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Titolo:
Sympathetic neuroeffector transmission in the rat anococcygeus muscle
Autore:
Bramich, NJ; Hirst, GDS;
Indirizzi:
Univ Melbourne, Dept Zool, Parkville, Vic 3052, Australia Univ Melbourne Parkville Vic Australia 3052 arkville, Vic 3052, Australia
Titolo Testata:
JOURNAL OF PHYSIOLOGY-LONDON
fascicolo: 1, volume: 516, anno: 1999,
pagine: 101 - 115
SICI:
0022-3751(19990401)516:1<101:SNTITR>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG ILEUM; SMOOTH-MUSCLE; NEUROMUSCULAR-TRANSMISSION; SARCOPLASMIC-RETICULUM; LONGITUDINAL MUSCLE; CALCIUM CHANNELS; PORTAL-VEIN; CELLS; NORADRENALINE; CHLORIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Hirst, GDS Univ Melbourne, Dept Zool, Parkville, Vic 3052, Australia Univ Melbourne Parkville Vic Australia 3052 ic 3052, Australia
Citazione:
N.J. Bramich e G.D.S. Hirst, "Sympathetic neuroeffector transmission in the rat anococcygeus muscle", J PHYSL LON, 516(1), 1999, pp. 101-115

Abstract

1. When intracellular recordings were made from preparations of rat anococcygeus muscle, transmural nerve stimulation evoked noradrenergic excitatoryjunction potentials (EJPs) made up of two distinct components. Both components were abolished by either guanethidine or alpha-adrenoceptor antagonists, indicating that they resulted from the release of transmitter from sympathetic nerves and the subsequent activation of alpha-adrenoceptors.2. 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.3. 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 (Ca-L 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.4. When the relationships between changes in [Ca2+](i), membrane depolarization and contraction produced by an increasing number of sympathetic nervestimuli 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+ contraction released from stores more readily triggers contraction and membrane depolarization than does Ca2+ entry via Ca-L channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/08/20 alle ore 14:20:28