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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Acta+Pharmacol+Sin
2015 ; 36
(12
): 1444-50
Nephropedia Template TP
gab.com Text
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English Wikipedia
The new antihypertensive drug iptakalim activates ATP-sensitive potassium
channels in the endothelium of resistance blood vessels
#MMPMID26592519
Wang SY
; Cui WY
; Wang H
Acta Pharmacol Sin
2015[Dec]; 36
(12
): 1444-50
PMID26592519
show ga
AIM: To investigate the mechanisms underlying the activation of ATP-sensitive
potassium channels (K(ATP)) by iptakalim in cultured rat mesenteric microvascular
endothelial cells (MVECs). METHODS: Whole-cell KATP currents were recorded in
MVECs using automated patch clamp devices. Nucleotides (ATP, ADP and UDP) were
added to the internal perfusion system, whereas other drugs were added to the
cell suspension on NPC-1 borosilicate glass chips. RESULTS: Application of
iptakalim (10 and 100 ?mol/L) significantly increased the whole-cell K(ATP)
currents, which were prevented by the specific K(ATP) blocker glibenclamide (1.0
?mol/L). The opening of K(ATP) channels by iptakalim depended upon the
intracellular concentrations of ATP or NDPs: iptakalim activated K(ATP) channels
when the intracellular ATP or NDPs were at 100 or 1000 ?mol/L, and was
ineffective when the non-hydrolysable ATP analogue ATP?S (1000 ?mol/L) was
infused into the cells. In contrast, the K(ATP) opener pinacidil activated K(ATP)
channels when the intracellular concentrations of ATP or NDPs ranged from 10 to
5000 ?mol/L, and even ATP?S (1000 ?mol/L) was infused into the cells. CONCLUSION:
Iptakalim activates K(ATP) channels in the endothelial cells of resistance blood
vessels with a low metabolic status, and this activation is dependent on both ATP
hydrolysis and ATP ligands.