Changes in α₁‐adrenoceptor coupling to Ca²⁺ channels during development in rat heart

Abstract

It has been reported in the literature that a,-adrenoceptor activation in adult rat heart does not cause an increase in Ca*' current but involves a decrease in I,. This may explain in part the positive inotropic effect of a,-adrenoceptor activation. In this study, the effect of phenylephrine, an a-adrenergic agonist, on L-type Ca*' channel current was compared in young and neonatal rat myocytes. In the presence of propranolol, phenylephrine increased the Ca*' current (reversed by prazosin) in neonatal but not in young rat myocytes suggesting that the coupling of the cc,-adrenoceptor to Ca'+ channels may switch during development.

Norepinephrine-induced calcium signaling and expression of adrenoceptors in avian tendon cells

“…Muscle from younger (5-8 wk old) chickens did not respond to NE with a Ca 2ϩ transient. In addition, rat myocyte adrenoceptor coupling to L-type Ca 2ϩ channels changes during development (37). Explant tissue may present fewer adrenoceptor-expressing cells.…”

Pharmacological support for children with myocardial dysfunction

“…The mature inhibitory response is usually mediated by the α 1B ‐adrenoreceptor, but only occurs following postnatal local release of neuropeptide Y from sympathetic nerve endings. The stimulation of α 1 ‐adrenoreceptors in young and adult rats results in the reduction of the transient outward K + current, but does not affect calcium currents (47). However, in neonatal rats, α 1 ‐adrenoreceptor stimulation causes an increased L ‐type calcium current (48) mediated by protein kinase C phosphorylation of calcium channel proteins (49).…”