Effects of Catecholamines in the Cat Superior Cervical Ganglion and Their Postulated Rôle as Physiological Modulators of Ganglionic Transmission

We, Haefely

doi:10.1016/s0079-6123(08)63228-8

Cited by 25 publications

(8 citation statements)

References 19 publications

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“…Investigations were also made in the 1970s of the ionic mechanisms involved in the action of alpha receptors found on cell bodies of adrenergic neurones. Catecholamines produce a hyperpolarization of the cell bodies of sympathetic ganglion cells [53,54], an effect that was shown to increase on removal of external calcium ions or following reduction of external potassium ions (Fig. 6B) [55], similar to that already reported for the effects of these ions on alpha-mediated inhibition of noradrenaline release [44,56].…”

Section: The Ionic Basis Of the Action Of Alpha 2 Adrenoceptorssupporting

confidence: 76%

One hundred years of adrenaline: the discovery of autoreceptors

Bennett

1999

Clinical Autonomic Research

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The active principle of suprenal extract that produces its pressor effects was isolated by the joint research of John Abel in 1899 and Jokichi Takamine in 1901. Within three years Elliott, working in Langley's laboratory, suggested that this active principle, referred to by British physiologists as "adrenaline" and named "Adrenalin" by Takamine, was released from sympathetic nerve terminals to act on smooth muscle cells. However, it was not until 1946 that von Euler showed that demythelated adrenaline (noradrenaline) rather than adrenaline is a sympathetic transmitter. The possibility that this sympathetic transmitter could also act on nerve terminals was not developed until 1971. Research on autoreceptors culminated in the identification of adrenergic receptors on nerve terminals different to those on muscle cells. This paper assesses the contributions that established the idea of the adrenergic autoreceptor, 100 years after the discovery of adrenaline.

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Section: The Ionic Basis Of the Action Of Alpha 2 Adrenoceptorssupporting

confidence: 76%

One hundred years of adrenaline: the discovery of autoreceptors

Bennett

1999

Clinical Autonomic Research

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“…That hyperpolarization of nerve terminals may be somehow involved in the mode of action of c-autoinhibition has been proposed by other workers (Dismukes et al 1977). a-Adrenoceptor mediated hyperpolarization of sympathetic ganglion cells has also been repeatedly described (De Groat & Volle, 1966;Haefely, 1969). This may be relevant for the present problem, since there seems to be reason to assume that noradrenergic cell bodies and nerve terminals possess the same type ofct2-adrenoceptors Brown & Caulfield, 1979).…”

Section: Estimation Of the Evoked Secretion Of [3h]noradrenalinementioning

confidence: 53%

Site(s) and ionic basis of α‐autoinhibition and facilitation of [³H]noradrenaline secretion in guinea‐pig vas deferens

