Influence of low extracellular pH upon the Ca inward current and isometric contractile force in mammalian ventricular myocardium

1976 ◽  
Vol 366 (1) ◽  
pp. 31-38 ◽  
Author(s):  
M. Kohlhardt ◽  
K. Haap ◽  
H. R. Figulla
Keyword(s):  
Ventricular Myocardium ◽  
Contractile Force ◽  
Extracellular Ph ◽  
Inward Current ◽  
Ca Inward Current

Effect of reduced Na gradient on electrical activity in isolated bovine and feline ventricular myocytes

1988 ◽  
Vol 66 (2) ◽  
pp. 222-232 ◽  
Author(s):  
Magda Horackova ◽  
Andrzej Beresewicz ◽  
Gerrit Isenberg
Keyword(s):  
Electrical Activity ◽  
Ventricular Myocytes ◽  
Ionic Current ◽  
Outward Current ◽  
Free Solution ◽  
Initial Part ◽  
Inward Current ◽  
Ca Inward Current ◽  
Sudden Decrease ◽  
K Currents

We have studied changes in electrical activity resulting from abrupt alterations of the Na gradient, using ventricular myocytes isolated from feline and bovine hearts. Attempting to investigate the ionic current possibly generated by Na–Ca exchange, we studied the effects of the changes in [Na]o in the presence of 20 mM CsCl to inhibit K currents. To facilitate the effect of Cs, we also used a K-free solution and a patch electrode filled with 150 mM cesium glutamate. The application of 20 mM Nao resulted in hyperpolarization and the action potential duration was reduced. Under voltage clamp, 20 or 45 mM Nao generated an outward current at all membrane potentials investigated. The initial part (100–200 ms) of this current was only partially inhibited by 5 mM NiCl2 which is known to fully block the Ca inward current. However, the outward current generated by the reduced [Na]o was fully inhibited by 20 mM MnCl2 (which presumably inhibits Na–Ca exchange). Our observations extend the work on multicellular cardiac preparations indicating that the outward current elicited by a sudden decrease in Na gradient could be generated by Na–Ca exchange. Although the characteristics of this outward current support certain concepts of the Na–Ca exchange in cardiac muscle, we cannot at present exclude a contribution of other membrane current(s).

Effect of sympathectomy on inotropic responsiveness to α-adrenoceptor stimulation in developing mouse myocardia

1995 ◽  
Vol 73 (9) ◽  
pp. 1285-1288 ◽  
Author(s):  
Hikaru Tanaka ◽  
Tomoyuki Matsuda ◽  
Mika Adachi ◽  
Koki Shigenobu
Keyword(s):  
Sympathetic Innervation ◽  
Ventricular Myocardium ◽  
Contractile Force ◽  
Inotropic Response ◽  
Maximum Decrease ◽  
6 Hydroxydopamine ◽  
Inotropic Responses

Effects of postnatal sympathectomy on inotropic responsiveness to α-adrenoceptor stimulation were examined in mouse myocardia to determine whether the developmental conversion of α-adrenoceptor-mediated inotropic responses from positive to negative is triggered by sympathetic innervation. Sympathectomy was performed chemically by consecutively administering 6-hydroxydopamine for 14 days after birth and confirmed by the absence of inotropic responses to tyramine. In newborn myocardia, phenylephrine, in the presence of propranolol, produced concentration-dependent positive inotropic responses. Three weeks after birth, phenylephrine, in the presence of propranolol, produced concentration-dependent negative inotropic responses, both in control and in sympathectomized myocardia; no difference was observed between the two groups of mice in the maximum decrease in contractile force produced by phenylephrine. The sensitivity (pD2 value) to phenylephrine was significantly higher in sympathectomized myocardia. In conclusion, sympathetic innervation of the mouse ventricular myocardium is not required for the developmental conversion of the α-adrenoceptor-mediated inotropic response from positive to negative.Key words: inotropism, α-adrenoceptor, supersensitivity, sympathetic innervation, development.

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