Angiotensin AT1–Receptor Blockers Enhance Cardiac Responses to Parasympathetic Nerve Stimulation via Presynaptic AT1 Receptors in Pithed Rats

Yamaki, Fumiko; Arai, Takami; Aoyama, Masato; Watanabe, A.; Takata, Yoshinobu

doi:10.1254/jphs.12283fp

Cited by 8 publications

(9 citation statements)

References 18 publications

(18 reference statements)

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“…It is unlikely to be via the canonical G q/11 -AT1R coupling, which signals via the inhibition of cAMP and the generation of ROS, respectively [65]. These studies indicate that this pathway may be an additional mode of action via which Ang II blockers may be beneficial [57,59]. In conclusion, these data taken together indicate that losartan and other clinically available AT1R blockers potentiate vagal tone.…”

Section: Ang II Tonically Inhibits Cardiac Vagal Tone-peripheral Actionsmentioning

confidence: 75%

“…However, how far the losartan can diffuse out of the dialysis probe to the vagal nerve terminals could not be determined so a role for the postsynaptic receptors cannot be ruled out. These actions of Ang II on vagal tone appear to be mediated via AT1Rs since no effect on vagal stimulation-mediated bradycardia is observed with an AT2R antagonist [57].…”

Section: Ang II Tonically Inhibits Cardiac Vagal Tone-peripheral Actionsmentioning

confidence: 97%

“…Several studies have suggested that cardiac parasympathetic tone is under tonic inhibition by Ang II [57][58][59]. Stimulation of the main vagal branch results in depolarisation-induced release of acetylcholine from postganglionic nerve fibres and reduces heart rate.…”

Section: Ang II Tonically Inhibits Cardiac Vagal Tone-peripheral Actionsmentioning

confidence: 99%

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Angiotensin II and the Cardiac Parasympathetic Nervous System in Hypertension

Shanks

Ramchandra

2021

IJMS

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The renin–angiotensin–aldosterone system (RAAS) impacts cardiovascular homeostasis via direct actions on peripheral blood vessels and via modulation of the autonomic nervous system. To date, research has primarily focused on the actions of the RAAS on the sympathetic nervous system. Here, we review the critical role of the RAAS on parasympathetic nerve function during normal physiology and its role in cardiovascular disease, focusing on hypertension. Angiotensin (Ang) II receptors are present throughout the parasympathetic nerves and can modulate vagal activity via actions at the level of the nerve endings as well as via the circumventricular organs and as a neuromodulator acting within brain regions. There is tonic inhibition of cardiac vagal tone by endogenous Ang II. We review the actions of Ang II via peripheral nerve endings as well as via central actions on brain regions. We review the evidence that Ang II modulates arterial baroreflex function and examine the pathways via which Ang II can modulate baroreflex control of cardiac vagal drive. Although there is evidence that Ang II can modulate parasympathetic activity and has the potential to contribute to impaired baseline levels and impaired baroreflex control during hypertension, the exact central regions where Ang II acts need further investigation. The beneficial actions of angiotensin receptor blockers in hypertension may be mediated in part via actions on the parasympathetic nervous system. We highlight important unknown questions about the interaction between the RAAS and the parasympathetic nervous system and conclude that this remains an important area where future research is needed.

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Section: Ang II Tonically Inhibits Cardiac Vagal Tone-peripheral Actionsmentioning

confidence: 75%

Section: Ang II Tonically Inhibits Cardiac Vagal Tone-peripheral Actionsmentioning

confidence: 97%

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Angiotensin II and the Cardiac Parasympathetic Nervous System in Hypertension

