Aldosterone Robustly Promotes Atrial Fibrillation in the Presence of Chronic Volume Overload in Rats

We investigated the modulatory effects of aldosterone on atrial remodeling induced by an abdominal aorto-venocaval shunt (AVS) in rats, as patients with primary hyperaldosteronism are suggested to have a higher risk of developing atrial fibrillation (AF). The rats were divided into four groups based...

Full description

Saved in:

Bibliographic Details
Published in:	Biological & pharmaceutical bulletin Vol. 47; no. 9; pp. 1525 - 1531
Main Authors:	Aimoto, Megumi, Nada, Mizuki, Nagasawa, Yoshinobu, Takahara, Akira
Format:	Journal Article
Language:	English
Published:	Japan The Pharmaceutical Society of Japan 13-09-2024 Japan Science and Technology Agency
Subjects:	Aldosterone Aldosterone - blood Animals atrial fibrillation Atrial Fibrillation - etiology Atrial Fibrillation - physiopathology atrial remodeling Atrial Remodeling - drug effects Cardiac arrhythmia chronic volume overload Fibrillation Fibrosis Heart Atria - drug effects Heart Atria - pathology Heart Atria - physiopathology Hypertrophy Male Rats Rats, Sprague-Dawley Surgery atrial remodeling atrial fibrillation chronic volume overload aldosterone
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Abstract	We investigated the modulatory effects of aldosterone on atrial remodeling induced by an abdominal aorto-venocaval shunt (AVS) in rats, as patients with primary hyperaldosteronism are suggested to have a higher risk of developing atrial fibrillation (AF). The rats were divided into four groups based on the basis of whether they underwent AVS surgery, received aldosterone using an intraperitoneally implanted osmotic minipump, or both. Aldosterone was started at 0.5 µg/h during the AVS surgery, and morphological and electrophysiological assessments were performed four weeks after AVS creation. The atrial structural changes induced by AVS, including atrial cell hypertrophy and fibrosis, were not modulated by aldosterone, whereas P-wave duration was longer in aldosterone-treated AVS rats than in non-treated rats. Although the average AF duration induced by burst pacing was 10–25 s in the untreated, aldosterone-treated, and AVS rats, the AF duration was approximately 100 s in the aldosterone-treated AVS rats. Meanwhile, there was no significant difference in the atrial effective refractory period among the four experimental groups. Notably, premature atrial contractions (PAC) were frequently observed in aldosterone-treated sham rats, while paroxysmal AF, in addition to PAC, was detected in aldosterone-treated AVS rats, which was not induced in non-treated AVS rats. These findings suggest that aldosterone robustly promotes AF, particularly in the presence of chronic volume overload.
AbstractList	We investigated the modulatory effects of aldosterone on atrial remodeling induced by an abdominal aorto-venocaval shunt (AVS) in rats, as patients with primary hyperaldosteronism are suggested to have a higher risk of developing atrial fibrillation (AF). The rats were divided into four groups based on the basis of whether they underwent AVS surgery, received aldosterone using an intraperitoneally implanted osmotic minipump, or both. Aldosterone was started at 0.5 µg/h during the AVS surgery, and morphological and electrophysiological assessments were performed four weeks after AVS creation. The atrial structural changes induced by AVS, including atrial cell hypertrophy and fibrosis, were not modulated by aldosterone, whereas P-wave duration was longer in aldosterone-treated AVS rats than in non-treated rats. Although the average AF duration induced by burst pacing was 10–25 s in the untreated, aldosterone-treated, and AVS rats, the AF duration was approximately 100 s in the aldosterone-treated AVS