Modulation of transmission in rat sympathetic ganglia by activation of presynaptic α‐ and β‐adrenoceptors

Medgett, Iain C.

doi:10.1111/j.1476-5381.1983.tb09358.x

Cited by 19 publications

(9 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, it cannot be excluded that some of the present effects d clonidine have been at a ganglionic level. However, in recent experiments on the superior cervical ganglion of the rat clonidine in supramaximal doses inhibited the compound action potential far less (Medgett 1983) than it reduced the amylase output in the present experiments, suggesting that its major effect in this case is likely to have been at the prejunctional level of the postganglionic neurons. Only receptors belonging to the a2-subgroup seemed to be involved in the response to clonidine, since the mainly a Iadrenoceptor activating agonist phenylephrine (Starke et al 1975b), which has been shown not to cause any amylase secretion from rabbit parotid gland (Asking & Gorjstrup 1980), was without effect on the secretion of amylase caused by sympathetic excitation.…”

Section: Discussioncontrasting

confidence: 82%

“…However, catecholamines have been shown to depress ganglionic transmission (Marazzi 1939, Lundberg 1952, de Groat & Volle 1966; some of these effects have been attributed to changes in the postsynaptic response (see Libet 1979, see Nishi 19791, and some to a decreased release of acetylcholine from preganglionic nerve endings, as shown in the superior cervical ganglion of the cat (Paton & Thomson 1953) and rabbit (Dawes & Vizi 1973). Whereas the postsynaptic effects seem primarily to have been attributed to dopamine release from SIFcells in the ganglion (Libet & Owman 1974) presynaptic effects in the rabbit and rat have been attributed to a-adrenoceptor activation (Dawes & Vizi 1973, Medgett 1983). Thus, it cannot be excluded that some of the present effects d clonidine have been at a ganglionic level.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Gjörstrup

1984

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

In rabbits under urethane anaesthesia parotid secretion of fluid and amylase in response to electrical stimulation of the sympathetic and parasympathetic nerves was measured before and after injections of various agents acting on alpha-adrenoceptors. Amylase secretion in response to sympathetic nerve stimulation at 0.5 and 1 Hz was markedly reduced by clonidine, 0.5-30 micrograms/kg, in a dose related manner. The effect was not due to an altered responsiveness of the gland, since isoprenaline still caused a large release of amylase. Phenylephrine, 10 micrograms/kg, and prazosine, 300 micrograms/kg, had no effect on the sympathetically evoked amylase secretion. Yohimbine in a dose of 0.5 mg/kg increased the amylase output in response to sympathetic nerve stimulation at 0.5 Hz by 70%, while the response at 1 Hz, which is close to maximum for the gland, was not significantly increased. The fluid and amylase secretion produced by parasympathetic nerve stimulation at 1.5, 5.0 and 10 Hz remained unchanged after clonidine, 1.0-30 micrograms/kg, or yohimbine 0.5 mg/kg. In rabbits provided with chronic parotid fistulae fluid and amylase secretion were studied after injections of clonidine, 30 micrograms/kg, and yohimbine, 1 mg/kg. In the conscious animal clonidine reduced not only amylase but also fluid secretion, by around 50 and 30%, respectively, indicating an effect on the activity in both the sympathetic and parasympathetic secretory nerves. Yohimbine increased the output of amylase during feeding, seen as an increased mean output of amylase due to an increased concentration of amylase in the saliva, while fluid secretion remained unchanged. The various experiments suggest that amylase secretion in response to sympathetic activation may be influenced by prejunctional control of transmitter release via alpha-2-adrenoceptors, and that this control may be of physiological significance. Parasympathetically evoked secretion does not seem to be under the influence of a similar control.

show abstract

Section: Discussioncontrasting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Gjörstrup

1984

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

show abstract

“…4, A and C). ␣ 2 -Adrenoreceptor agonists inhibit excitatory transmitter release in sympathetic ganglia (32). Therefore, as a positive control, we used the agonist of ␣ 2 -adrenoreceptors, UK-14304, 1 M. The amplitudes of fast EPSPs before UK-14304 was added were 26.1 Ϯ 5.3 mV and in the presence of UK-14304 amplitudes were 15.0 Ϯ 4.8 mV, a significant difference (P Ͻ 0.01, t-test, 2-tail, n ϭ 5).…”