Shanks

Ramchandra

2021

IJMS

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“…Òàêaeå äëÿ ñîåäèíåíèÿ KT3-671 ïîêàçàíà ñïîñîáíîñòü óñèëèâàòü ïàðàñèìïà-òè÷åñêîå âëèÿíèå íà ñåðäöå. Â ñðàâíåíèè ñ ëîçàðòàíîì, äàííûé ïàðàñèìïàòèêî-ñòèìóëèðóþùèé ýôôåêò ïðàòîñàðòàíà ÿâëÿåòñÿ áîëåå âûðàaeåííûì [55]. Ó ïðîèçâîäíîãî èìèäàçî [5,4-b ]ïèðèäèíà L-158,809 áûëà âûÿâëåíà âûñîêîñåëåêòèâíàÿ AT 1 -àíòàãîíèñòè-÷åñêàÿ àêòèâíîñòü íà ìîäåëÿõ èçó÷åíèÿ ñèñòåìíîé ãåìîäèíàìèêè (ÀÄ, îáùåå ïåðèôåðè÷åñêîå ñîñóäèñòîå ñîïðîòèâëåíèå) è ôóíêöèè ñåðäöà (÷àñòîòà ñåðäå÷íûõ ñîêðàùåíèé, ñåðäå÷íûé âûáðîñ) ó íàðêîòèçèðîâàííûõ ãàëîòàíîì ñîáàê ñ çàêðûòîé ãðóäíîé êëåòêîé [40].…”

Section: ëèãàíäû At 1 -ðåöåïòîðîâunclassified

Ангиотензиновые AT<sub>1</sub>-рецепторы и их лиганды (обзор)

Спасов¹,

Яковлев²,

Бригадирова³

2017

Хим.-фарм. ж.

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В обзоре рассматривается одна из наиболее интенсивно изучающихся биологических мишеней организма — ангиотензиновые рецепторы первого типа. Отдельно сфокусировано внимание на строении рецептора и его взаимодействии с различными внутриклеточными сигнальными молекулами. Представлены данные о давно существующих и недавно созданных лигандах, способных влиять на AT1-рецепторы. Описаны отдельные структурные фрагменты молекул AT1-антагонистов, являющиеся функционально значимыми для проявления данного вида активности. Кратко приводится анализ перспектив клинического использования AT1-антагонистов при ряде патологических состояний в дополнение к зарегистрированным показаниям, включающим артериальную гипертензию, хроническую сердечную недостаточность и нефропатию при сахарном диабете 2 типа. Это обусловлено открытием дополнительных аспектов механизма действия антагонистов и проявления ими таких эффектов, как нейропротекторный и противовоспалительный, а также различных органопротективных свойств.

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“…Recent studies in rats demonstrated evidence for presynaptic AT 1 receptors that can reduce parasympathetic responses to vagal stimulation by inhibiting ACh release (28). To test for the presence of this mechanism in guinea pigs, we determined the output frequency of intracardiac neurons from control animals with and without 100 nM ANG II in the bath solution.…”

Section: Effects Of Ang II Modulators In Healthy Animalsmentioning

confidence: 99%

Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus

Hardwick

Ryan

Powers

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg Ϫ1 ·day Ϫ1 ) on remodeling of the guinea pig intrinsic cardiac plexus following chronic myocardial infarction (MI). MI was surgically induced and animals recovered for 6 or 7 wk, with or without drug treatment. Intracellular voltage recordings from whole mounts of the cardiac plexus were used to monitor changes in neuronal responses to norepinephrine (NE), muscarinic agonists (bethanechol), or ANG II. MI produced an increase in neuronal excitability with NE and a loss of sensitivity to ANG II. MI animals treated with captopril exhibited increased neuronal excitability with NE application, while MI animals treated with CGP42112A did not. Losartan treatment of MI animals did not alter excitability with NE compared with untreated MIs, but these animals did show an enhanced synaptic efficacy. This effect on synaptic function was likely due to presynaptic AT1 receptors, since ANG II was able to reduce output to nerve fiber stimulation in control animals, and this effect was prevented by inclusion of losartan in the bath solution. Analysis of AT receptor expression by Western blot showed a decrease in both AT 1 and AT2 receptors with MI that was reversed by all three drug treatments. These data indicate that neuronal remodeling of the guinea pig cardiac plexus following MI is mediated, in part, by activation of both AT 1 and AT2 receptors.

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Angiotensin AT1–Receptor Blockers Enhance Cardiac Responses to Parasympathetic Nerve Stimulation via Presynaptic AT1 Receptors in Pithed Rats

Cited by 8 publications

References 18 publications

Angiotensin II and the Cardiac Parasympathetic Nervous System in Hypertension

Angiotensin II and the Cardiac Parasympathetic Nervous System in Hypertension

Ангиотензиновые AT<sub>1</sub>-рецепторы и их лиганды (обзор)

Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus

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