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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F14%3A00431288" target="_blank" >RIV/67985823:_____/14:00431288 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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. 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 isnecessary 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

Název v anglickém jazyce

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

Popis výsledku anglicky

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. 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 isnecessary 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

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Physiological Research

ISSN

0862-8408

e-ISSN

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Svazek periodika

63

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

11

Strana od-do

275-285

Kód UT WoS článku

000339879900001

EID výsledku v databázi Scopus

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