Role of adenosine A2A receptor signaling in the nicotine-evoked attenuation of reflex cardiac sympathetic control

El‐Mas, Mahmoud M.; El‐Gowilly, Sahar M.; Fouda, Mohamed A.; Saad, Evan I.

doi:10.1016/j.taap.2011.04.014

Cited by 24 publications

(29 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In male rats, nicotine impaired the baroreceptor-mediated control of reflex tachycardia, but not bradycardia, through a mechanism that involved disruption of adenosine A 2A receptor-mediated facilitation of reflex cardiac sympathoexcitation (El-Mas et al, 2011a). The depressant effect of nicotine on reflex tachycardia was also demonstrated in female rats with depleted estrogen levels (OVX or diestrus rats), but not physiological estrogen levels (proestrus rats or estrogen-replaced OVX rats), suggesting a protective effect for estrogen against the nicotine-baroreflex interaction (El-Mas et al, 2012).…”

Section: Introductionmentioning

confidence: 91%

“…The method described in our previous studies (El-Mas and AbdelRahman, 1993;El-Mas et al, 2011a) was adopted. In brief, rats were anesthetized with thiopental (50 mg/kg i.p.).…”

Section: Intravascular Cannulationmentioning

confidence: 99%

“…Experiments started 2 days later in conscious freely moving rats. This time period has been shown to be adequate for recovery from surgery and restoration of normal rat activity (El-Mas and Abdel-Rahman, 1993;El-Mas et al, 2011a).…”

Section: Intravascular Cannulationmentioning

confidence: 99%

“…Recent experimental reports from our laboratory showed that the interaction of acutely administered nicotine with reflex chronotropic responses depended on the animal's sex, hormonal milieu, and nature of the baroreflex heart rate (HR) response (El-Mas et al, 2011a. In male rats, nicotine impaired the baroreceptor-mediated control of reflex tachycardia, but not bradycardia, through a mechanism that involved disruption of adenosine A 2A receptor-mediated facilitation of reflex cardiac sympathoexcitation (El-Mas et al, 2011a).…”

Section: Introductionmentioning

confidence: 99%

“…Because nicotine was given acutely in our previous studies (El-Mas et al, 2011a, the issue of whether the preferential depressant action of nicotine on reflex tachycardia could be replicated when nicotine is administered on a chronic basis has not been explored. Therefore, this study reports on the dose dependence of chronic nicotine on cardiovascular and baroreflex functions in conscious female rats.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Estrogen Provokes the Depressant Effect of Chronic Nicotine on Vagally Mediated Reflex Chronotropism in Female Rats

El‐Mas

El‐Gowelli²,

El‐Gowilly³

et al. 2012

J Pharmacol Exp Ther

Self Cite

View full text Add to dashboard Cite

We recently reported that acute nicotine impairs reflex tachycardic activity in estrogen-depleted, but not estrogen-repleted, female rats, suggesting a restraining influence for estrogen against the nicotine effect. In this study, we tested whether the baroreflex-protective effect of estrogen can be replicated when nicotine was administered chronically. We also report on the dose dependence and autonomic modulation of the nicotinebaroreflex interaction. The effects of nicotine (0.5, 1, or 2 mg/ kg/day for 14 days) on baroreflex curves relating changes in heart rate to increases [phenylephrine (PE)] or decreases [sodium nitroprusside (SNP)] in blood pressure were evaluated in sham-operated (SO), ovariectomized (OVX), and estrogen-replaced OVX (OVXE 2 ) rats. Slopes of the curves were taken as a measure of baroreflex sensitivity (BRS PE and BRS SNP ). In SO rats, both reflex bradycardic and tachycardic responses were attenuated by nicotine in a dose-related fashion. In nicotinetreated rats, blockade of ␤-adrenergic (propranolol), but not muscarinic (atropine), receptors caused additional reductions in reflex chronotropic responses, implying that nicotine selectively impairs reflex vagal activity. OVX selectively decreased BRS PE but not BRS SNP and abolished the nicotine-induced impairment of either response. These effects of OVX were reversed after treatment with estrogen or the estrogen receptor modulator raloxifene. In atropine-treated rats, comparable BRS values were demonstrated in all rat preparations regardless of the estrogen or nicotine milieu. Collectively, the inhibition of vagal activity accounts for the depressant effect of chronic nicotine on baroreflex activity. Furthermore, contrary to nicotine's acute effects, the baroreflex-attenuating effect of chronic nicotine is exacerbated by estrogen.

show abstract

Section: Introductionmentioning

confidence: 91%

“…The method described in our previous studies (El-Mas and AbdelRahman, 1993;El-Mas et al, 2011a) was adopted. In brief, rats were anesthetized with thiopental (50 mg/kg i.p.).…”

Section: Intravascular Cannulationmentioning

confidence: 99%

Section: Intravascular Cannulationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Estrogen Provokes the Depressant Effect of Chronic Nicotine on Vagally Mediated Reflex Chronotropism in Female Rats

El‐Mas

El‐Gowelli²,

El‐Gowilly³

et al. 2012

J Pharmacol Exp Ther

Self Cite

View full text Add to dashboard Cite

show abstract

Involvement of β‐adrenoceptors in the cardiovascular responses induced by selective adenosine A_2A and A_2B receptor agonists

