Impaired control of L-type voltage-dependent calcium channels in experimental hypertension
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
20131936
DOI
10.33549/physiolres.931914
PII: 931914
Knihovny.cz E-resources
- MeSH
- Receptors, Adrenergic, alpha metabolism MeSH
- Chloride Channels metabolism MeSH
- Ion Channel Gating MeSH
- Genetic Predisposition to Disease MeSH
- Hypertension etiology metabolism physiopathology MeSH
- Blood Pressure * MeSH
- Rats MeSH
- Sodium Chloride, Dietary adverse effects MeSH
- Humans MeSH
- Disease Models, Animal MeSH
- Nucleotides, Cyclic metabolism MeSH
- Nitric Oxide metabolism MeSH
- Rats, Inbred SHR MeSH
- GTP-Binding Protein alpha Subunits, Gi-Go metabolism MeSH
- Sympathetic Nervous System physiopathology MeSH
- Calcium metabolism MeSH
- Calcium Signaling * MeSH
- Calcium Channels, L-Type metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Receptors, Adrenergic, alpha MeSH
- Chloride Channels MeSH
- Sodium Chloride, Dietary MeSH
- Nucleotides, Cyclic MeSH
- Nitric Oxide MeSH
- GTP-Binding Protein alpha Subunits, Gi-Go MeSH
- Calcium MeSH
- Calcium Channels, L-Type MeSH
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).
References provided by Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension
