Serotonin stimulates a Ca2+ permeant nonspecific cation channel in hepatic endothelial cells.
The contraction of hepatic endothelial cell fenestrae after exposure to serotonin is associated with an increase in intracellular Ca2+ which is derived from extracellular Ca2+, is inhibited by pertussis toxin and is not associated with activation of phosphoinositol turnover or cAMP. Using cell-attached and excised patches in primary cultures of rat hepatic endothelial cells, we identified a serotonin-activated channel with conductance of 26.4+/-2.3 pS. The channel was also permeant to Na+, K+ and Ca++ but not to anions. In cell-attached patch recordings, addition of serotonin to the bath significantly increased channel activity with Ca2+ or Na+ as the charge-carrying ions. This channel provides a mechanism whereby serotonin can raise the cytosolic Ca2+ concentration in hepatic endothelial cells.
Brauneis
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Department of Physiology, Tufts University School of Medicine, Boston, MA 02111.
Gatmaitan
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Arias
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D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002412:Cations; D004553:Electric Conductivity; D004730:Endothelium, Vascular / Q000502:physiology*; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D037342:Pertussis Toxin; D011169:Portal Vein / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012701:Serotonin / Q000494:pharmacology*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D002412:Cations; D007473:Ion Channels; D010566:Virulence Factors, Bordetella; D012701:Serotonin; D037342:Pertussis Toxin; D002118:Calcium