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2018 ; 7
(7
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
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English Wikipedia
The Unexpected Role of Calcium-Activated Potassium Channels: Limitation of
NO-Induced Arterial Relaxation
#MMPMID29574460
Schmid J
; Müller B
; Heppeler D
; Gaynullina D
; Kassmann M
; Gagov H
; Mladenov M
; Gollasch M
; Schubert R
J Am Heart Assoc
2018[Mar]; 7
(7
): ä PMID29574460
show ga
BACKGROUND: Multiple studies have shown that an NO-induced activation of vascular
smooth muscle BK channels contributes to the NO-evoked dilation in many blood
vessels. In vivo, NO is released continuously. NO attenuates vessel constrictions
and, therefore, exerts an anticontractile effect. It is unknown whether the
anticontractile effect of continuously present NO is mediated by BK channels.
METHODS AND RESULTS: This study tested the hypothesis that BK channels mediate
the vasodilatory effect of continuously present NO. Experiments were performed on
rat and mouse tail and rat saphenous arteries using isometric myography and
FURA-2 fluorimetry. Continuously present NO donors, as well as endogenous NO,
attenuated methoxamine-induced vasoconstrictions. This effect was augmented in
the presence of the BK channel blocker iberiotoxin. Moreover, the contractile
effect of iberiotoxin was reduced in the presence of NO donors. The effect of the
NO donor sodium nitroprusside was abolished by an NO scavenger and by a guanylyl
cyclase inhibitor. In addition, the effect of sodium nitroprusside was reduced
considerably by a protein kinase G inhibitor, but was not altered by inhibition
of H(2)S generation. Sodium nitroprusside attenuated the intracellular calcium
concentration response to methoxamine. Furthermore, sodium nitroprusside strongly
reduced methoxamine-induced calcium influx, which depends entirely on L-type
calcium channels. It did not affect methoxamine-induced calcium release.
CONCLUSIONS: In summary, this study demonstrates the following: (1) continuously
present NO evokes a strong anticontractile effect on rat and mouse arteries; (2)
the iberiotoxin-induced augmentation of the effect of NO is associated with an
NO-induced reduction of the effect of iberiotoxin; and (3) NO evoked a reduction
of calcium influx via L-type calcium channels.
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