Adenosine‐activated potassium current in smooth muscle cells isolated from the pig coronary artery.

Abstract

SUMMARY1. The perforated patch technique with nystatin or amphotericin was used to record whole cell currents activated by adenosine in smooth muscle cells isolated enzymatically from pig coronary arteries.2. Adenosine (5-40 /SM) activated an outward current at a holding potential of 0 mV in 5 mm [K+]. and an inward current at -60 mV in 143 mm [K+] Openings became more frequent after the application of adenosine, with several levels then being detected. Openings of channels with a larger conductance were sometimes also seen in the presence of adenosine. Fluctuation analysis gave somewhat lower estimates of unitary current than did direct measurements.5. The effect of adenosine could be mimicked by the A1 receptor agonist CCPA (2-chloro-NM-cyclopentyladenosine), while the A2 agonist CGS 21680 (2-p-(2-carboxethyl)phenethylamino-5'-N-ethylcarboxamido adenosine hydrochloride) was without effect. The response to adenosine was inhibited by the A, antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine), but was unaffected by the A2antagonist CGS 15943A (5-amino-9-chloro-2-(2-furanyl)-1,2,4-triazolo[1,5-C]quinazoline monomethanesulphonate). 6. Our results suggest that adenosine acts at an A1 receptor to activate K+ channels. We consider it most likely that these are ATP-dependent K+ channels. We discuss the mechanism by which K+ channel activation may lead to hyperpolarization and so vasorelaxation.

Gender-specific K+-channel contribution to adenosine-induced relaxation in coronary arterioles

“…Similar to isoproterenol, adenosine is proposed to activate K ϩ channels via cAMP/ PKA-dependent phosphorylation or direct G-protein activation of the channel (9,33). However, the contribution of K V channels to adenosine or other cAMPmediated relaxation in isolated, intact arteries has not been reported previously.…”

A2B adenosine receptors mediate relaxation of the pig intravesical ureter: adenosine modulation of non adrenergic non cholinergic excitatory neurotransmission

“…This notion, however, does not unequivocally mean that any adenosine mediated relaxation is exerted through an action at the A 2 -receptor, as there are references describing A 1 -receptor mediated relaxations. Thus, in the adenosinemediated relaxation of the rat duodenum (Nicholls et al, 1992), in the pig coronary arteries (Merkel et al, 1992;Dart & Standen, 1993) and in rat diaphragmatic arterioles (Danialou et al, 1997), the involvement of both the A 1 -and A 2 -receptor subtypes has been suggested. In the present study, the contribution of the A 1 -receptor to pig intravesical ureter relaxation has been discarded because of the low potency shown by adenosine and CPA, as well as by the lack of e ect of 10 78 M DPCPX, a concentration selective for blocking the A 1 -receptor, on relaxations to adenosine and NECA.…”

Potassium channel activation and relaxation by nicorandil in rat small mesenteric arteries

“…adenosine or hypoxia in cells freshly isolated from the same tissue (35 pS, Dart & Standen, 1993;. In rabbit portal vein, the channel activated may have a slightly lower conductance of 26 pS (Kamouchi & Kitamura, 1994), though a higher conductance channel has also been reported to be activated by another K ATP channel opener, pinacidil, in this tissue (50 pS, Kajioka et al, 1991).…”

“…The low level of background channel activity in arterial smooth muscle cells sometimes makes it possible to resolve single channel events in whole cell recordings (Dart & Standen, 1993;. We were able to use this approach to study the channels activated by nicorandil in mesenteric arterial cells.…”