Angiotensin II increases electrical coupling in mammalian ventricular myocardium.
Electrical measurements of current flow in ventricular myocardium immersed in silicone oil showed that angiotensin II increases the cell-to-cell spread of current within seconds. The increases in current spread and conduction velocity occur without any changes in resting membrane potential or maximum rate of rise of the action potential. The concentration range was 10 nM to 10 microM, with an ED50 of 100 nM for angiotensin exposures lasting about 10 seconds. The larges effects were an apparent decrease in resistance through the cellular pathway to 50% of control and a 40% increase in conduction velocity, which returned to control in about 15 minutes. Continuous or repeated exposure to angiotensin caused desensitization to appear. These effects were found with or without denervation by 6-hydroxydopamine and beta-adrenergic blockade by 1 microM propranolol in calf, pig, sheep, and rabbit ventricular myocardium. Therefore, angiotensin appears to increase electrical conduction rapidly and directly in cardiac muscle by decreasing resistance through the cellular pathway.
D000200:Action Potentials; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002417:Cattle; D004305:Dose-Response Relationship, Drug; D004560:Electricity; D005110:Extracellular Space; D006168:Guinea Pigs; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D011817:Rabbits; D012504:Saralasin / Q000494:pharmacology; D012756:Sheep; D013552:Swine; D013997:Time Factors; D016276:Ventricular Function
D000804:Angiotensin II; D012504:Saralasin; D009638:Norepinephrine