scholarly journals Beta-adrenergic and cholinergic modulation of inward rectifier K+ channel function and phosphorylation in guinea-pig ventricle.

1995 ◽  
Vol 486 (3) ◽  
pp. 661-678 ◽  
Author(s):  
S Koumi ◽  
J A Wasserstrom ◽  
R E Ten Eick
Keyword(s):  
Guinea Pig ◽  
Inward Rectifier ◽  
K Channel ◽  
Cholinergic Modulation ◽  
Beta Adrenergic ◽  
Channel Function

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.

Xenon Does Not Alter Cardiac Function or Major Cation Currents in Isolated Guinea Pig Hearts or Myocytes

2000 ◽  
Vol 92 (2) ◽  
pp. 516-516 ◽  
Author(s):  
David F. Stowe ◽  
Georg C. Rehmert ◽  
Wai-Meng Kwok ◽  
Henry U. Weigt ◽  
Michael Georgieff ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Guinea Pig ◽  
Salt Solution ◽  
Left Ventricular ◽  
Inward Rectifier ◽  
K Channel ◽  
Conduction Time ◽  
Patch Clamp Technique ◽  
Isolated Hearts ◽  
Major Cation

Background The noble gas xenon (Xe) has been used as an inhalational anesthetic agent in clinical trials with little or no physiologic side effects. Like nitrous oxide, Xe is believed to exert minimal unwanted cardiovascular effects, and like nitrous oxide, the vapor concentration to achieve 1 minimum alveolar concentration (MAC) for Xe in humans is high, i.e., 70-80%. In the current study, concentrations of up to 80% Xe were examined for possible myocardial effects in isolated, erythrocyte-perfused guinea pig hearts and for possible effects on altering major cation currents in isolated guinea pig cardiomyocytes. Methods Isolated guinea pigs hearts were perfused at 70 mm Hg via the Langendorff technique initially with a salt solution at 37 degrees C. Hearts were then perfused with fresh filtered (40-microm pore) and washed canine erythrocytes diluted in the salt solution equilibrated with 20% O2 in nitrogen (control), with 20% O2, 40% Xe, and 40% N2, (0.5 MAC), or with 20% O2 and 80% Xe (1 MAC), respectively. Hearts were perfused with 80% Xe for 15 min, and bradykinin was injected into the blood perfusate to test endothelium-dependent vasodilatory responses. Using the whole-cell patch-clamp technique, 80% Xe was tested for effects on the cardiac ion currents, the Na+, the L-type Ca2+, and the inward-rectifier K+ channel, in guinea pig myocytes suffused with a salt solution equilibrated with the same combinations of Xe, oxygen, and nitrogen as above. Results In isolated hearts, heart rate, atrioventricular conduction time, left ventricular pressure, coronary flow, oxygen extraction, oxygen consumption, cardiac efficiency, and flow responses to bradykinin were not significantly (repeated measures analysis of variance, P&gt;0.05) altered by 40% or 80% Xe compared with controls. In isolated cardiomyocytes, the amplitudes of the Na+, the L-type Ca2+, and the inward-rectifier K+ channel over a range of voltages also were not altered by 80% Xe compared with controls. Conclusions Unlike hydrocarbon-based gaseous anesthetics, Xe does not significantly alter any measured electrical, mechanical, or metabolic factors, or the nitric oxide-dependent flow response in isolated hearts, at least partly because Xe does not alter the major cation currents as shown here for cardiac myocytes. The authors' results indicate that Xe, at approximately 1 MAC for humans, has no physiologically important effects on the guinea pig heart.

scholarly journals Estrogen Regulation of Genes Important for K+ Channel Signaling in the Arcuate Nucleus

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4937-4951 ◽  
Author(s):  
Troy A. Roepke ◽  
Anna Malyala ◽  
Martha A. Bosch ◽  
Martin J. Kelly ◽  
Oline K. Rønnekleiv
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Arcuate Nucleus ◽  
Neuronal Excitability ◽  
Estradiol Benzoate ◽  
K Channel ◽  
Pcr Analysis ◽  
Estrogen Regulation ◽  
K Channels ◽  
Channel Function

Estrogen affects the electrophysiological properties of a number of hypothalamic neurons by modulating K+ channels via rapid membrane actions and/or changes in gene expression. The interaction between these pathways (membrane vs. transcription) ultimately determines the effects of estrogen on hypothalamic functions. Using suppression subtractive hybridization, we produced a cDNA library of estrogen-regulated, brain-specific guinea pig genes, which included subunits from three prominent K+ channels (KCNQ5, Kir2.4, Kv4.1, and Kvβ1) and signaling molecules that impact channel function including phosphatidylinositol 3-kinase (PI3K), protein kinase Cε (PKCε), cAMP-dependent protein kinase (PKA), A-kinase anchor protein (AKAP), phospholipase C (PLC), and calmodulin. Based on these findings, we dissected the arcuate nucleus from ovariectomized guinea pigs treated with estradiol benzoate (EB) or vehicle and analyzed mRNA expression using quantitative real-time PCR. We found that EB significantly increased the expression of KCNQ5 and Kv4.1 and decreased expression of KCNQ3 and AKAP in the rostral arcuate. In the caudal arcuate, EB increased KCNQ5, Kir2.4, Kv4.1, calmodulin, PKCε, PLCβ4, and PI3Kp55γ expression and decreased Kvβ1. The effects of estrogen could be mediated by estrogen receptor-α, which we found to be highly expressed in the guinea pig arcuate nucleus and, in particular, proopiomelanocortin neurons. In addition, single-cell RT-PCR analysis revealed that about 50% of proopiomelanocortin and neuropeptide Y neurons expressed KCNQ5, about 40% expressed Kir2.4, and about 60% expressed Kv4.1. Therefore, it is evident that the diverse effects of estrogen on arcuate neurons are mediated in part by regulation of K+ channel expression, which has the potential to affect profoundly neuronal excitability and homeostatic functions, especially when coupled with the rapid effects of estrogen on K+ channel function.

scholarly journals Pathologically Entangled: Brain trauma-evoked ROS imbalance disrupts Kir channel function in distant peripheral vessels

Function ◽  
2021 ◽  
Author(s):  
Nick Weir ◽  
Thomas A Longden
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Potassium Channels ◽  
Vascular Function ◽  
Inward Rectifier ◽  
Brain Trauma ◽  
Channel Function ◽  
Inward Rectifier Potassium Channels ◽  
Kir Channel

Abstract A Perspective on "Traumatic Brain Injury Impairs Systemic Vascular Function Through Disruption of Inward-Rectifier Potassium Channels"

Sign in / Sign up

Export Citation Format

Share Document