Mechanisms underlying contraction of rat isolated coronary artery induced by acidosis
10.3969/j.issn.1000-4718.2017.05.012
- VernacularTitle:酸中毒致大鼠离体冠状动脉收缩的机制
- Author:
Zefang HE
;
Xiaomin HOU
;
Rong YANG
;
Fangwen FAN
;
Pengmei GUO
;
Yu LIU
;
Mingsheng ZHANG
- Keywords:
Acidosis;
Coronary artery;
Na+-H+ exchanger;
Na+-HCO-3 cotransporter;
Chloride channels
- From:
Chinese Journal of Pathophysiology
2017;33(5):838-842
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the mechanisms underlying contraction induced by extracelluar acidosis (pHex6.8) in rat isolated coronary artery (RCA).METHODS:Using the microvessel tension recorder system, the effects of acid-base transporters on RCA contraction induced by pHex6.8 were explored by applying the selective pharmacological inhibitors of Na+-H+ exchanger 1 (NHE-1) and Na+-HCO-3 cotransporter (NBC), HOE-642 and S0859, respectively.The effects of chloride channel on RCA contraction induced by pHex6.8 were explored by applying the inhibitors of chloride channel (NPPB and NFA), and by replacing the extracellular NaCl with equimolar NaBr.RESULTS:pHex6.8 augmented the resting tension of RCA, and the maximum contraction was (3.90±0.95) mN.HOE-642 at 30 μmol/L and S0859 at 100 μmol/L both inhibited the contraction of RCA induced by pHex6.8 (P<0.01).NPPB and NFA both inhibited the contraction of RCA induced by pHex6.8 or KCl (60 mmol/L) in a concentration-dependent manner.NPPB and NFA (100 μmol/L) both inhibited the contraction of RCA induced by U46619 (1 μmol/L).Replacing the extracellular NaCl with equimolar NaBr almost completely inhibited RCA contraction induced by pHex6.8 (P<0.01), but had no obvious effect on the contraction induced by KCl (60 mmol/L) or U46619 (1 μmol/L).CONCLUSION:Extracellular acidosis-induced contraction in RCA may be related to the activated NHE-1 and NBC, and it may be also related to the enhanced chloride transport across the membrane.
