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[Modulation of electrical responses of endothelial cells by nicotinic cholinoreceptors].
Fiziol Zh. 2009; 55(2):17-23.FZ

Abstract

Because the sustained component of hyperpolarization of endothelial cells evoked by acetylcholine in isolated rat aorta may partially be mediated by the reversed Na(+)-Ca(2+) exchanger and Na(+)-K(+) ATPase, the mechanisms which transport Na(+) out of cells, we compared the electrical responses of endothelial cells from isolated rat aorta to acetylcholine with other Ca(2+) mobilizing agents and studied the effect of nicotine on endothelial membrane potential in order to asses the functional activity of nicotinic cholinoreceptors. Ca(2+) ionophores A23187 and ionomycin, as well as inhibitors of endoplasmic reticulum Ca(2+) ATPase cyclopiazonic acid and 2,5-di-tert-butylhydroquinone evoked a short-lived hyperpolarization which turned to a sustained depolarization of endothelial cells, a time course that substantially differed from that evoked by acetylcholine. Nicotine evoked a Na+ dependent depolarization of endothelial cells confirming functional activity ofnicotinic cholinoreceptors in rat aortic endothelial cells. The results suggest that stimulation of Na+ permeant nicotinic receptors by acetylcholine may contribute to sustained hyperpolarizatiom via stimulation of Na+ extrusion mechanisms.

Authors

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Pub Type(s)

Journal Article

Language

ukr

PubMed ID

19526844

Citation

Bondarenko, O I., and V F. Sahach. "[Modulation of Electrical Responses of Endothelial Cells By Nicotinic Cholinoreceptors]." Fiziolohichnyi Zhurnal (Kiev, Ukraine : 1994), vol. 55, no. 2, 2009, pp. 17-23.
Bondarenko OI, Sahach VF. [Modulation of electrical responses of endothelial cells by nicotinic cholinoreceptors]. Fiziol Zh. 2009;55(2):17-23.
Bondarenko, O. I., & Sahach, V. F. (2009). [Modulation of electrical responses of endothelial cells by nicotinic cholinoreceptors]. Fiziolohichnyi Zhurnal (Kiev, Ukraine : 1994), 55(2), 17-23.
Bondarenko OI, Sahach VF. [Modulation of Electrical Responses of Endothelial Cells By Nicotinic Cholinoreceptors]. Fiziol Zh. 2009;55(2):17-23. PubMed PMID: 19526844.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Modulation of electrical responses of endothelial cells by nicotinic cholinoreceptors]. AU - Bondarenko,O I, AU - Sahach,V F, PY - 2009/6/17/entrez PY - 2009/6/17/pubmed PY - 2009/8/11/medline SP - 17 EP - 23 JF - Fiziolohichnyi zhurnal (Kiev, Ukraine : 1994) JO - Fiziol Zh VL - 55 IS - 2 N2 - Because the sustained component of hyperpolarization of endothelial cells evoked by acetylcholine in isolated rat aorta may partially be mediated by the reversed Na(+)-Ca(2+) exchanger and Na(+)-K(+) ATPase, the mechanisms which transport Na(+) out of cells, we compared the electrical responses of endothelial cells from isolated rat aorta to acetylcholine with other Ca(2+) mobilizing agents and studied the effect of nicotine on endothelial membrane potential in order to asses the functional activity of nicotinic cholinoreceptors. Ca(2+) ionophores A23187 and ionomycin, as well as inhibitors of endoplasmic reticulum Ca(2+) ATPase cyclopiazonic acid and 2,5-di-tert-butylhydroquinone evoked a short-lived hyperpolarization which turned to a sustained depolarization of endothelial cells, a time course that substantially differed from that evoked by acetylcholine. Nicotine evoked a Na+ dependent depolarization of endothelial cells confirming functional activity ofnicotinic cholinoreceptors in rat aortic endothelial cells. The results suggest that stimulation of Na+ permeant nicotinic receptors by acetylcholine may contribute to sustained hyperpolarizatiom via stimulation of Na+ extrusion mechanisms. SN - 2522-9028 UR - https://www.unboundmedicine.com/medline/citation/19526844/[Modulation_of_electrical_responses_of_endothelial_cells_by_nicotinic_cholinoreceptors]_ DB - PRIME DP - Unbound Medicine ER -