Comparison of signalling mechanisms underlying UTP-evoked vasoconstriction of rat pulmonary and tail arteries

European Journal of Pharmacology
Asrin TengahCharles Kennedy

Abstract

The endogenous nucleotide, UTP, acts at smooth muscle P2Y receptors to constrict rat pulmonary and tail arteries, but the underlying signalling pathways are poorly understood. The aim was to characterise the contribution of Ca2+ release and influx, rho kinase and protein kinase C to these contractions. Isometric tension was recorded from endothelium-denuded rat intralobar pulmonary and tail artery rings mounted on a wire myograph. Contractions were evoked by UTP and peak amplitude measured. Thapsigargin (1 µM), but not ryanodine (10 µM), significantly depressed contractions in both by 30-40% (P < 0.05). Nifedipine (1 µM) significantly reduced contractions in tail artery by ~60% (P < 0.01). Y27632 (10 µM), a rho kinase inhibitor and GF109203X (10 µM), a protein kinase C inhibitor, each significantly reduced pulmonary vasoconstriction by ~20%, and tail artery contractions by ~80% and ~40%, respectively (P < 0.01). In pulmonary artery, Y27632, GF109203X and thapsigargin, acted in an additive manner, but nifedipine less so. Adding all four together abolished the UTP response. In tail artery, Y27632 plus thapsigargin or GF109203X or nifedipine abolished contractions. Thapsigargin, GF109203X and nifedipine, coapplied pair-wise, acted...Continue Reading

Citations

Jan 12, 2021·Naunyn-Schmiedeberg's Archives of Pharmacology·Annabel SpekMartin Hennenberg

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