rats. Meanwhile, there was no significant difference in the atrial effective refractory period among the four experimental groups. Notably, premature atrial contractions (PAC) were frequently observed in aldosterone-treated sham rats, while paroxysmal AF, in addition to PAC, was detected in aldosterone-treated AVS rats, which was not induced in non-treated AVS rats. These findings suggest that aldosterone robustly promotes AF, particularly in the presence of chronic volume overload. We investigated the modulatory effects of aldosterone on atrial remodeling induced by an abdominal aorto-venocaval shunt (AVS) in rats, as patients with primary hyperaldosteronism are suggested to have a higher risk of developing atrial fibrillation (AF). The rats were divided into four groups based on the basis of whether they underwent AVS surgery, received aldosterone using an intraperitoneally implanted osmotic minipump, or both. Aldosterone was started at 0.5 µg/h during the AVS surgery, and morphological and electrophysiological assessments were performed four weeks after AVS creation. The atrial structural changes induced by AVS, including atrial cell hypertrophy and fibrosis, were not modulated by aldosterone, whereas P-wave duration was longer in aldosterone-treated AVS rats than in non-treated rats. Although the average AF duration induced by burst pacing was 10-25 s in the untreated, aldosterone-treated, and AVS rats, the AF duration was approximately 100 s in the aldosterone-treated AVS rats. Meanwhile, there was no significant difference in the atrial effective refractory period among the four experimental groups. Notably, premature atrial contractions (PAC) were frequently observed in aldosterone-treated sham rats, while paroxysmal AF, in addition to PAC, was detected in aldosterone-treated AVS rats, which was not induced in non-treated AVS rats. These findings suggest that aldosterone robustly promotes AF, particularly in the presence of chronic volume overload.We investigated the modulatory effects of aldosterone on atrial remodeling induced by an abdominal aorto-venocaval shunt (AVS) in rats, as patients with primary hyperaldosteronism are suggested to have a higher risk of developing atrial fibrillation (AF). The rats were divided into four groups based on the basis of whether they underwent AVS surgery, received aldosterone using an intraperitoneally implanted osmotic minipump, or both. Aldosterone was started at 0.5 µg/h during the AVS surgery, and morphological and electrophysiological assessments were performed four weeks after AVS creation. The atrial structural changes induced by AVS, including atrial cell hypertrophy and fibrosis, were not modulated by aldosterone, whereas P-wave duration was longer in aldosterone-treated AVS rats than in non-treated rats. Although the average AF duration induced by burst pacing was 10-25 s in the untreated, aldosterone-treated, and AVS rats, the AF duration was approximately 100 s in the aldosterone-treated AVS rats. Meanwhile, there was no significant difference in the atrial effective refractory period among the four experimental groups. Notably, premature atrial contractions (PAC) were frequently observed in aldosterone-treated sham rats, while paroxysmal AF, in addition to PAC, was detected in aldosterone-treated AVS rats, which was not induced in non-treated AVS rats. These findings suggest that aldosterone robustly promotes AF, particularly in the presence of chronic volume overload.
ArticleNumber	b24-00445
Author	Nagasawa, Yoshinobu Takahara, Akira Aimoto, Megumi Nada, Mizuki
