Altered neural and vascular mechanisms in hypertension

Title:

Altered neural and vascular mechanisms in hypertension

Creator:

Mária Pintérová, Jaroslav Kuneš, and Jiří Zicha

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:2d7bd059-81bb-41e8-8182-0fe9dcbe06cd
uuid:2d7bd059-81bb-41e8-8182-0fe9dcbe06cd

Subject:

Fyziologie člověka a srovnávací fyziologie, bílkoviny, sympatický nervový systém, krevní tlak, proteins, sympathetic nervous system, blood pressure, spontaneously hypertensive rats, alpha- and beta-adrenoceptors, G proteins, L-type voltage-dependent calcium channels, calcium influx, potassium channels, PhoA/Rho-kinase pathway, calcium sensitization, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print

Description:

b1_Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in th e 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., b2_ there is considerable information on th e complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing., M. Pintérová, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

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

Source:

Physiological research | 2011 Volume:60 | Number:3

Harvested from:

CDK

Metadata only:

false