The antiarrhythmic effects of exogenous adenosine and Valsalva on this form of VT may be due to receptor-mediated inhibition of adenylate cyclase or to noncardiac receptor-mediated effects, i.e., exogenous << adenosine >> may modulate VT through alterations in autonomic tone by activation of arterial [[ chemoreceptors ]], and Valsalva has been shown to decrease venous return, resulting in a reduction in cardiac dimensions and myocardial stretch.