Cardiac alphai-adrenergic receptor stimulation: Positive inotropism and arrhythmias (part 12). CONCLUSIONS
The situation is markedly different in tissues in which the sodium load is not perfectly controlled, such as ischemia or reperfusion. In these physiopathological conditions, alpha1-adrenergic receptor-mediated activation of the Na-H antiport and Na-HCO3 symport further increases sodium load and consequently leads to calcium overload. Such a condition is known to trigger calcium release from sarcoplasmic reticulum and would cause membrane depolarization by both opening of nonspecific cationic conductance and activation of the reverse mode of the Na/Ca exchanger. Major work is still required to understand the roles and intracellular pathways of alpha1-adrenoreceptor subtypes. Furthermore, our understanding if alpha1-adrenergic stimulation in pathological conditions is limited. Some studies report a further enhancement of phosphatidylinositol turnover in hypoxia, in diabetic rats (buy diabetes drug) or in malignant hyperthermia-susceptible swine. Moreover, cardiac cells are simultaneously submitted to several neurohormonal stimulations, which can add to or counteract each other and which may vary according to pathophysiological status.Thus, alpha1- and beta-adrenergic stimulations are not additive, although both independently increase inotropism; also, alpha1-adrenergic stimulation appears to be more active in pathological conditions, while the alpha1-adrenergic pathway is often inhibited due to a reduction in beta-adrenergic receptor and an increase in Gi-protein. The clinical interest in these studies is obvious due to the reported increase of alpha1-adrenergic receptors in patients with chronic heart failure. Cheapest treatment – buy levaquin 500 mg only here to always have a wide choice of options.
Tags: Contractility, Electrical activity, Neurostimulation, Phosphorylation