Adrenergic Regulation of Vascular Smooth Muscle

Bevan, John A.; Bevan, Rosemary D.; Duckles, Sue Piper

doi:10.1002/cphy.cp020218

Cited by 109 publications

(70 citation statements)

References 280 publications

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“…Most blood vessels are innervated by noradrenergic nerves (Bevan et al, 1980), and the cellular responses of vascular smooth muscles to perivascular nerve stimulation are either an excitatory junction potential (e.j.p.) or a slow depolarization, or both.…”

Section: Introductionmentioning

confidence: 99%

Adrenergic transmission in the dog mesenteric vein and its modulation by α‐adrenoceptor antagonists

Suzuki

1984

British J Pharmacology

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Adrenergic transmission was investigated in the dog mesenteric vein by recording electrical responses of single smooth muscle cells to perivascular nerve stimulation. Perivascular nerve stimulation generated an excitatory junction potential (e.j.p.) and a slow depolarization of the membrane. The amplitude of the e.j.p. was increased by increasing the stimulus intensity, and at high intensity, a spike potential was generated. Repetitive stimulation of the nerves showed facilitation of e.j.ps and enhanced the amplitude of slow depolarization. A linear relationship was observed between the amplitude of the e.j.p. and of slow depolarization. The slow depolarization was inhibited by application of yohimbine or phentolamine, but not by prazosin. The amplitude of e.j.p. was increased by prazosin and was decreased by yohimbine. Both e.j.p. and slow depolarization were inhibited by guanethidine or tetrodotoxin. Exogenously applied noradrenaline depolarized the muscle membrane and, in high concentrations (> 10−7 m), generated slow waves. These effects of noradrenaline were blocked by yohimbine. High concentrations of prazosin (> 10−6m) showed weak inhibitory effects on the noradrenaline actions. The amplitude of e.j.p. was decreased by exogenously applied noradrenaline in a dose‐dependent manner. The inhibitory effect of noradrenaline on the e.j.p. was suppressed by yohimbine, but not by prazosin or phentolamine. Phentolamine, but not prazosin, enhanced the facilitation process of e.j.ps. This effect was not suppressed by exogenously applied noradrenaline. Application of neostigmine but not of atropine, reduced the e.j.p. amplitude without affecting the slow depolarization. It was concluded that, in the dog mesenteric vein, perivascular nerve stimulation produced three types of electrical responses of the smooth muscle membrane, i.e., e.j.p., slow depolarization and spike potential. The slow depolarization was generated by activation of α2‐adrenoceptors. Exogenously applied noradrenaline reduced the e.j.p. amplitude through activation of prejunctional α2‐adrenoceptors, but the reduction may not involve α‐autoinhibitory mechanisms.

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Section: Introductionmentioning

confidence: 99%

Adrenergic transmission in the dog mesenteric vein and its modulation by α‐adrenoceptor antagonists

Suzuki

1984

British J Pharmacology

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“…For comparison with peripheral arteries, parallel studies were done on the rabbit ear artery, a well innervated vessel (Bevan, Bevan & Duckles, 1980 (Su, Duckles & Florence, 1977 (Su & Bevan, 1970 Transmural electrical stimulation was delivered across the electrodes via a stimulator (Grass S-88) and coupling device to provide a low source impedance (Duckles & Silverman, 1980). Stimulation parameters (0.3 ms, 6 V across the electrodes) were selected to achieve supramaximal nerve stimulation.…”

