Cardiac alphai-adrenergic receptor stimulation: Positive inotropism and arrhythmias (part 11). CONCLUSIONS
It appears that alpha1-adrenergic-induced positive inotropism results from the interplay of three major mechanisms: prolongation of action potential due to potassium current inhibition; alkalinization related to both Na-H antiport and Na-HCO3 symport activation; and calcium sensitization of the contractile proteins following their phosphorylation. The relative importance of these three mechanisms is unknown; it should depend on species and most probably on the physiological state of the cells. Alpha1-adrenergic stimulation also induces activation of the phosphatidylinositol pathway associated with IP3 increase. Actually no significant role is known for this IP3 increase in cardiac tissues; IP3 does not seem to induce calcium release from the sarcoplasmic reticulum, nor does it alter contractile protein sensitivity to calcium ions, and no IP3 effect has been observed on cardiac membrane currents.It is noteworthy that purinergic stimulation, which also activates the phosphatidylinositol pathway, has no significant effect on myofilament sensitivity to calcium ions while it increases calcium current. Furthermore, in control conditions, alpha1-adrenergic stimulation has a beneficial inotropic effect without significant chronotropic action. Learn how to save money – buy alesse just now to enjoy your shopping and your treatment.
Tags: Contractility, Electrical activity, Neurostimulation, Phosphorylation