Guanylate cyclase, potassium channels and eNOS are involved in TERPY effect in resistance vessels of SHR

Abstract

The hypotensive effect of the nitric oxide donor ([RU(TERPY)(BDQ)NO]3+) (TERPY) is slowly and long lasting in spontaneously hypertensive rats (SHR). Endothelium improves the relaxant effect of TERPY in SHR aorta. TERPY effect in resistance vessel of SHR was not studied yet. The aim of this study was evaluate the mechanism of TERPY effect in 2nd or 3rd branches of mesentery artery of SHR. Rings were pre‐contract with Phenylephrine and TERPY curves (0,1nmol/L to 100mmol/L) were performed using DMT‐myograf system (PowerLab 8/35). The presence of the endothelium was verified by acetylcholine effect (80%). Rings were pre‐incubated with ODQ (1 mmol/L), TEA (1 mmol/L), L‐NAME (100 mmol/L), ODQ+TEA or ODQ+TEA+L‐NAME. Endothelium improves TERPY´s effect. In rings with endothelium, L‐NAME reduced the potency of TERPY, ODQ or TEA decreased the potency and maximun effect (Emax) of TERPY. ODQ+TEA+L‐NAME reduced Emax, but did not abolish the TERPY effect. In rings without endothelium, both ODQ or TEA decreased the potency and Emax of TERPY and ODQ+TEA abolished TERPY effect. In conclusion, TERPY´s effect in resistance vessel of SHR is dependent of guanylate cyclase (GC), potassium (K+) channel and NOS activation.