Funny channels in the control of cardiac rhythm and mode of action of selective blockers

2006 ◽  
Vol 53 (5) ◽  
pp. 399-406 ◽  
Author(s):  
D DIFRANCESCO
1966 ◽  
Vol 17 (1) ◽  
pp. 447-462 ◽  
Author(s):  
T Killip ◽  
C T Lambrew

Cardiology ◽  
1976 ◽  
Vol 61 (1) ◽  
pp. 20-36 ◽  
Author(s):  
Walter C. Randall ◽  
David E. Euler ◽  
Kurt Jacobs ◽  
William Wehrmacher ◽  
Michael P. Kaye ◽  
...  

2021 ◽  
Vol 118 (9) ◽  
pp. e2018220118
Author(s):  
Charlotte D. Koopman ◽  
Jessica De Angelis ◽  
Swati P. Iyer ◽  
Arie O. Verkerk ◽  
Jason Da Silva ◽  
...  

The establishment of cardiac function in the developing embryo is essential to ensure blood flow and, therefore, growth and survival of the animal. The molecular mechanisms controlling normal cardiac rhythm remain to be fully elucidated. From a forward genetic screen, we identified a unique mutant, grime, that displayed a specific cardiac arrhythmia phenotype. We show that loss-of-function mutations in tmem161b are responsible for the phenotype, identifying Tmem161b as a regulator of cardiac rhythm in zebrafish. To examine the evolutionary conservation of this function, we generated knockout mice for Tmem161b. Tmem161b knockout mice are neonatal lethal and cardiomyocytes exhibit arrhythmic calcium oscillations. Mechanistically, we find that Tmem161b is expressed at the cell membrane of excitable cells and live imaging shows it is required for action potential repolarization in the developing heart. Electrophysiology on isolated cardiomyocytes demonstrates that Tmem161b is essential to inhibit Ca2+ and K+ currents in cardiomyocytes. Importantly, Tmem161b haploinsufficiency leads to cardiac rhythm phenotypes, implicating it as a candidate gene in heritable cardiac arrhythmia. Overall, these data describe Tmem161b as a highly conserved regulator of cardiac rhythm that functions to modulate ion channel activity in zebrafish and mice.


JAMA ◽  
1973 ◽  
Vol 226 (8) ◽  
pp. 881-886 ◽  
Author(s):  
P. M. Zoll

1973 ◽  
pp. 287-291
Author(s):  
Yu. A. Vlasov ◽  
A. T. Kolotov

2019 ◽  
Vol 514 (3) ◽  
pp. 759-764 ◽  
Author(s):  
Yue Cheng ◽  
Haitao Li ◽  
Hong Lei ◽  
Chan Jiang ◽  
Panpan Rao ◽  
...  

1955 ◽  
Vol 33 (3) ◽  
pp. 175-181 ◽  
Author(s):  
E. R. Bellemare ◽  
Jean Belcourt

The mode of action, on the heart of Periplaneta americana, of the cyanide analogue of DDT has been studied. Results of preliminary tests with rotenone confirm the findings of other investigators. Tests made with DDT produce a slight reduction of the cardiac rhythm. With the cyanide analogue of DDT, the rate of heart beat is also slightly reduced but, as with DDT, the pulsations continue long after paralysis has set in. The general intoxication symptoms produced by the injection of the cyanide analogue (in suspension) are likewise identical with those of DDT. The above results, together with results of experiments found in the literature, seem to be at variance with the hypothesis proposed by Krijgsman et al. that the heart mechanism of insects consists of a neurogenic pacemaker with adrenergic properties, controlled by a cholinergic accelerating nerve.


Sign in / Sign up

Export Citation Format

Share Document