A Ca²⁺-dependent chloride current and Ca²⁺ influx via Ca(v)1.2 ion channels play major roles in P2Y receptor-mediated pulmonary vasoconstriction.

ABSTRACT:

Background and purpose

ATP, UTP and UDP act at smooth muscle P2X and P2Y receptors to constrict rat intrapulmonary arteries, but the underlying signalling pathways are poorly understood. Here, we determined the roles of the Ca²⁺ -dependent chloride ion current (I(Cl,Ca)), Ca(v)1.2 ion channels and Ca²⁺ influx.

Experimental approach

Isometric tension was recorded from endothelium-denuded rat intrapulmonary artery rings (i.d. 200-500 µm) mounted on a wire myograph.

Key results

The I(Cl,Ca) blockers, niflumic acid and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid and the Ca(v)1.2 channel blocker, nifedipine, reduced peak amplitude of contractions evoked by UTP and UDP by ∼45-50% and in a non-additive manner. Ca²⁺-free buffer inhibited responses by ∼70%. Niflumic aci

SUBMITTER: Mitchell C 

PROVIDER: S-EPMC3417463 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature