{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:49:11Z","timestamp":1790617751416,"version":"4.1.0"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1993,8,1]],"date-time":"1993-08-01T00:00:00Z","timestamp":744163200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1993,8]]},"abstract":"<jats:p>1. The modulation of whole\u2010cell K+ and Ca2+ currents by stimulation of histamine H1\u2010receptors in freshly isolated single smooth muscle cells from the rabbit coronary artery was characterized using the patch\u2010clamp technique at 35 degrees C. Single\u2010channel K+ currents were also analysed using the cell\u2010attached patch configuration. 2. The histamine H1\u2010receptor agonist, 2\u2010(2\u2010aminoethyl)pyridine (AEP) (0.1 mM), increased the amplitude of voltage\u2010activated inward Ba2+ currents, recorded using the perforated\u2010patch recording technique, which could be completely blocked by the dihydropyridine antagonist, nicardipine (1 microM). 3. Whole\u2010cell outward K+ currents in rabbit coronary artery cells could be classified into at least two components: (a) a slowly inactivating, 4\u2010aminopyridine (4\u2010AP)\u2010sensitive low\u2010noise current, and (b) a non\u2010inactivating, tetraethylammonium (TEA)\u2010sensitive high\u2010noise current. 4. AEP (0.1 mM) caused changes in whole\u2010cell outward K+ currents which depended upon membrane voltage. Specifically: (a) AEP enhanced the amplitude of outward currents at voltages between \u201030 and 0 mV, and (b) AEP decreased the outward currents at more positive potentials. 5. The removal of extracellular Ca2+ caused little inhibition of the effects of AEP on K+ currents, whereas the depletion of intracellular Ca2+ stores by pretreatment with ryanodine and caffeine prevented the effects of AEP on K+ channels. Moreover, acute exposure to ryanodine (10 microM) or thapsigargin (1 microM), a Ca(2+)\u2010ATPase inhibitor, caused voltage\u2010dependent changes in the outward currents similar to those observed with AEP. These results suggest that the voltage\u2010dependent effects of AEP on K+ currents are mainly mediated by release of Ca2+ from intracellular stores. 6. The dual stimulatory and inhibitory effect of AEP on whole\u2010cell K+ currents was shown to be due to a differential effect on two distinct types of K+ channels. The stimulatory effect observed over the voltage range \u201030 to 0 mV was prevented by pretreatment of cells with low concentrations of TEA (1 mM), whereas the inhibitory effect observed at positive potentials was prevented by pretreatment of cells with 4\u2010AP (3 mM). 7. Single\u2010channel recordings revealed two types of unitary K+ currents with conductances of 225 and 70 pS in the cell\u2010attached configuration with symmetrical K+ solutions (150 mM K+ in pipette\u2010150 mM K+ in bath). Bath application of AEP (0.1 mM) caused a marked increase in the open probability of the large conductance channels.(ABSTRACT TRUNCATED AT 400 WORDS)<\/jats:p>","DOI":"10.1113\/jphysiol.1993.sp019777","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T14:09:30Z","timestamp":1418825370000},"page":"379-400","source":"Crossref","is-referenced-by-count":53,"title":["Modulation of K+ and Ca2+ channels by histamine H1\u2010receptor stimulation in rabbit coronary artery cells."],"prefix":"10.1113","volume":"468","author":[{"given":"T","family":"Ishikawa","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J R","family":"Hume","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K D","family":"Keef","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1993,8]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1993.sp019777","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1993.sp019777","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,25]],"date-time":"2023-10-25T01:51:20Z","timestamp":1698198680000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1993.sp019777"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1993,8]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1993,8]]}},"alternative-id":["10.1113\/jphysiol.1993.sp019777"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1993.sp019777","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1993,8]]}}}