Effects of endogenous and exogenous noradrenaline on the smooth muscle of guinea‐pig mesenteric vein

Abstract

SUMMARYMembrane responses of smooth muscles of the guinea-pig mesenteric vein to noradrenaline released from perivascular nerves or applied exogenously were investigated.1. Exogenously applied noradrenaline depolarized the muscle membrane at concentrations ofover 10-6 M, and generated slow waves or action potentials. Application of phentolamine but not propranolol suppressed the depolarization.2. The depolarization induced by exogenous noradrenaline was associated with increase in the membrane resistance. The level of the membrane depolarization was3. Repetitive but not single stimulation ofthe nerves produced slow depolarization of the membrane. The amplitude of the slow depolarization was dependent on the frequency or number of stimuli within a certain range, but beyond this an increased frequency or an increased number of stimulating pulses produced no further increase in amplitude of the slow depolarization.4. The slow depolarization induced by nerve stimulation was analysed in relation to the diffusion of transmitter. The rising phase of the slow depolarization fitted well with the theoretically predicted one, while the falling phase did not.5. Stimulation of nerves with a high frequency and a large number of pulses produced slow waves or action potentials superimposed on the slow depolarization of the membrane.6. Membrane responses induced by nerve stimulation did not appear in the presence of TTX or phentolamine. TEA enhanced the nerve-induced responses.7. Myogenic electrical activities insensitive to TTX and phentolamine were recorded from the mesenteric vein. These activities were induced by nerve stimulation only in the fresh tissues, were usually irregular in shape, size and frequency, and lasted for 5-20 min.8. It was concluded that alpha-adrenergic receptors on the muscle membrane reacted in a similar manner to noradrenaline either released from the nerves or applied exogenously. Noradrenaline depolarized the muscle membrane by the decrease in potassium conductance of the membrane.

Ca2+ channel activation and membrane depolarization mediated by Cl− channels in response to noradrenaline in vascular myocytes

“…Recent results obtained from single venous smooth muscle cells indicated that the NA-induced depolarization is mainly mediated by an increase in chloride conductance (Byrne & Large, 1988a;Van Helden, 1988;Pacaud et al, 1989). However, an increase in a non-specific cation channel (Byrne & Large, 1988b) and a decrease in potassium conductance (Suzuki, 1981) could also be involved.…”

Noradrenaline activates a calcium‐activated chloride conductance and increases the voltage‐dependent calcium current in cultured single cells of rat portal vein

“…Two other ionic mechanisms 1 Author for correspondence. involved in noradrenaline action have been described: an increase in a non specific cation channel (Byrne & Large, 1988b) and a decrease in potassium conductance (Suzuki, 1981; Van Helden, 1988). Furthermore, noradrenaline increases the cytoplasmic calcium concentration as measured with fluorescent indicators (Satoh et al, 1987).…”

Purinergic receptors in the splanchnic circulation

“…For instance, in the guinea-pig mesenteric artery, sympathetic nerve stimulation gives rise to rapidly rising excitatory junction potentials of brief duration that are resistant to prazosin, but are blocked by α,β-meATP [67,82]. In contrast, in the guinea-pig mesenteric vein a slow depolarization [166] that is resistant to purinoceptor desensitization with α,β-meATP [65,67] is observed rather than fast EJPs. This has led to the conclusion that ATP is not involved in these junctional events [65,67] and, hence, is not released during nerve stimulation.…”