5-Hydroxytryptamine inhibits the tachycardia induced by selective preganglionic sympathetic stimulation in pithed rats

Villalón, Carlos M.; Centurión, David; Fernández, María del Mar; Morán, Asunción; Sánchez-López, Araceli

doi:10.1016/s0024-3205(99)00126-5

Cited by 25 publications

(70 citation statements)

References 21 publications

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“…after the last stimulation, cardioaccelerator or vasopressor responses were elicited by giving i.v. bolus injections of exogenous noradrenaline (0.03, 0.1, 0.3, 1 and 3 μg/kg), as reported earlier .…”

Section: Methodsmentioning

confidence: 83%

Cardiovascular Alterations during the Interictal Period in Awake and Pithed Amygdala‐Kindled Rats

Ruiz-Salinas

Rocha

Marichal‐Cancino

et al. 2016

Basic Clin Pharma Tox

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Epileptic seizures are often accompanied by increased sympathetic cardiovascular activity (even interictally), but it remains unknown whether this increased activity is of central and/or peripheral origin. Hence, this study investigated the cardiovascular alterations produced by amygdala kindling in awake and pithed Wistar rats. Blood pressure (BP) and heart rate (HR) were initially recorded by tail cuff plethysmography in awake control, sham-operated and amygdala-kindled rats before and 24 hr after the kindling process. The after-discharge threshold (ADT) was measured under different conditions to correlate brain excitability with BP and HR in kindled rats. Twenty-four hours after the last kindling seizure, (i) HR, systolic and diastolic BP were increased and (ii) only higher HR values correlated with lower ADT values. Forty-eight hr after the last kindled seizure, all rats were pithed and prepared for analysing the tachycardic, vasopressor and vasodepressor responses by (i) stimulation of the sympathetic or sensory vasodepressor CGRPergic out-flows (stimulus-response curves, S-R curves) and (ii) intravenous injections of noradrenaline or a-CGRP (dose-response curves, D-R curves). Interestingly, (i) the tachycardic S-R and D-R curves were attenuated, whilst the CGRPergic S-R and D-R curves were potentiated in kindled rats, and (ii) the vasopressor noradrenergic S-R and D-R curves were not significantly different in all groups. Therefore, the kindling process may be associated with overstimulation in the central sympathetic and sensory out-flows interictally, producing (i) peripheral attenuation of cardiac sympathetic out-flow and b-adrenoceptor activity and (ii) peripheral potentiation of vasodepressor sensory CGRPergic out-flow and CGRP receptor activity.Epilepsy is a disorder characterized by a pre-disposition to generate spontaneous and recurrent seizures [1]. Postictal (period after a seizure characterized by a reduced susceptibility to present subsequent seizures) and interictal (period between seizures characterized by a susceptibility to present subsequent seizures) phenomena reflect changes in the brain induced by epilepsy such as depression, aggressive behaviour and autonomic dysfunction [2]. In this regard, seizures induce severe autonomic changes such as hyperventilation, apnoea and changes in blood pressure (BP) and heart rate (HR) [3,4] (even interictally). Moreover, several lines of evidence have shown (i) interictal cardiac autonomic dysfunction in patients with temporal lobe epilepsy, such as impaired HR responses and diminished HR variability [5,6], and (ii) higher basal HR in patients with complex partial and secondarily generalized seizures than in control or other epileptic patients [7].Further studies in animal models have also demonstrated a possible autonomic dysfunction associated with epilepsy. For example, Pansani et al. [8] have observed in amygdala-kindled rats (i) a correlation between the number of seizures induced by electrical amygdala kindling and ictal tachycardia, wh...

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Section: Methodsmentioning

confidence: 83%

Cardiovascular Alterations during the Interictal Period in Awake and Pithed Amygdala‐Kindled Rats

Ruiz-Salinas

Rocha

Marichal‐Cancino

et al. 2016

Basic Clin Pharma Tox

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“…The simplest interpretation of these findings suggests that the cardioaccelerator sympathetic outflow in diabetic (as compared to normoglycaemic) rats involves a differential activation of α 2 ‐adrenergic, dopamine D 2 ‐like and histamine H 3 /H 4 receptors. Admittedly, we did not measure directly the release of noradrenaline from sympathetic nerves, but it was determined indirectly by assessment of the evoked tachycardic responses induced by sympathetic stimulation, as previously reported . In this respect, it is noteworthy that, unlike exogenous noradrenaline given i.v., sympathetic nerves can release, in addition to noradrenaline, several co‐transmitters including neuropeptide Y, ATP, galanin, etc.…”

Section: Discussionmentioning

confidence: 97%

Differential cardiac sympatho‐inhibitory responses produced by the agonists B‐HT 933, quinpirole and immepip in normoglycaemic and diabetic pithed rats

