Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation.

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Research Abstract Details 

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Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Abstract Text:

Toru Kawada,Toji Yamazaki,Tsuyoshi Akiyama,Meihua Li,Can Zheng,Toshiaki Shishido,Hidezo Mori,Masaru Sugimachi,Toru Kawada,Toji Yamazaki,Tsuyoshi Akiyama,Meihua Li,Can Zheng,Toshiaki Shishido,Hidezo Mori,Masaru Sugimachi,

Although ANG II exerts a variety of effects on the cardiovascular system, its effects on the peripheral parasympathetic neurotransmission have only been evaluated by changes in heart rate (an effect on the sinus node). To elucidate the effect of ANG II on the parasympathetic neurotransmission in the left ventricle, we measured myocardial interstitial ACh release in response to vagal stimulation (1 ms, 10 V, 20 Hz) using cardiac microdialysis in anesthetized cats. In a control group (n = 6), vagal stimulation increased the ACh level from 0.85 +/- 0.03 to 10.7 +/- 1.0 (SE) nM. Intravenous administration of ANG II at 10 microg x kg(-1) x h(-1) suppressed the stimulation-induced ACh release to 7.5 +/- 0.6 nM (P < 0.01). In a group with pretreatment of intravenous ANG II receptor subtype 1 (AT(1) receptor) blocker losartan (10 mg/kg, n = 6), ANG II was unable to inhibit the stimulation-induced ACh release (8.6 +/- 1.5 vs. 8.4 +/- 1.7 nM). In contrast, in a group with local administration of losartan (10 mM, n = 6) through the dialysis probe, ANG II inhibited the stimulation-induced ACh release (8.0 +/- 0.8 vs. 5.8 +/- 1.0 nM, P < 0.05). In conclusion, intravenous ANG II significantly inhibited the parasympathetic neurotransmission through AT(1) receptors. The failure of local losartan administration to nullify the inhibitory effect of ANG II on the stimulation-induced ACh release indicates that the site of this inhibitory action is likely at parasympathetic ganglia rather than at postganglionic vagal nerve terminals.

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Publishing Authors By Initials

T Kawada,T Yamazaki,T Akiyama,M Li,C Zheng,T Shishido,H Mori,M Sugimachi,T Kawada,T Yamazaki,T Akiyama,M Li,C Zheng,T Shishido,H Mori,M Sugimachi,

For similar nervous system: peripheral nervous system: autonomic nervous system: autonomic pathways: vagus nerve research abstracts see: nervous system: peripheral nervous system: autonomic nervous system: autonomic pathways: vagus nerve research

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Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: American journal of physiology. Heart and circulat

VOLUME: 293

Page Numbers: H2516-22

Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

ISSN: 0363-6135

DAY: 20

MONTH: 07

YEAR: 2007

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Information

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LANGUAGE: eng

NlmUniqueID: 100901228

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Keywords Mesh Terms:

KEYWORDS: Vagus Nerve

MESH TERMS: physiology

Chemical & Substance for Abstract: Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation. Information

Substance Name: Acetylcholine

Registry Number: 51-84-3

Grant and Affiliation Information for Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation.

AFFILIATION: Dept. of Cardiovascular Dynamics, Advance Medical Engineering Center, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan. torukawa@res.ncvc.go.jp

Country: United States

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MEDLINETA: Am J Physiol Heart Circ Physio

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