTOR MEDIATED FORMATION OF CYCLIC-AMP IN RAT SPINAL-CORD

  • 1 January 1980
    • journal article
    • research article
    • Vol. 6  (2) , 133-141
Abstract
Methoxamine and phenylephrine (PE), postsynaptic .alpha. adrenergic agonists, stimulated the accumulation of cyclic[c]AMP in spinal cord tissue slices. Naphazoline, oxymetazoline and clonidine presynpatic .alpha. receptors did not alter accumulation and blocked the PE response. The PE stimulation was completely inhibited by postsynaptic .alpha. antagonists, incompletely by agents which block presynaptic .alpha. receptors and slightly by the .beta. blocker propranolol. PE-stimulated accumulation was potentiated by phosphodiesterase inhibition (RO 20-1724 [4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone]). In contrast to reports on the requirement of the copresence of adenosine for .alpha. receptor-stimulated accumulation of cAMP in neuronal tissue, the PE stimulation in spinal cord slices was unchanged by adenosine receptor blockade (theophylline), hydrolysis of endogenous adenosine (adenosine deaminase), inhibition of adenosine deaminase (EHNA [erythro-9-(2-hydroxyl-3-nonyl)adenine hydrochloride]) or blockade of adenosine uptake (dipyridamole). Added adenosine increased basal accumulation and produced a marked potentiation of the PE response. In spinal cord tissue slices a postsynaptic .alpha. adrenergic receptor linked to cAMP accumulation occurs which does not require the presence of other neurohumoral agents for activation.