Sympathetic neuroeffector transmission in the rat anococcygeus muscle

1. When intracellular recordings were made from preparations of rat anococc ygeus muscle, transmural nerve stimulation evoked noradrenergic excitatory junction potentials (EJPs) made up of two distinct components. Both compone nts were abolished by either guanethidine or alpha-adrenoceptor antagonists , indicating that they resulted from the release of transmitter from sympat hetic nerves and the subsequent activation of alpha-adrenoceptors. 2. The first component was associated with a transient increase in the intr acellular concentration of calcium ions ([Ca2+](i)) and a contraction. Alth ough the second component was often associated with a long lasting increase in [Ca2+](i) it was not associated with a contraction unless the second co mponent initiated an action potential. 3. The increase in [Ca2+](i) associated with the first component resulted f rom 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 C a2+ channels (Ca-L channels). The depolarization associated with the initia l increase in [Ca2+](i) was abolished by reducing the external concentratio n of chloride ions ([Cl-](o)), suggesting that it involved the activation o f a Cl- conductance. 4. When the relationships between changes in [Ca2+](i), membrane depolariza tion 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 nifedipi ne produced a larger contraction and larger membrane depolarization than di d a similar increase in [Ca2+](i) recorded in either control or caffeine-co ntaining solutions. These observations indicate that Ca2+ contraction relea sed from stores more readily triggers contraction and membrane depolarizati on than does Ca2+ entry via Ca-L channels.