Pharmacological evidence that α2A- and α2C-adrenoceptors mediate the inhibition of cardioaccelerator sympathetic outflow in pithed rats

Cobos-Puc, Luis E.; Villalón, Carlos M.; Sánchez-López, Araceli; Lozano-Cuenca, Jair; Pertz, Heinz H.; Görnemann, Tilo; Centurión, David

doi:10.1016/j.ejphar.2006.09.068

Cited by 18 publications

(22 citation statements)

References 20 publications

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“…The electrically-induced tachycardic responses are due to selective sympathetic stimulation, as only negligible changes in diastolic blood pressure were observed (see Fig. 2), as shown earlier (15,17).…”

Section: Initial Effects Of Sympathetic Stimulation or Exogenous Noramentioning

confidence: 49%

“…Moreover, the potentiation of sympathetically-induced tachycardic responses after desipramine (see Results) made it possible to reveal more marked sympatho-inhibitory responses at lower frequencies of stimulation (Fig. 3: b and d), as previously was described (15,17).…”

Section: Systemic Haemodynamic Changesmentioning

confidence: 65%

“…In the second group of rats (n = 6), the effect of desipramine on the tachycardic responses induced by electrical stimulation was determined (see below). Under these conditions, in the first group of rats, the tachycardic responses to lower stimulation frequencies are greater than those elicited without desipramine as previously described (15). Then, the cardiac sympathetic outflow was stimulated with a S88X square pulse stimulator (Grass Technologies) by applying trains of 10 s (monophasic rectangular pulses of 2 ms and 50 V), at increasing frequencies of stimulation (0.03, 0.1, 0.3, 1, and 3 Hz).…”

Section: Experimental Protocolsmentioning

confidence: 77%

“…2a). Thus, the electrically-induced neurotransmitter release in the sinus node could be estimated indirectly by measurement of the evoked tachycardia (15).…”

Section: Discussionmentioning

confidence: 99%

“…However, we cannot rule out an action at both the sympathetic ganglia and post-ganglionic sympathetic neurons that have modulatory D 2 -like receptors (4,23,24) or a 2A/2C -adrenoceptors (15) for which dopamine displays affinity (Table 1) and dopamine reduced the stimulation-evoked release of norepinephrine (25,26). Moreover, the inhibition elicited by 1.8 mg/kg•min dopamine over 3 mg/kg of noradrenaline (Fig.…”

Section: Possible Mechanisms In the Inhibition To Dopamine And Quinpimentioning

confidence: 99%

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Pharmacological Evidence That Dopamine Inhibits the Cardioaccelerator Sympathetic Outflow via D2-Like Receptors in Pithed Rats

et al. 2013

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Abstract. It has been suggested that N,N-di-n-propyl-dopamine (dopamine analogue) decreased heart rate in rats through stimulation of dopamine receptors. Nevertheless, the role of prejunctional dopamine D 1/2 -like receptors or even a 2 -adrenoceptors to mediate cardiac sympatho-inhibition induced by dopamine remains unclear. Hence, this study identified the pharmacological profile of the cardiac sympatho-inhibition to dopamine in pithed rats. Male Wistar rats were pithed and prepared to stimulate the cardiac sympathetic outflow or to receive i.v. bolus of exogenous noradrenaline. I.v. continuous infusions of dopamine (endogenous ligand) or quinpirole (D 2 -like agonist) dose-dependently inhibited the tachycardic responses to sympathetic stimulation, but not those to exogenous noradrenaline. In contrast, SKF-38393 (100 mg/kg•min, D 1 -like agonist) failed to modify both of these responses. The sympatho-inhibition to dopamine (1.8 mg/kg•min) or quinpirole (100 mg/kg•min): i) remained unaltered after saline or the antagonists SCH-23390 (D 1 -like, 300 mg/kg) and rauwolscine (a 2 -adrenoceptors, 300 mg/kg); and ii) was significantly antagonized by raclopride (D 2 -like, 300 mg/kg). These antagonists, at the above doses, failed to modify the sympatheticallyinduced tachycardic responses. The above results suggest that the inhibition of the cardiac sympathetic outflow to dopamine and quinpirole is primarily mediated by prejunctional D 2 -like receptors but not D 1 -like receptors or a 2 -adrenoceptors.

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Section: Initial Effects Of Sympathetic Stimulation or Exogenous Noramentioning

confidence: 49%

Section: Systemic Haemodynamic Changesmentioning

confidence: 65%

Section: Experimental Protocolsmentioning

confidence: 77%

“…2a). Thus, the electrically-induced neurotransmitter release in the sinus node could be estimated indirectly by measurement of the evoked tachycardia (15).…”

Section: Discussionmentioning

confidence: 99%

Section: Possible Mechanisms In the Inhibition To Dopamine And Quinpimentioning

confidence: 99%

See 3 more Smart Citations

Pharmacological Evidence That Dopamine Inhibits the Cardioaccelerator Sympathetic Outflow via D2-Like Receptors in Pithed Rats

et al. 2013

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Pharmacological characterization of ergotamine-induced inhibition of the cardioaccelerator sympathetic outflow in pithed rats

Cobos-Puc

Villalón

Sánchez-López

et al. 2008

Naunyn-Schmied Arch Pharmacol

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Ergotamine inhibits the sympathetically-induced tachycardia in pithed rats. The present study identified the pharmacological profile of this response. Male Wistar rats were pithed and prepared to stimulate the preganglionic (C(7)-T(1)) cardiac sympathetic outflow. Intravenous continuous infusions of ergotamine dose-dependently inhibited the tachycardic responses to sympathetic stimulation, but not those to exogenous noradrenaline. Using several antagonists, the sympatho-inhibition to ergotamine was: (1) partially blocked by rauwolscine (alpha(2)), haloperidol (D(1/2)-like) or rauwolscine plus GR127935 (5-HT(1B/1D)); (2) abolished by rauwolscine plus haloperidol; and (3) unaffected by either saline or GR127935. In animals systematically pretreated with haloperidol, this sympatho-inhibition was: (1) unaffected by BRL44408 (alpha(2A)), partially antagonized by MK912 (alpha(2C)); and (3) abolished by BRL44408 plus MK912. These antagonists failed to modify the sympathetically induced tachycardic responses per se. Thus, the cardiac sympatho-inhibition by ergotamine may be mainly mediated by alpha(2A)/alpha(2C)-adrenoceptors, D(2)-like receptors and, to a lesser extent, by 5-HT(1B/1D) receptors.

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The role of purinergic P2Y12 and P2Y13 receptors in ADPβS-induced inhibition of the cardioaccelerator sympathetic drive in pithed rats

Villanueva-Castillo

Rivera‐Mancilla

Haanes

et al. 2020

Purinergic Signalling

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Pharmacological evidence that α2A- and α2C-adrenoceptors mediate the inhibition of cardioaccelerator sympathetic outflow in pithed rats

Cited by 18 publications

References 20 publications

Pharmacological Evidence That Dopamine Inhibits the Cardioaccelerator Sympathetic Outflow via D2-Like Receptors in Pithed Rats

Pharmacological Evidence That Dopamine Inhibits the Cardioaccelerator Sympathetic Outflow via D2-Like Receptors in Pithed Rats

Pharmacological characterization of ergotamine-induced inhibition of the cardioaccelerator sympathetic outflow in pithed rats

The role of purinergic P2Y12 and P2Y13 receptors in ADPβS-induced inhibition of the cardioaccelerator sympathetic drive in pithed rats

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