scholarly journals Effects of Development and Thyroid Hormone on K+Currents and K+Channel Gene Expression in Rat Ventricle

1997 ◽  
Vol 504 (2) ◽  
pp. 271-286 ◽  
Author(s):  
A. D. Wickenden ◽  
R. Kaprielian ◽  
T. G. Parker ◽  
O. T. Jones ◽  
P. H. Backx
2006 ◽  
Vol 128 (4) ◽  
pp. 405-411 ◽  
Author(s):  
Patricia Ortega-Sáenz ◽  
Alberto Pascual ◽  
Raquel Gómez-Díaz ◽  
José López-Barneo

Hemeoxygenase-2 (HO-2) is an antioxidant enzyme that can modulate recombinant maxi-K+ channels and has been proposed to be the acute O2 sensor in the carotid body (CB). We have tested the physiological contribution of this enzyme to O2 sensing using HO-2 null mice. HO-2 deficiency leads to a CB phenotype characterized by organ growth and alteration in the expression of stress-dependent genes, including the maxi-K+ channel α-subunit. However, sensitivity to hypoxia of CB is remarkably similar in HO-2 null animals and their control littermates. Moreover, the response to hypoxia in mouse and rat CB cells was maintained after blockade of maxi-K+ channels with iberiotoxin. Hypoxia responsiveness of the adrenal medulla (AM) (another acutely responding O2-sensitive organ) was also unaltered by HO-2 deficiency. Our data suggest that redox disregulation resulting from HO-2 deficiency affects maxi-K+ channel gene expression but it does not alter the intrinsic O2 sensitivity of CB or AM cells. Therefore, HO-2 is not a universally used acute O2 sensor.


1997 ◽  
Vol 500 (1) ◽  
pp. 65-73 ◽  
Author(s):  
Y Shimoni ◽  
C Fiset ◽  
R B Clark ◽  
J E Dixon ◽  
D McKinnon ◽  
...  

Circulation ◽  
2003 ◽  
Vol 107 (14) ◽  
pp. 1917-1922 ◽  
Author(s):  
Takeshi Yamashita ◽  
Akiko Sekiguchi ◽  
Yu-ki Iwasaki ◽  
Kouichi Sagara ◽  
Hiroyuki Iinuma ◽  
...  

1996 ◽  
Vol 35 (7) ◽  
pp. 1001-1006 ◽  
Author(s):  
E.S. LEVITAN ◽  
K.M. HERSHMAN ◽  
T.G. SHERMAN ◽  
K. TAKIMOTO

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