scholarly journals Temperature Dependence of the Inward Rectifier K+ Channel Gating in Guinea-Pig Ventricular Cells.

1997 ◽  
Vol 47 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Tamotsu MITSUIYE ◽  
Yasuko SHINAGAWA ◽  
Akinori NOMA
Keyword(s):  
Guinea Pig ◽  
Temperature Dependence ◽  
Channel Gating ◽  
Inward Rectifier ◽  
K Channel ◽  
Ventricular Cells

Inhibitory effects of class I and IV antiarrhythmic drugs on the Na+-activated K+ channel current in guinea pig ventricular cells

1998 ◽  
Vol 358 (6) ◽  
pp. 641-648 ◽  
Author(s):  
Katsumi Mori ◽  
Satoru Kobayashi ◽  
Toshihiro Saito ◽  
Yoshiaki Masuda ◽  
H. Nakaya
Keyword(s):  
Guinea Pig ◽  
Antiarrhythmic Drugs ◽  
Class I ◽  
K Channel ◽  
Inhibitory Effects ◽  
Channel Current ◽  
Ventricular Cells

scholarly journals Secretory modulation of basolateral membrane inwardly rectified K+ channel in guinea pig distal colonic crypts

2002 ◽  
Vol 282 (4) ◽  
pp. C719-C735 ◽  
Author(s):  
Yingjun Li ◽  
Dan R. Halm
Keyword(s):  
Guinea Pig ◽  
Basolateral Membrane ◽  
Inward Rectifier ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Prostaglandin E ◽  
Open Probability ◽  
Pipette Solution ◽  
Colonic Crypts ◽  
Activity Mode

Cell-attached recordings revealed K+ channel activity in basolateral membranes of guinea pig distal colonic crypts. Inwardly rectified currents were apparent with a pipette solution containing 140 mM K+. Single-channel conductance (γ) was 9 pS at the resting membrane potential. Another inward rectifier with γ of 19 pS was observed occasionally. At a holding potential of −80 mV, γ was 21 and 41 pS, respectively. Identity as K+ channels was confirmed after patch excision by changing the bath ion composition. From reversal potentials, relative permeability of Na+ over K+ ( P Na/ P K) was 0.02 ± 0.02, with P Rb/ P K = 1.1 and P Cl/ P K < 0.03. Spontaneous open probability ( P o) of the 9-pS inward rectifier (gpKir) was voltage independent in cell-attached patches. Both a low ( P o = 0.09 ± 0.01) and a moderate ( P o = 0.41 ± 0.01) activity mode were observed. Excision moved gpKir to the medium activity mode; P o ofgpKir was independent of bath Ca2+activity and bath acidification. Addition of Cl− and K+ secretagogues altered P o ofgpKir. Forskolin or carbachol (10 μM) activated the small-conductance gpKir in quiescent patches and increased P o in low-activity patches. K+ secretagogues, either epinephrine (5 μM) or prostaglandin E2 (100 nM), decreased P o of gpKir in active patches. This gpKir may be involved in electrogenic secretion of Cl− and K+ across the colonic epithelium, which requires a large basolateral membrane K+ conductance during maximal Cl− secretion and, presumably, a lower K+ conductance during primary electrogenic K+ secretion.

scholarly journals Distribution of the Muscarinic K+ Channel Proteins Kir3.1 and Kir3.4 in the Ventricle, Atrium, and Sinoatrial Node of Heart

2001 ◽  
Vol 49 (10) ◽  
pp. 1221-1234 ◽  
Author(s):  
Halina Dobrzynski ◽  
David D.R. Marples ◽  
Hanny Musa ◽  
Tomoko T. Yamanushi ◽  
Zaineb Hendersonxyl ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Muscarinic Receptor ◽  
Western Blotting ◽  
K Channel ◽  
Outer Cell ◽  
Sa Node ◽  
Ventricular Cells ◽  
M2 Muscarinic Receptor ◽  
Vagal Nerves ◽  
Rat Ventricle

The functionally important effects on the heart of ACh released from vagal nerves are principally mediated by the muscarinic K+ channel. The aim of this study was to determine the abundance and cellular location of the muscarinic K+ channel subunits Kir3.1 and Kir3.4 in different regions of heart. Western blotting showed a very low abundance of Kir3.1 in rat ventricle, although Kir3.1 was undetectable in guinea pig and ferret ventricle. Although immunofluorescence on tissue sections showed no labeling of Kir3.1 in rat, guinea pig, and ferret ventricle and Kir3.4 in rat ventricle, immunofluorescence on single ventricular cells from rat showed labeling in t-tubules of both Kir3.1 and Kir3.4. Kir3.1 was abundant in the atrium of the three species, as shown by Western blotting and immunofluorescence, and Kir3.4 was abundant in the atrium of rat, as shown by immunofluorescence. Immunofluorescence showed Kir3.1 expression in SA node from the three species and Kir3.4 expression in the SA node from rat. The muscarinic K+ channel is activated by ACh via the m2 muscarinic receptor and, in atrium and SA node from ferret, Kir3.1 labeling was co-localized with m2 muscarinic receptor labeling throughout the outer cell membrane.

scholarly journals Inward rectifier K + current under physiological cytoplasmic conditions in guinea‐pig cardiac ventricular cells

2002 ◽  
Vol 540 (3) ◽  
pp. 831-841 ◽  
Author(s):  
Keiko Ishihara ◽  
Ding‐Hong Yan ◽  
Shintaro Yamamoto ◽  
Tsuguhisa Ehara
Keyword(s):  
Guinea Pig ◽  
Inward Rectifier ◽  
Ventricular Cells ◽  
K Current
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