Sympathetic neuroeffector transmission in the rat anococcygeus muscle

摘要

class="enumerated" style="list-style-type:decimal">When intracellular recordings were made from preparations of rat anococcygeus muscle, transmural nerve stimulation evoked noradrenergic excitatory junction potentials (EJPs) made up of two distinct components. Both components were abolished by either guanethidine or α-adrenoceptor antagonists, indicating that they resulted from the release of transmitter from sympathetic nerves and the subsequent activation of α-adrenoceptors.The first component was associated with a transient increase in the intracellular concentration of calcium ions ([Ca²⁺]i) and a contraction. Although the second component was often associated with a long lasting increase in [Ca²⁺]i it was not associated with a contraction unless the second component initiated an action potential.The increase in [Ca²⁺]i associated with the first component resulted from Ca²⁺ release from an intracellular store and from entry of Ca²⁺ through voltage-dependent Ca²⁺ channels. The increase in [Ca²⁺]i associated with the second component resulted only from the entry of Ca²⁺ through L-type Ca²⁺ channels (CaL channels). The depolarization associated with the initial increase in [Ca²⁺]i was abolished by reducing the external concentration of chloride ions ([Cl⁻]o), suggesting that it involved the activation of a Cl⁻ conductance.When the relationships between changes in [Ca²⁺]i, membrane depolarization and contraction produced by an increasing number of sympathetic nerve stimuli were determined in control, and caffeine- and nifedipine-containing solutions, it was found that an increase in [Ca²⁺]i recorded in nifedipine produced a larger contraction and larger membrane depolarization than did a similar increase in [Ca²⁺]i recorded in either control or caffeine-containing solutions. These observations indicate that Ca²⁺ released from stores more readily triggers contraction and membrane depolarization than does Ca²⁺ entry via CaL channels.