Section: Introductionmentioning

confidence: 99%

Functional Activity of the Noradrenergic Innervation of Large Cerebral Arteries

Duckles

1980

British J Pharmacology

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The role of the sympathetic innervation of cerebral arteries remains controversial. Therefore, the functional activity of the adrenergic innervation of the rabbit basilar artery was characterized and compared to that of a peripheral artery, the ear artery. Both the ear artery and basilar artery have similar endogenous noradrenaline (NA) contents but accumulation of [3H]‐NA was considerably greater in the basilar artery. Studies of tritium efflux after loading with [3H]‐NA demonstrated a considerable non‐neuronal component since neither guanethidine nor tetrodotoxin completely blocked tritium efflux during nerve stimulation. Pretreatment with blockers of uptake2 did not eliminate this problem. Comparison of methods for estimating the functional activity of adrenergic nerves showed that, for the vessels studied, NA content and [3H]‐NA accumulation gave markedly different answers. Fractional release of [3H]‐NA did not correspond to fractional release of endogenous NA. Adrenergic nerves innervating cerebral arteries are shown to have a high activity relative to a peripheral artery. While cerebrovascular sympathetic innervation may not play an important role in normal circumstances, its influence may be seen in pathological conditions.

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“…Involvement of sympathetic nerve in regulation of the cerebral vascular tone has been receiving increased attention (PURVES, 1978), because this nerve regulates smooth muscle tone in the majority of peripheral vasculatures (BEVAN et al, 1980). However, evidence shows that in cerebral vascular smooth muscles, sufficient receptors for the sympathetic neurotransmitter substances are lacking (LAHER and BEVAN, 1985), or that stimulation of sympathetic nerves fails to modulate the cerebral blood flow (SHIBATA, 1977).…”

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Non-neural electrical responses of smooth muscle cells of the rabbit basilar artery to electrical field stimulation.

Nagao

Suzuki

1987

Jpn.J.Physiol

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In smooth muscle cells of the rabbit basilar artery, field stimulation evoked a depolarizing response which consisted of a fast (1-3 s duration) and a following slow (1-4min duration) component. The amplitude of these responses increased in an intensity-dependent manner and, when exceeding 10-15 mV, a spike potential was generated. During generation of the slow depolarization, ionic conductances of the membrane were increased. When outward current pulses with long duration (2-3 s) were applied to the smooth muscle using the partition stimulating method, electrotonic potentials and spike potentials were generated. The cessation of the current pulse caused repolarization of the membrane with time constant of 250-350 ms. The depolarizing responses were resistant to tetrodotoxin, sympathetic transmission blocking agents (guanethidine, bretylium, or 6-hydroxydopamine treatment), receptor antagonists for 5-hydroxytryptamine (methysergide), dopamine (haloperidol), ACh (atropine), noradrenaline (phentolamine), ATP (a,f-mATP) or histamine (mepyramine), blockade of synthesis of prostaglandins or thromboxane A2 (indomethacin) or high Mgt + j low Cat + solution. Smooth muscle cell membrane of the basilar artery was depolarized by 5-hydroxytryptamine (above 0.1 µM) or histamine (above 10 µM) but not by ACh (up to 100 µM) or noradrenaline (up to 10 µM). The depolarization induced by 5-hydroxytryptamine or histamine was antagonized by methysergide or mepyramine, respectively. Denervation of the vessel by storing in a cold condition (4°C) decreased but did not abolish the depolarizing response. The decrease in amplitude of the depolarizing response during cold storage was attributed to associated depolarization of the smooth muscle membrane. Internal perfusion of the vessel with distilled water abolished generation of the depolarizing response, and this procedure also abolished the endothelium-dependent relaxation induced by ACh during the potassium contraction. The results suggest that the depolarizing response evoked by field stimulation is generated by substances released from nonneural components, possibly from the endothelial cells.

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Adrenergic Regulation of Vascular Smooth Muscle

Cited by 109 publications

References 280 publications

Adrenergic transmission in the dog mesenteric vein and its modulation by α‐adrenoceptor antagonists

Adrenergic transmission in the dog mesenteric vein and its modulation by α‐adrenoceptor antagonists

Functional Activity of the Noradrenergic Innervation of Large Cerebral Arteries

Non-neural electrical responses of smooth muscle cells of the rabbit basilar artery to electrical field stimulation.

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