Involvement of BKCa and KV potassium channels in cAMP-induced vasodilatation: their insufficient function in genetic hypertension

Title:

Involvement of BKCa and KV potassium channels in cAMP-induced vasodilatation: their insufficient function in genetic hypertension

Creator:

Mária Pintérová, Behuliak, M., Jaroslav Kuneš, and Josef Zicha

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:82a8e189-6a12-49bf-b29a-1b422cd04b53
uuid:82a8e189-6a12-49bf-b29a-1b422cd04b53
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, isoprenaline, cyclic AMP, potassium channels, genetic hypertension, calcium channels, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Spontaneously hypertensive rats (SHR) are characterized by enhanced sympathetic vasoconstriction, whereas their vasodilator mechanisms are relatively attenuated compared to their high BP. The objective of our in vivo study was to evaluate whether the impaired function of BKCa and/or KV channels is responsible for abnormal cAMP-induced vasodilatation in genetic hypertension. Using conscious SHR and normotensive WKY rats we have shown that under the basal conditions cAMP overproduction elicited by the infusion of β-adrenoceptor agonist (isoprenaline) caused a more pronounced decrease of baseline blood pressure (BP) in SHR compared to WKY rats. Isoprenaline infusion prevented BP rises induced by acute NO synthase blockade in both strains and it also completely abolished the fully developed BP response to NO synthase blockade. These cAMP-induced vasodilator effects were diminished by the inhibition of either BKCa or KV channels in SHR but simultaneous blockade of both K+ channel types was necessary in WKY rats. Under basal conditions, the vasodilator action of both K+ channels was enhanced in SHR compared to WKY rats. However, the overall contribution of K+ channels to cAMP-induced vasodilator mechanisms is insufficient in genetic hypertension since a concurrent activation of both K+ channels by cAMP overproduction is necessary for the prevention of BP rise elicited by acute NO/cGMP deficiency in SHR. This might be caused by less effective activation of these K+ channels by cAMP in SHR. In conclusion, K+ channels seem to have higher activity in SHR, but their vasodilator action cannot match sufficiently the augmented vasoconstriction in this hypertensive strain., M. Pintérová, M. Behuliak, J. Kuneš, J. Zicha., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2014 Volume:63 | Number:3

Harvested from:

CDK

Metadata only:

false