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1 School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia; Department of Cell and Molecular Physiological and Pharmacological Sciences, University of Pavia, Pavia, Italy
2 School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia
3 Department of Cell and Molecular Physiological and Pharmacological Sciences, University of Pavia, Pavia, Italy
* To whom correspondence should be addressed. E-mail: dadams{at}uq.edu.au.
The expression and function of nicotinic acetylcholine receptors (nAChRs) in rat coronary microvascular endothelial cells (CMECs) was examined using reverse
transcriptase-polymerase chain reaction (RT-PCR) and whole cell patch clamp recording methods. RT-PCR revealed expression of mRNA encoding for the subunits
2,3,4,5,7,
2 and 4 but not the 3 subunit. Focal application of ACh evoked an inward current in isolated CMECs voltage-clamped at negative membrane potentials. The current-voltage relationship of the ACh-induced current exhibited marked inward rectification and a reversal potential (Erev) close to 0 mV. The cholinergic agonists, nicotine, epibatidine and cytisine, activated membrane currents similar to that evoked by ACh. The nicotine-induced current was abolished by the neuronal nAChR antagonist, mecamylamine. The direction and magnitude of the shift in Erev of nicotine-induced current as a function of extracellular Na+ concentration indicates the nAChR channel is cation selective and follows that predicted by the Goldman-Hodgkin-Katz equation assuming PK/PNa of 1.11. In fura-2 loaded CMECs, application of ACh, but not of nicotine, elicited a transient increase in intracellular free Ca 2+ concentration. Taken together, these results demonstrate that neuronal nAChRs activation by cholinergic
agonists evokes an inward current in CMECs carried primarily by Na+ , which may contribute to the plasma nicotine-induced changes in microvascular permeability and reactivity induced by elevations in plasma nicotine.
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