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

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

Research output: Contribution to journalArticle

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Abstract

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 normotensive WKY rats were mounted on tension myograph and ACh concentration-response curves were obtained. Westernblotting of eNOS and KCa 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.

Original languageEnglish
Pages (from-to)39-49
Number of pages11
JournalPhysiological Research
Volume64
Issue number1
Publication statusPublished - 2015

Fingerprint

Lisinopril
Mesenteric Arteries
Inbred SHR Rats
Vasodilation
Acetylcholine
Nitric Oxide
Apamin
omega-N-Methylarginine
Indomethacin
Inbred WKY Rats
Proteins

Keywords

  • ACE inhibition
  • Endothelium
  • K channels
  • Lisinopril
  • Nitric oxide
  • Small mesenteric arteries

ASJC Scopus subject areas

  • Physiology

Cite this

Lisinopril alters contribution of nitric oxide and KCa channels to vasodilatation in small mesenteric arteries of spontaneously hypertensive rats. / Albarwani, S.; Al-Siyabi, S.; Al-Husseini, I.; Al-Ismail, A.; Al-Lawati, I.; Al-Bahrani, I.; Tanira, M. O.

In: Physiological Research, Vol. 64, No. 1, 2015, p. 39-49.

Research output: Contribution to journalArticle

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AU - Albarwani, S.

AU - Al-Siyabi, S.

AU - Al-Husseini, I.

AU - Al-Ismail, A.

AU - Al-Lawati, I.

AU - Al-Bahrani, I.

AU - Tanira, M. O.

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AB - 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 normotensive WKY rats were mounted on tension myograph and ACh concentration-response curves were obtained. Westernblotting of eNOS and KCa 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.

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