Alberts

Bartfai

Stjärne

1981

The Journal of Physiology

132

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SUMMARY1. Mechanisms controlling the secretion of [3H]noradrenaline from the noradrenergic nerves of guinea-pig isolated vas deferens, prelabelled by incubation with [3H]noradrenaline, were studied using (a) different modes of (extramural or transmural) electrical nerve stimulation (a total of 300 shocks of varying strength, and a duration of 2 msec) at or (b) depolarizing concentrations of K+ (60-110 mM).2. The fractional rise in efflux of 3H-labelled material (At) was used to measure the secretion of [3H]noradrenaline.3. Thedependence of[3H]noradrenalinesecretionontheexternalCa2+ concentration (1-8 mM) was essentially hyperbolic. Double reciprocal plot analysis (1/At vs. 1/Ca2+) of the data yields that blockade of a-autoinhibition (phentolamine 1 /SM) does not increase the maximal secretary velocity, but does enhance the apparent affinity of the secretary mechanism for external Ca2+. Exogenous noradrenaline has (qualitatively) opposite effects. The interaction between a-autoinhibition and external Caa2+ thus shows a 'competitive' pattern, indicating that restriction of the utilization of external. Ca2+ is a major mechanism in a-autoinhibition of noradrenaline secretion, in this system. 4. Phenoxybenzamine (10 ,uM) and phentolamine (1 /LM) increased the secretion of[3H]noradrenaline evoked by depolarization with K+ much less than that caused by electrical nerve stimulation (frequencies up to 10 Hz). Exogenous noradrenaline (1)(2)(3)(4)(5) /SM) depressed the secretion evoked by both modes of stimulation. The results indicate that a-autoinhibition of [3H]noradrenaline secretion is mainly operative when the secretary stimulus requires conduction of nerve impulses between varicosities.5. The frequency dependence of [3H]noradrenaline secretion was hyperbolic, both in the presence and in the absence ofa-autoinhibition; at each frequency the secretion (At per shock) increased with the Ca2+ concentration in the medium (0'6-8 mM). Double reciprocal plot analysis (1/At vs. 1/frequency) of the data yields that the pattern of interaction between external Ca2+ and facilitation depends on the presence or absence of a-autoinhibition (phentolamine 1 /SM); in the former case it is 'noncompetitive', in the latter 'competitive'. Similar analysis of the effect of facilitation byThe experiments reported in this paper were carried out at the Department of Physiology, Karolinska Institutet. Authors' names are in alphabetical order.0022-3751/81/3710-0802 $07.50 ©D 1981 The Physiological Society 298 P. ALBERTS, T. BARTFAI AND L. STJARNE increasing the length of stimulus trains (from 5 to 300 pulses) at a constant frequency (5 Hz), on the Ca2+ dependence ofAt (1/At vs. 1/Ca2+) in the absence ofa-autoinhibition also yields that facilitation promotes utilization of external Ca2+. These results apparently imply that a rise in external Ca2 , in the presence of a-autoinhibition, augments the secretary response to electrical nerve stimulation mainly by promoting recruitment of active units (varicosities?), without markedly altering their 'a...

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“…De Groat & Volle (1966) and Haefely (1969) discerned two forms of potential change in cat superior cervical ganglia in situ following local application of catecholamines: an a-mediated hyperpolarization and a ,B-mediated depolarization. In previous experiments on rat isolated sympathetic ganglia, only the a-mediated hyperpolarization could be recorded and no catecholamine-induced depolarization was detected (Suzuki & Volle, 1978;Brown & Caulfield, 1979).…”

Section: Introductionmentioning

confidence: 99%

Depolarization of rat isolated superior cervical ganglia mediated by β₂‐adrenoceptors

Brown

Dunn

1983

British J Pharmacology

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Effects of Catecholamines in the Cat Superior Cervical Ganglion and Their Postulated Rôle as Physiological Modulators of Ganglionic Transmission

Cited by 25 publications

References 19 publications

One hundred years of adrenaline: the discovery of autoreceptors

One hundred years of adrenaline: the discovery of autoreceptors

Site(s) and ionic basis of α‐autoinhibition and facilitation of [³H]noradrenaline secretion in guinea‐pig vas deferens

Depolarization of rat isolated superior cervical ganglia mediated by β₂‐adrenoceptors

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Effects of Catecholamines in the Cat Superior Cervical Ganglion and Their Postulated Rôle as Physiological Modulators of Ganglionic Transmission

Cited by 25 publications

References 19 publications

One hundred years of adrenaline: the discovery of autoreceptors

One hundred years of adrenaline: the discovery of autoreceptors

Site(s) and ionic basis of α‐autoinhibition and facilitation of [3H]noradrenaline secretion in guinea‐pig vas deferens

Depolarization of rat isolated superior cervical ganglia mediated by β2‐adrenoceptors

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Site(s) and ionic basis of α‐autoinhibition and facilitation of [³H]noradrenaline secretion in guinea‐pig vas deferens

Depolarization of rat isolated superior cervical ganglia mediated by β₂‐adrenoceptors