Wragg

Pannucci

Hill

et al. 2022

Pharmacology Res & Perspec

View full text Add to dashboard Cite

A2A and A2B adenosine receptors produce regionally selective regulation of vascular tone and elicit differing effects on mean arterial pressure (MAP), whilst inducing tachycardia. The tachycardia induced by the stimulation of A2A or A2B receptors has been suggested to be mediated by a reflex increase in sympathetic activity. Here, we have investigated the role of β1‐ and β2‐adrenoceptors in mediating the different cardiovascular responses to selective A2A and A2B receptor stimulation. Hemodynamic variables were measured in conscious male Sprague‐Dawley rats (350–450 g) via pulsed Doppler flowmetry. The effect of intravenous infusion (3 min per dose) of the A2A‐selective agonist CGS 21680 (0.1, 0.3, 1.0 µg.kg−1.min−1) or the A2B‐selective agonist BAY 60–6583 (4.0, 13.3, 40.0 µg.kg−1.min−1) in the absence or following pre‐treatment with the non‐selective β‐antagonist propranolol (1.0 mg.kg−1), the selective β1‐antagonist CGP 20712A (200 µg.kg−1), or the selective β2‐antagonist ICI 118,551 (2.0 mg.kg−1) was investigated (maintenance doses also administered). CGP 20712A and propranolol significantly reduced the tachycardic response to CGS 21680, with no change in the effect on MAP. ICI 118,551 increased BAY 60–6583‐mediated renal and mesenteric flows, but did not affect the heart rate response. CGP 20712A attenuated the BAY 60–6583‐induced tachycardia. These data imply a direct stimulation of the sympathetic activity via cardiac β1‐adrenoceptors as a mechanism for the A2A‐ and A2B‐induced tachycardia. However, the regionally selective effects of A2B agonists on vascular conductance were independent of sympathetic activity and may be exploitable for the treatment of acute kidney injury and mesenteric ischemia.

show abstract

Central GABAA receptors are involved in inflammatory and cardiovascular consequences of endotoxemia in conscious rats

Sallam

El‐Gowilly

Abdel-Galil

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

γ-Aminobutyric acid (GABA), the principal brain inhibitory neurotransmitter, modulates inflammatory and neurodegenerative disease. Here, we tested the hypothesis that central GABAergic neurotransmission mediates the detrimental inflammatory, hemodynamic, and cardiac autonomic actions of endotoxemia. The effects of drugs that block GABA receptors or interfere with GABA uptake or degradation on blood pressure (BP), heart rate (HR), and HR variability (HRV) responses elicited by i.v. lipopolysaccharide (LPS) were assessed in conscious rats. The hypotensive effect of LPS (10 mg/kg) was blunted after intracisternal (i.c.) administration of bicuculline (GABAA receptor antagonist) or saclofen (GABAB receptor antagonist). By contrast, the concomitant LPS-evoked tachycardia and decreases in time domain and frequency domain indices of HRV (measures of cardiac autonomic control) were abolished upon treatment with bicuculline but not saclofen. Increases in serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) caused by LPS disappeared in the presence of bicuculline or saclofen, whereas LPS-evoked increases in serum nitric oxide metabolites (NOx) were counteracted by bicuculline only. None of the endotoxemia effects was altered in rats treated with i.c. tiagabine (GABA reuptake inhibitor) or vigabatrin (GABA transaminase inhibitor). These data suggest a major role for central GABAA receptors in the inflammatory and cardiovascular effects of endotoxemia.

show abstract

Role of adenosine A2A receptor signaling in the nicotine-evoked attenuation of reflex cardiac sympathetic control

Cited by 24 publications

References 44 publications

Estrogen Provokes the Depressant Effect of Chronic Nicotine on Vagally Mediated Reflex Chronotropism in Female Rats

Estrogen Provokes the Depressant Effect of Chronic Nicotine on Vagally Mediated Reflex Chronotropism in Female Rats

Involvement of β‐adrenoceptors in the cardiovascular responses induced by selective adenosine A_2A and A_2B receptor agonists

Central GABAA receptors are involved in inflammatory and cardiovascular consequences of endotoxemia in conscious rats

Contact Info

Product

Resources

About

Role of adenosine A2A receptor signaling in the nicotine-evoked attenuation of reflex cardiac sympathetic control

Cited by 24 publications

References 44 publications

Estrogen Provokes the Depressant Effect of Chronic Nicotine on Vagally Mediated Reflex Chronotropism in Female Rats

Estrogen Provokes the Depressant Effect of Chronic Nicotine on Vagally Mediated Reflex Chronotropism in Female Rats

Involvement of β‐adrenoceptors in the cardiovascular responses induced by selective adenosine A2A and A2B receptor agonists

Central GABAA receptors are involved in inflammatory and cardiovascular consequences of endotoxemia in conscious rats

Contact Info

Product

Resources

About

Involvement of β‐adrenoceptors in the cardiovascular responses induced by selective adenosine A_2A and A_2B receptor agonists