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Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction

  • Authors:
    • Hui‑Juan Wan
    • Yang Wang
    • Jun‑Qiang Si
    • Li Li
  • View Affiliations / Copyright

    Affiliations: Department of Physiology, Shihezi University Medical College, Shihezi, Xinjiang 832002, P.R. China
    Copyright: © Wan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2960-2968
    |
    Published online on: July 26, 2018
       https://doi.org/10.3892/etm.2018.6527
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Abstract

The present study aimed to investigate the role of propofol in mediating the vasomotor activity of the mesenteric arteriole (MA) of Sprague Dawley (SD) rats, and to elucidate the underlying mechanisms. The pressure myograph technique was used to examine the effect of different concentrations of propofol on the relaxation of blood vessels in the 2‑3 mm MA segments freshly separated from the SD rats. The whole‑cell patch‑clamp technique was applied to observe the outward current of single vascular smooth muscle cells (VSMCs) obtained from the MAs of the SD rats. Furthermore, immunofluorescence was utilized to assess the expression of connexin (Cx) in the MAs of SD rats. The results indicated the following: i) Propofol relaxed the MA of SD rats in a concentration‑dependent manner from 1x10‑7 to 3x10‑4 mol/l; ii) in the acutely dissociated VSMCs, propofol (1x10‑7 to 3x10‑4 mol/l) enhanced the outward current of VSMCs in a concentration‑dependent manner; iii) the enhanced outward currents induced by propofol (1x10‑5 mol/l) may be reversed by tetraethylammonium (TEA; 1 mmol/l), a calcium‑activated K+ channel inhibitor; iv) the effect of propofol on the relaxation of the vasculature wAS reduced after perfusion with 1 mmol/l TEA; v) Cx40, Cx43 and Cx45 were expressed on the MA; 6) 18β‑glycyrrhetintic acid and 2‑aminoethoxydiphenyl borate, two types of gap junction blocker, inhibited the propofol‑induced relaxation. The present study provides evidence that propofol relaxes the MA, which may be associated with its effect of enhancing the channel current of large‑conductance calcium voltage‑activated potassium channels, contributing to the K+ outflow and leading to VSMC hyperpolarization; the gap junction may facilitate the hyperpolarization, which may lead to vascular synchronized relaxation and thereby reduce the blood pressure.
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Copy and paste a formatted citation
Spandidos Publications style
Wan HJ, Wang Y, Si JQ and Li L: Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction. Exp Ther Med 16: 2960-2968, 2018.
APA
Wan, H., Wang, Y., Si, J., & Li, L. (2018). Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction. Experimental and Therapeutic Medicine, 16, 2960-2968. https://doi.org/10.3892/etm.2018.6527
MLA
Wan, H., Wang, Y., Si, J., Li, L."Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction". Experimental and Therapeutic Medicine 16.4 (2018): 2960-2968.
Chicago
Wan, H., Wang, Y., Si, J., Li, L."Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction". Experimental and Therapeutic Medicine 16, no. 4 (2018): 2960-2968. https://doi.org/10.3892/etm.2018.6527
Copy and paste a formatted citation
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Spandidos Publications style
Wan HJ, Wang Y, Si JQ and Li L: Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction. Exp Ther Med 16: 2960-2968, 2018.
APA
Wan, H., Wang, Y., Si, J., & Li, L. (2018). Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction. Experimental and Therapeutic Medicine, 16, 2960-2968. https://doi.org/10.3892/etm.2018.6527
MLA
Wan, H., Wang, Y., Si, J., Li, L."Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction". Experimental and Therapeutic Medicine 16.4 (2018): 2960-2968.
Chicago
Wan, H., Wang, Y., Si, J., Li, L."Propofol‑induced vasodilation of mesenteric arterioles via BKCa channel and gap junction". Experimental and Therapeutic Medicine 16, no. 4 (2018): 2960-2968. https://doi.org/10.3892/etm.2018.6527
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