Angiotensin II reduced junctional conductance by about 55% within 20 seconds, whereas enalapril increased junctional conductance by 106% within 2 minutes in isolated rat ventricular cell pairs.
Does modulation of the renin-angiotensin system alter junctional conductance in isolated adult rat ventricular cell pairs?
Inhibition of the renin-angiotensin system with enalapril increases electrical coupling between cardiac myocytes, providing a potential cellular mechanism for its antiarrhythmic and heart failure benefits.
The influence of the renin-angiotensin system on the control of cell communication was investigated in isolated ventricular cell pairs of adult rats. It was found that angiotensin II (1 microgram/ml) reduced the junctional conductance (gj) by about 55% within 20 s. This effect of angiotensin II was suppressed by DuP 753--an angiotensin receptor blocking agent. Enalapril (1 microgram/ml)--an angiotensin converting enzyme inhibitor--caused an increase in junctional conductance (106%) within 2 min. The effect of enalapril on gj was not related to activation of beta-adrenergic receptors or cAMP-dependent protein kinase. The effect of angiotensin II on gj was suppressed by staurosporine--a potent inhibitor of protein kinase C. This finding indicates that the peptide is changing gj through activation of protein kinase C. The increase in cell coupling caused by enalapril raises the possibility that the antiarrhythmic action of enalapril as well its effect in congestive heart failure are related to an increase in electrical synchronization of cardiac myocytes.
Mello et al. (Thu,) reported a other. Angiotensin II and Enalapril was evaluated on Junctional conductance (gj). Angiotensin II reduced junctional conductance by about 55% within 20 seconds, whereas enalapril increased junctional conductance by 106% within 2 minutes in isolated rat ventricular cell pairs.
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