Show simple item record

dc.contributor.advisorWang, Ruien_US
dc.creatorHanna, Salma Tomaen_US
dc.date.accessioned2004-12-23T14:29:14Zen_US
dc.date.accessioned2013-01-04T05:12:45Z
dc.date.available2005-01-04T08:00:00Zen_US
dc.date.available2013-01-04T05:12:45Z
dc.date.created2004-12en_US
dc.date.issued2004-12-09en_US
dc.date.submittedDecember 2004en_US
dc.identifier.urihttp://hdl.handle.net/10388/etd-12232004-142914en_US
dc.description.abstractATP-sensitive K+ channels (KATP) channels were first described in the cardiac muscles. KATP channels are a complex of regulatory sulphonylurea receptor subunits and pore-forming inward rectifier subunits such as Kir6.1. Nicotine, an exogenous substance, adversely affects cardiovascular function in humans. Acetylcholine (ACh) is well known as a key neurotransmitter of the parasympathetic nervous system. ACh effects are usually related to binding to muscarinic receptors and stimulating second messengers that relay and direct the extracellular signals to different intracellular destinations, resulting in modulated cellular activity. We hypothesize that nicotine and ACh may modulate Kir6.1 channels via different mechanisms. Using the whole cell patch-clamp technique, the interactions of nicotine and ACh with Kir6.1 subunit permanently expressed in Human Embryonic Kidney (HEK-293) cells as well as the underlying mechanisms were studied. Non-transfected HEK-293 cells possess an endogenous K+ current with current density of –3.2 ± 1.4 pA/pF at –150 mV (n = 9). Stable expression of Kir6.1 subunits cloned from rat mesenteric artery in HEK-293 cells yielded a detectable inward rectifier KATP current (-23.9 ± 1.6 pA/pF at –150 mV, n = 6). In the presence of 0.3 mM ATP in the pipette solution, nicotine at 30 and 100 µM increased the expressed Kir6.1 currents by 42 ± 11.8 and 26.2 ± 14.6%, respectively (n = 4-6, pen_US
dc.language.isoen_USen_US
dc.subjectHEK-293 cellsen_US
dc.subjectKir6.1 channelsen_US
dc.subjectnicotineen_US
dc.subjectAChen_US
dc.subjectpatch-clampen_US
dc.titleModulation of Kir6.1 channels heterologously expressed in HEK-293 cells by nicotine and acetylocholineen_US
thesis.degree.departmentPhysiologyen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.grantorUniversity of Saskatchewanen_US
thesis.degree.levelDoctoralen_US
thesis.degree.nameDoctor of Philosophy (Ph.D.)en_US
dc.type.materialtexten_US
dc.type.genreThesisen_US
dc.contributor.committeeMemberSulakhe, Prakashen_US
dc.contributor.committeeMemberGopalakrishnan, Venkaten_US
dc.contributor.committeeMemberFisher, Thomas E.en_US
dc.contributor.committeeMemberDesautels, Michelen_US
dc.contributor.committeeMemberAnand-Srivastava, M.en_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record