Lisinopril alters contribution of nitric oxide and KCa channels to vasodilatation in small mesenteric arteries of spontaneously hypertensive rats

Title:

Lisinopril alters contribution of nitric oxide and KCa channels to vasodilatation in small mesenteric arteries of spontaneously hypertensive rats

Creator:

Albarwani, S., Al-Siyabi, S., Al-Husseini, I., Al-Ismail, A., Al-Lawati, I., Al-Bahrani, I., and Tanira, M. O.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:233c030c-bb5c-489b-b7eb-eb4d4611153c
uuid:233c030c-bb5c-489b-b7eb-eb4d4611153c
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, endotel, oxid dusnatý, endothelium, nitric oxide, small mesenteric arteries, lisinopril, KCa channels, ACE inhibition, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

To investigate lisinopril effect on the contribution of nitric oxide (NO) and KCa 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 normotensi ve 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 (SKCa and IKCa 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, SKCa and BKCa proteins. Lisinopril treatment increased expression of eNOS, SKCa , BKCa 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 SKCa and IKCa 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 SKCa and IKCa channels is reduced, S. Albarwani, S. Al-Siyabi, I. Al-Husseini, A. Al-Ismail, I. Al-Lawati, I. Al-Bahrani, M. O. Tanira., and Obsahuje bibliografii

Language:

English

Rights:

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

Source:

Physiological research | 2015 Volume:64 | Number:1

Harvested from:

CDK

Metadata only:

false