Lisinopril alters contribution of nitric oxide and K(Ca) channels to vasodilatation in small mesenteric arteries of spontaneously hypertensive rats
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25194131
DOI
10.33549/physiolres.932780
PII: 932780
Knihovny.cz E-resources
- MeSH
- Antihypertensive Agents pharmacology MeSH
- Mesenteric Arteries drug effects metabolism physiopathology MeSH
- Potassium Channel Blockers pharmacology MeSH
- Potassium Channels, Calcium-Activated drug effects metabolism MeSH
- Hypertension drug therapy metabolism physiopathology MeSH
- Angiotensin-Converting Enzyme Inhibitors pharmacology MeSH
- Lisinopril pharmacology MeSH
- Disease Models, Animal MeSH
- Small-Conductance Calcium-Activated Potassium Channels drug effects metabolism MeSH
- Nitric Oxide metabolism MeSH
- Rats, Inbred SHR MeSH
- Rats, Inbred WKY MeSH
- Signal Transduction drug effects MeSH
- Nitric Oxide Synthase Type III antagonists & inhibitors metabolism MeSH
- Large-Conductance Calcium-Activated Potassium Channel alpha Subunits drug effects metabolism MeSH
- Intermediate-Conductance Calcium-Activated Potassium Channels drug effects metabolism MeSH
- Vasodilation drug effects MeSH
- Vasodilator Agents pharmacology MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antihypertensive Agents MeSH
- Potassium Channel Blockers MeSH
- Potassium Channels, Calcium-Activated MeSH
- Angiotensin-Converting Enzyme Inhibitors MeSH
- Kcnma1 protein, rat MeSH Browser
- Lisinopril MeSH
- Small-Conductance Calcium-Activated Potassium Channels MeSH
- Nos3 protein, rat MeSH Browser
- Nitric Oxide MeSH
- Nitric Oxide Synthase Type III MeSH
- Large-Conductance Calcium-Activated Potassium Channel alpha Subunits MeSH
- Intermediate-Conductance Calcium-Activated Potassium Channels MeSH
- Vasodilator Agents MeSH
To investigate lisinopril effect on the contribution of nitric oxide (NO) and K(Ca) channels to acetylcholine (ACh)-induced relaxation in isolated mesenteric arteries of spontaneously hypertensive rats (SHRs). Third branch mesenteric arteries isolated from lisinopril treated SHR rats (20 mg/kg/day for ten weeks, SHR-T) or untreated (SHR-UT) or normotensive WKY rats were mounted on tension myograph and ACh concentration-response curves were obtained. Westernblotting of eNOS and K(Ca) channels was performed. ACh-induced relaxations were similar in all groups while L-NMMA and indomethacin caused significant rightward shift only in SHR-T group. Apamin and TRAM-34 (SK(Ca) and IK(Ca) channels blockers, respectively) significantly attenuated ACh-induced maximal relaxation by similar magnitude in vessels from all three groups. In the presence of L-NMMA, indomethacin, apamin and TRAM-34 further attenuated ACh-induced relaxation only in SHR-T. Furthermore, lisinopril treatment increased expression of eNOS, SK(Ca) and BK(Ca) proteins. Lisinopril treatment increased expression of eNOS, SK(Ca), BK(Ca) channel proteins and increased the contribution of NO to ACh-mediated relaxation. This increased role of NO was apparent only when EDHF component was blocked by inhibiting SK(Ca) and IK(Ca) channels. Such may suggest that in mesenteric arteries, non-EDHF component functions act as a reserve system to provide compensatory vasodilatation if (and when) hyperpolarization that is mediated by SK(Ca) and IK(Ca) channels is reduced.
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