Rivera‐Mancilla

Altamirano-Espinoza

Manrique-Maldonado

et al. 2018

Clin Exp Pharma Physio

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This study compared the cardiac sympatho-inhibitory responses produced by agonists at α -adrenergic (B-HT 933), dopamine D -like (quinpirole) and histamine H /H (immepip) receptors between normoglycaemic and streptozotocin-pretreated (diabetic) pithed rats. Intravenous (i.v.) continuous infusions of B-HT 933, quinpirole or immepip were used in normoglycaemic and diabetic pithed rats to analyse their sympatho-inhibitory effects on the electrically-stimulated cardioaccelerator sympathetic outflow. Both in normoglycaemic and diabetic animals, B-HT 933 (until 100 μg/kg per minute) and quinpirole (until 10 μg/kg per minute) inhibited the tachycardic responses to electrical sympathetic stimulation, but not those to i.v. bolus of exogenous noradrenaline. These sympatho-inhibitory responses were more pronounced in diabetic than in normoglycaemic animals. Accordingly, the areas under the curve for 100 μg/kg per minute B-HT 933 and 10 μg/kg per minute quinpirole in diabetic rats (1065 ± 70 and 920 ± 35, respectively) were significantly smaller (P < .05) than those in normoglycaemic rats (1220 ± 45 and 1360 ± 42, respectively). In contrast, immepip infusions produced cardiac sympatho-inhibition in normoglycaemic (until 10 μg/kg per minute), but not in diabetic (until 100 μg/kg per minute) animals. Our results suggest that in diabetic pithed rats: (i) the more pronounced cardiac sympatho-inhibition to B-HT 933 and quinpirole may be probably due to up-regulation of α -adrenergic and dopamine D -like receptors, respectively; (ii) the histamine H /H receptors do not seem to play a sympatho-inhibitory role; and (iii) there is a differential participation of α -adrenergic and dopamine D -like receptors, which may certainly represent therapeutic targets for the treatment of diabetic complications such as cardiovascular autonomic neuropathy.

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“…[21][22][23] Previous studies performed in our laboratory have revealed the existence of different serotonergic mechanisms that increase or inhibit sympathetic vascular and cardiac neurotransmission. These mechanisms involve a decrease in the release of noradrenaline through the activation of presynaptic 5-HT1 receptors 14,17,24 or increases in noradrenaline levels as a result of 5-HT3 receptor activation. 14 The possible interaction between the above two systems has been also investigated by our group in mesenteric and renal autoperfused vascular beds (E Calama et al, unpubl.…”

Section: Discussionmentioning

confidence: 99%

Effect of 5‐hydroxytryptamine on neurogenic vasoconstriction in the isolated, autoperfused hindquarters of the rat

Calama

Urbina

Morán

et al. 2005

Clin Exp Pharma Physio

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1. In the present study, we analysed the effect of different doses of 5-hydroxytryptamine (5-HT; intravenous infusions of 0.001-40 microg/kg per min) in the autoperfused hindquarters of the rat subjected to electrical stimulation (frequencies of 0.5-20 Hz) of the lumbar chains, investigating the relationship between the adrenergic and serotonergic systems in this vascular bed. 2. Because we observed that 5-HT inhibited the increases in perfusion pressure induced by electrical stimulation of the lumbar chains, we used different agonists and antagonists to analyse the mechanism of action of 5-HT. 3. The effect of 5-HT was inhibited by methiothepin (a non-specific 5-HT receptor antagonist), but not by ritanserin (a selective 5-HT2 receptor antagonist). The effects of 5-HT were mimicked by 5-carboxamidotryptamine (a 5-HT1 receptor agonist) and L-694 247 (a selective 5-HT1D receptor agonist), but not by 8-hydroxy-2-dipropylaminotetralin (a 5-HT1A receptor agonist), CGS-12066B (a 5-HT1B receptor agonist), alpha-methyl-5-HT (a 5-HT2 receptor agonist), 1-(3-chlorophenyl) piperazine (a 5-HT2C receptor agonist) or 1-phenylbiguanide (a 5-HT3 receptor agonist). The selective 5-HT1D/1B receptor antagonist BRL 15572 inhibited the effect of the agonist L-694 247. 4. Our data suggest that 5-HT inhibits the increases in perfusion pressure induced by the electrical stimulation of the lumbar chains, acting on presynaptic 5-HT1D receptors and decreasing the release of noradrenaline from the sympathetic nerves in the hindquarter vascular bed of the rat.

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5-Hydroxytryptamine inhibits the tachycardia induced by selective preganglionic sympathetic stimulation in pithed rats

Cited by 25 publications

References 21 publications

Cardiovascular Alterations during the Interictal Period in Awake and Pithed Amygdala‐Kindled Rats

Cardiovascular Alterations during the Interictal Period in Awake and Pithed Amygdala‐Kindled Rats

Differential cardiac sympatho‐inhibitory responses produced by the agonists B‐HT 933, quinpirole and immepip in normoglycaemic and diabetic pithed rats

Effect of 5‐hydroxytryptamine on neurogenic vasoconstriction in the isolated, autoperfused hindquarters of the rat

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