About: Altered neural and vascular mechanisms in hypertension

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
Description	This review is focused on two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins This review is focused on two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins (en)
Title	Altered neural and vascular mechanisms in hypertension Altered neural and vascular mechanisms in hypertension (en)
skos:prefLabel	Altered neural and vascular mechanisms in hypertension Altered neural and vascular mechanisms in hypertension (en)
skos:notation	RIV/67985823:_____/11:00364294!RIV12-AV0-67985823
http://linked.open...avai/riv/aktivita	P Z
http://linked.open...avai/riv/aktivity	P(GA305/09/0336), Z(AV0Z50110509)
http://linked.open...iv/cisloPeriodika	3
http://linked.open...vai/riv/dodaniDat	2012
http://linked.open...aciTvurceVysledku	Zicha, Josef Pintérová, Mária Kuneš, Jaroslav
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Fyziologický ústav AV ČR, v. v. i.
http://linked.open...dnocenehoVysledku	185265
http://linked.open...ai/riv/idVysledku	RIV/67985823:_____/11:00364294
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	adrenoceptors; G proteins; L-type voltage-dependent calcium channels; potassium channels; RhoA/Rho kinase; genetic hypertension (en)
http://linked.open.../riv/klicoveSlovo	G proteins L-type voltage-dependent calcium channels RhoA/Rho kinase adrenoceptors genetic hypertension potassium channels
http://linked.open...odStatuVydavatele	CZ - Česká republika
http://linked.open...ontrolniKodProRIV	[15DECA788FBA]
http://linked.open...i/riv/nazevZdroje	Physiological Research
http://linked.open...in/vavai/riv/obor	FA
http://linked.open...ichTvurcuVysledku	3 (xsd:int)
http://linked.open...cetTvurcuVysledku	3 (xsd:int)
http://linked.open...vavai/riv/projekt	Mechanisms of antihypertensive action of high potassium intake in salt hypertension
http://linked.open...UplatneniVysledku	2011
http://linked.open...v/svazekPeriodika	60
http://linked.open...iv/tvurceVysledku	Kuneš, Jaroslav Pintérová, Mária Zicha, Josef
http://linked.open...ain/vavai/riv/wos	000293138600002
http://linked.open...n/vavai/riv/zamer	Výzkum molekulárních a buněčných základů fyziologických a patofyziologických procesů s cílem objasnit mechanismy vzniku závažných onemocnění člověka
issn	0862-8408
number of pages	22 (xsd:int)

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