| pubmed-article:7687726 | pubmed:abstractText | During acute myocardial ischemia, a combination of increased extracellular K+ concentration and sympathetic nerve activation exists. Using a perfused innervated rat heart model, we studied the influence of increased extracellular K+ concentrations on neural norepinephrine (NE) release, adrenergic stimulation-induced K+ uptake by the heart, and the occurrence of ventricular arrhythmias. Hearts were globally perfused with control (4 mM) or increased concentrations of K+ (7-16 mM). Sympathetic nerve stimulation-induced NE release was analyzed by radioenzymatic assay. Cardiac K+ uptake was assessed by the reduction in K+ concentration in the coronary venous effluent induced by nerve stimulation. Neural NE release was not influenced by increasing K+ from 4 mM to 7, 10, and 13 mM, but was suppressed by 16 mM K+ (-40 +/- 10%). Nerve stimulation induced cardiac uptake of K+, which was blocked by the beta-adrenoceptor antagonist timolol. This stimulated K+ uptake was substantially enhanced by increasing extracellular K+ and was also dependent on the intensity of sympathetic stimulation at 10 mM K+. Sympathetic nerve stimulation, together with a high K+ of 10 mM, was potent in initiating ventricular tachyarrhythmias, and quantitative NE release was well correlated with the frequency of ventricular arrhythmias. Our results demonstrate the synergistic effects of increased extracellular K+ and sympathetic activation, which may be involved in the genesis of ventricular arrhythmias. | lld:pubmed |
