The role of potassium channels in relaxant effect of levosimendan in rat small mesenteric arteries

Ozdem S. S., Yalcin Z., Meiselman H. J., Baskurt O. K., Usta C.

CARDIOVASCULAR DRUGS AND THERAPY, vol.20, no.2, pp.123-127, 2006 (SCI-Expanded, Scopus)

  • Publication Type: Article / Article
  • Volume: 20 Issue: 2
  • Publication Date: 2006
  • Doi Number: 10.1007/s10557-006-7294-y
  • Journal Name: CARDIOVASCULAR DRUGS AND THERAPY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.123-127
  • Keywords: levosimendan, ATP-dependent potassium channels, rat, small mesenteric arteries, vasodilatation, SENSITIVE K+ CHANNEL, CARDIAC TROPONIN-C, CALCIUM SENSITIZER, CORONARY-ARTERY, NITRIC-OXIDE, CA2+ SENSITIZER, HEART-FAILURE, SMOOTH-MUSCLE, VASCULAR BED, BLOOD-FLOW
  • Akdeniz University Affiliated: No

Abstract

We investigated both the effect of levosimendan and the role of various potassium channels in KCI-precontracted rat small mesenteric arteries. Levosimendan (10(-6)-10(-3) M) or cromakalim (CRO, 10(-7)-10(-4) M) produced concentration-dependent relaxation responses in small mesenteric arteries precontracted by 30 mM KCI. The relaxant responses to levosimendan in KCI-precontracted arteries did not differ significantly between endothelium-intact and endothelium-denuded preparations. Incubation of rat small mesenteric arterial segments with ATP-dependent potassium channel (KATP) blocker glibenclamide (GLI, 10(-6) M) for 30 min significantly inhibited the relaxant responses to both levosimendan and CRO. Neither the Ca2+-activated potassium channel (KCa) blocker iberi-otoxin (10(-7) M) nor the voltage-dependent potassium channel (K-V) blocker 4-aminopyridine (5 mM) incubation for 30 min caused significant alterations in relaxant responses to levosimendan in KCI-precontracted small mesenteric arteries. These findings suggested that levosimendan-induced relaxation responses in isolated rat small mesenteric arteries were neither depended on endothelium nor inhibited by the blockers of KV or KCa but, they rather seem to depend on the activation of KATP.

We investigated both the effect of levosimendan and the role of various potassium channels in KCI-precontracted rat small mesenteric arteries. Levosimendan (10(-6)-10(-3) M) or cromakalim (CRO, 10(-7)-10(-4) M) produced concentration-dependent relaxation responses in small mesenteric arteries precontracted by 30 mM KCI. The relaxant responses to levosimendan in KCI-precontracted arteries did not differ significantly between endothelium-intact and endothelium-denuded preparations. Incubation of rat small mesenteric arterial segments with ATP-dependent potassium channel (KATP) blocker glibenclamide (GLI, 10(-6) M) for 30 min significantly inhibited the relaxant responses to both levosimendan and CRO. Neither the Ca2+-activated potassium channel (KCa) blocker iberi-otoxin (10(-7) M) nor the voltage-dependent potassium channel (K-V) blocker 4-aminopyridine (5 mM) incubation for 30 min caused significant alterations in relaxant responses to levosimendan in KCI-precontracted small mesenteric arteries. These findings suggested that levosimendan-induced relaxation responses in isolated rat small mesenteric arteries were neither depended on endothelium nor inhibited by the blockers of KV or KCa but, they rather seem to depend on the activation of KATP.