Impaired control of L-type voltage-dependent calcium channels in experimental hypertension

Title:

Impaired control of L-type voltage-dependent calcium channels in experimental hypertension

Creator:

Mária Pintérová, Silvia Líšková, Zdena Dobešová, Behuliak, M., Jaroslav Kuneš, and Josef Zicha

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:7951c070-48ef-4084-9f4a-9e7368a39d4e
uuid:7951c070-48ef-4084-9f4a-9e7368a39d4e

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, krevní tlak, human physiology, blood pressure, L-type voltage-dependent calcium channels, calcium-activated K+ and Cl- channels, vasoactive systems, EDCF (endothelium-derived contracting factor), isolated arteries, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

Blood pressure (BP) level results from the balance of vasoconstrictors (mainly sympathetic nervous system) and vasodilators (predominantly nitric oxide and endothelium-derived hyperpolarizing factor). Most of the forms of experimental hypertension are associated with sympathetic hyperactivity and endothelial dysfunction. It is evident that nitric oxide and norepinephrine are antagonists in the control of calcium influx through L-type voltage-dependent calcium channels (L-VDCC). Their effects on L-VDCC are mediated by cGMP and cAMP, respectively. Nevertheless, it remains to determine whether these cyclic nucleotides have direct effects on L-VDCC or they act through a modulation of calcium-activated K+ and Cl- channels which influence membrane potential. Rats with genetic or salt hypertension are characterized by a relative (but not absolute) NO deficiency compared to the absolute enhancement of sympathetic vasoconstriction. This dysbalance of vasoconstrictor and vasodilator systems in hypertensive animals is reflected by greater calcium influx through L-VDCC susceptible to the inhibition by nifedipine. However, when the modulatory influence of cyclic nucleotides is largely attenuated by simultaneous ganglionic blockade and NO synthase inhibition, BP of spontaneously hypertensive rats remains still elevated compared to normotensive rats due to augmented nifedipine-sensitive BP component. It remains to determine why calcium influx through L-VDCC of hypertensive rats is augmented even in the absence of modulatory influence of major vasoactive systems (sympathetic nervous system, nitric oxide)., M. Pintérová ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

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

Source:

Physiological research | 2009 Volume:58 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false