{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T09:31:43Z","timestamp":1772703103704,"version":"3.50.1"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,8,10]],"date-time":"2005-08-10T00:00:00Z","timestamp":1123632000000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:p>Voltage\u2010gated potassium (Kv) currents of human pancreatic islet cells were studied by whole\u2010cell patch clamp recording. On average, 75% of the cells tested were identified as \u03b2\u2010cells by single cell, post\u2010recording RT\u2010PCR for insulin mRNA. In most cells, the dominant Kv current was a delayed rectifier. The delayed rectifier activated at potentials above \u221220 mV and had a <jats:italic>V<\/jats:italic><jats:sub>\u00bd<\/jats:sub> for activation of \u22125.3 mV. Onset of inactivation was slow for a major component (\u03c4= 3.2 s at +20 mV) observed in all cells; a smaller component (\u03c4= 0.30 s) with an amplitude of \u223c25% was seen in some cells. Recovery from inactivation had a \u03c4 of 2.5 s at \u221280 mV and steady\u2010state inactivation had a <jats:italic>V<\/jats:italic><jats:sub>\u00bd<\/jats:sub> of \u221239 mV. In 12% of cells (21\/182) a low\u2010threshold, transient Kv current (A\u2010current) was present. The A\u2010current activated at membrane potentials above \u221240 mV, inactivated with a time constant of 18.5 ms at \u221220 mV, and had a <jats:italic>V<\/jats:italic><jats:sub>\u00bd<\/jats:sub> for steady\u2010state inactivation of \u221252 mV. TEA inhibited total Kv current with an <jats:styled-content>IC<jats:sub>50<\/jats:sub>= 0.54 m<jats:sc>m<\/jats:sc><\/jats:styled-content> and PAC, a disubstituted cyclohexyl Kv channel inhibitor, inhibited with an <jats:styled-content>IC<jats:sub>50<\/jats:sub>= 0.57 \u03bc<jats:sc>m<\/jats:sc><\/jats:styled-content>. The total Kv current was insensitive to margatoxin (100 n<jats:sc>m<\/jats:sc>), agitoxin\u20102 (50 n<jats:sc>m<\/jats:sc>), kaliotoxin (50 n<jats:sc>m<\/jats:sc>) and ShK (50 n<jats:sc>m<\/jats:sc>). Hanatoxin (100 n<jats:sc>m<\/jats:sc>) inhibited total Kv current by 65% at +20 mV. Taken together, these data provide evidence of at least two distinct types of Kv channels in human pancreatic \u03b2\u2010cells and suggest that more than one type of Kv channel may be involved in the regulation of glucose\u2010dependent insulin secretion.<\/jats:p>","DOI":"10.1113\/jphysiol.2005.089375","type":"journal-article","created":{"date-parts":[[2005,6,3]],"date-time":"2005-06-03T00:13:56Z","timestamp":1117757636000},"page":"159-175","source":"Crossref","is-referenced-by-count":40,"title":["Biophysical and pharmacological properties of the voltage\u2010gated potassium current of human pancreatic 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