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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/H2516    most recent 00424.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kawada, T. Articles by Sugimachi, M. Search for Related Content PubMed PubMed Citation Articles by Kawada, T. Articles by Sugimachi, M.

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

¹Department of Cardiovascular Dynamics, Advanced Medical Engineering Center and ²Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Osaka; and ³Japan Association for the Advancement of Medical Equipment, Tokyo, Japan

Submitted 5 April 2007 ; accepted in final form 19 July 2007

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 µg·kg^–1·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 (AT₁ 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 AT₁ 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.

cardiac microdialysis; cats; losartan

This article has been cited by other articles:

				T. Kawada, M. Mizuno, S. Shimizu, K. Uemura, A. Kamiya, and M. Sugimachi Angiotensin II disproportionally attenuates dynamic vagal and sympathetic heart rate controls Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1666 - H1674. [Abstract] [Full Text] [PDF]