Section: Ghsr1a Receptor Agonists Did Not Inhibit Transmission In Symmentioning

confidence: 99%

Sites of action of ghrelin receptor ligands in cardiovascular control

Callaghan

Hunne

Hirayama

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Circulating ghrelin reduces blood pressure, but the mechanism for this action is unknown. This study investigated whether ghrelin has direct vasodilator effects mediated through the growth hormone secretagogue receptor 1a (GHSR1a) and whether ghrelin reduces sympathetic nerve activity. Mice expressing enhanced green fluorescent protein under control of the promoter for growth hormone secretagogue receptor (GHSR) and RT-PCR were used to locate sites of receptor expression. Effects of ghrelin and the nonpeptide GHSR1a agonist capromorelin on rat arteries and on transmission in sympathetic ganglia were measured in vitro. In addition, rat blood pressure and sympathetic nerve activity responses to ghrelin were determined in vivo. In reporter mice, expression of GHSR was revealed at sites where it has been previously demonstrated (hypothalamic neurons, renal tubules, sympathetic preganglionic neurons) but not in any artery studied, including mesenteric, cerebral, and coronary arteries. In rat, RT-PCR detected GHSR1a mRNA expression in spinal cord and kidney but not in the aorta or in mesenteric arteries. Moreover, the aorta and mesenteric arteries from rats were not dilated by ghrelin or capromorelin at concentrations >100 times their EC(50) determined in cells transfected with human or rat GHSR1a. These agonists did not affect transmission from preganglionic sympathetic neurons that express GHSR1a. Intravenous application of ghrelin lowered blood pressure and decreased splanchnic nerve activity. It is concluded that the blood pressure reduction to ghrelin occurs concomitantly with a decrease in sympathetic nerve activity and is not caused by direct actions on blood vessels or by inhibition of transmission in sympathetic ganglia.

show abstract

“…Clonidine has been reported previously to depress transmission in the superior cervical ganglion by an action at &2-adrenoceptors (Brown & Caulfield, 1979;Medgett, 1983). Thus it was of interest to compare depressant potencies of the x2-adrenoceptor agonists at this peripheral site with their potencies for depression of the spinal preparation.…”

Section: Effects On Ganglionic Transmissionmentioning

confidence: 99%

The effect of centrally acting myorelaxants on NMDA receptor‐mediated synaptic transmission in the immature rat spinal cord in vitro

Siarey

Long

Evans

1992

British J Pharmacology

View full text Add to dashboard Cite

1 The effect of the myorelaxant drugs baclofen, diazepam and tizanidine have been compared on in vitro preparations of baby rat spinal cord and adult rat superior cervical ganglion. 2 Dorsal root-elicited long duration (time to half decay 9.71 ± 0.29 s.e.mean, n = 31) ipsilateral ventral root reflexes (DR-VRP), measured as integrated area, of immature rat spinal cord preparations were abolished by RS-2-amino-5-phosphonopentanoate (AP5) (EC50 8.13 ± 0.92 ILM, n = 3). The initial short latency component of DR-VRP was resistant to AP5. 3 Baclofen abolished both components of the DR-VRP. Respective EC50 values for the AP5-insensitive and AP5-sensitive components were 237 ± 68 nM (n ± 7) and 57 ± 10 nM (n = 7). These effects of baclofen were reversed by the GABAB antagonist, CGP35348. The apparent Kd values (16.7 ± 6.4 pLM, n = 3 and 14.3 ± 3.9 JtM, n = 6 respectively) for this reversal were not significantly different. 4 Tizanidine, clonidine and diazepam had no effect on the AP5-insensitive component of the DR-VRP. 5 The AP5-sensitive long duration component of the DR-VRP was depressed to respective maximal levels of 23.2 ± 1.4% (n = 7), 18.8 ± 3.8% (n = 4) and 47.6 ± 1.6% (n = 5) of control (100%) levels by tizanidine (EC50 135 ± 33 nM), clonidine (EC50 26.0 ± 2.2 nM) and diazepam (EC25 114 ± 12 nM, n = 4).The depressant effects of tizanidine and clonidine were reversed by idazoxan (1 1AM). Flumazenil (I tiM) failed to reverse the depressant effect of tizanidine. The depressant effect of diazepam was reversed by flumazenil (1 jLM) but not by idazoxan (1 JAM). Naloxone 1 jAM did not reverse the effects of either tizanidine or diazepam. 6 In the presence of tetrodotoxin (0.1 SAM) which abolished synaptic activity, clonidine, tizanidine or diazepam (10, 100 and 101JM respectively) produced no significant antagonism of NMDA-induced depolarizations recorded from ventral roots. 7 Control (100%) synaptic responses of rat superior cervical ganglion preparations were depressed respectively to near maximal levels of 60.0 ± 5.2% (n = 4) and 60.7 ± 5.6% (n = 5) by clonidine (0.5 JAM, EC25 15.3 ± 3.0 nM) and tizanidine (1 JAM, EC25 227 ± 83 nM). These depressant effects were reversed by idazoxan (1 AM). Baclofen (EC25 28.7 ± 10.0, n = 3) depressed the postganglionic response to a maximum level of 71.8 + 2.4% (n = 4) control at a concentration of 100 JAM. The latter depressant action was reversed by the GABAB receptor antagonist, CGP35348 (1 mM). Diazepam (1 JAM) had no significant effect on ganglionic transmission. 8 It is concluded that the activation of benzodiazepine or M2-noradrenaline receptors can modulate NMDA receptor-mediated excitatory synaptic pathways whereas synaptic excitation from primary afferent terminals, mediated by non-NMDA receptors, appears to lack the propensity for this type of modulation. The results show also that the isolated spinal preparation can be used to (Davies & Quinlan, 1985). Thus in the present investigation the action of the myorelaxant, tizanidine, has been compared with the prototypic...

show abstract

Modulation of transmission in rat sympathetic ganglia by activation of presynaptic α‐ and β‐adrenoceptors

Cited by 19 publications

References 14 publications

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Sites of action of ghrelin receptor ligands in cardiovascular control

The effect of centrally acting myorelaxants on NMDA receptor‐mediated synaptic transmission in the immature rat spinal cord in vitro

Contact Info

Product

Resources

About