Author_xml	– sequence: 1 fullname: Aimoto, Megumi organization: Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Toho University – sequence: 2 fullname: Nada, Mizuki organization: Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Toho University – sequence: 3 fullname: Nagasawa, Yoshinobu organization: Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Toho University – sequence: 4 fullname: Takahara, Akira organization: Department of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Toho University
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/39284736$$D View this record in MEDLINE/PubMed
BookMark	eNpd0M9LHDEcBfBQlLraHnstAS-9jOb3zByXpbYFQRHba0gy33WzZCZrkin43zfr6h56SQ755PF45-hkihMg9IWSK8pEd2139soy0RAihPyAFpSLtpGMyhO0ID3tGkVld4bOc94SQlrC-Ed0xnvWiZarBRqWYYi5QKqp-CHaOZfwgu9THGOBjJcleRPwjbfJh2CKjxP2Ey4bqAYyTA5wXOPVpv73Dv-JYR4B3_2FFKIZ9vTBlPwJna5NyPD57b5Av2--P65-Nrd3P36tlreNE6wvDVjiOuZkrSYp2fdzre0cV2CGduj7bs1kZ9ggFB8ktdQ4IpkCZgW3LaXAL9C3Q-4uxecZctGjzw5q8QninDWnRBGhqJKVXv5Ht3FOU21XFVWiV7IlVTUH5VLMOcFa75IfTXrRlOj9_LrOr-v8-nX-6r--pc52hOGo3_euYHUA21zMExyBScW7AK9xotX9_jjGHl_dxiQNE_8HNkyZvw
Cites_doi	10.3390/ijms242015472 10.1161/CIRCULATIONAHA.104.503706 10.1093/eurheartj/ehr266 10.3389/fcvm.2014.00007 10.1152/ajpheart.01060.2005 10.1161/CIRCEP.107.754564 10.1016/S0140-6736(14)61774-8 10.1210/jc.2002-021476 10.1161/CIRCULATIONAHA.116.023163 10.1248/bpb.b22-00031 10.1016/j.jphs.2017.12.009 10.1016/j.jacc.2005.01.015 10.1016/j.cardiores.2005.05.009 10.1111/j.1469-7793.2001.0151k.x 10.1016/j.jacc.2019.06.066 10.1161/CIRCEP.111.964080 10.1113/jphysiol.2005.092692 10.1161/01.RES.85.12.1139 10.1097/00005344-200407000-00017 10.1161/CIRCULATIONAHA.108.805804 10.1161/JAHA.119.013133
ContentType	Journal Article
Copyright	2024 Author(s) This is an open access article distributed under the terms of Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/). Published by The Pharmaceutical Society of Japan 2024. This work is published under https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml	– notice: 2024 Author(s) This is an open access article distributed under the terms of Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/). Published by The Pharmaceutical Society of Japan – notice: 2024. This work is published under https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID	CGR CUY CVF ECM EIF NPM AAYXX CITATION 7QP 7QR 7TK 7U9 8FD FR3 H94 P64 7X8
DOI	10.1248/bpb.b24-00445
DatabaseName	Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Neurosciences Abstracts Virology and AIDS Abstracts Technology Research Database Engineering Research Database AIDS and Cancer Research Abstracts Biotechnology and BioEngineering Abstracts MEDLINE - Academic
DatabaseTitle	MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef Virology and AIDS Abstracts Technology Research Database AIDS and Cancer Research Abstracts Chemoreception Abstracts Engineering Research Database Calcium & Calcified Tissue Abstracts Neurosciences Abstracts Biotechnology and BioEngineering Abstracts MEDLINE - Academic
DatabaseTitleList	Virology and AIDS Abstracts MEDLINE - Academic MEDLINE
Database_xml	– sequence: 1 dbid: ECM name: MEDLINE url: https://search.ebscohost.com/login.aspx?direct=true&db=cmedm&site=ehost-live sourceTypes: Index Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Anatomy & Physiology Chemistry Pharmacy, Therapeutics, & Pharmacology
EISSN	1347-5215
EndPage	1531
ExternalDocumentID	10_1248_bpb_b24_00445 39284736 article_bpb_47_9_47_b24_00445_article_char_en
Genre	Journal Article
GroupedDBID	--- 23N 2WC 5GY 6J9 ACGFO ACIWK ACPRK ADBBV AENEX AFFNX AFRAH ALMA_UNASSIGNED_HOLDINGS BAWUL BKOMP CS3 DIK DU5 E3Z EBS EJD F5P GX1 HH5 JMI JSF JSH KQ8 MOJWN OK1 P2P RJT RZJ TR2 XSB .55 1CY 53G ABJNI ABTAH AI. CGR CUY CVF ECM EIF NPM TKC VH1 X7M ZXP ZY4 AAYXX CITATION 7QP 7QR 7TK 7U9 8FD FR3 H94 P64 7X8
ID	FETCH-LOGICAL-c429t-eb0c82c58475104736c7b8c36ead7d998f258a2d463d51b1ac0526e2b43b711e3
ISSN	0918-6158 1347-5215
IngestDate	Sat Oct 26 03:58:07 EDT 2024 Tue Oct 15 10:10:49 EDT 2024 Wed Nov 13 12:40:04 EST 2024 Sat Nov 02 12:27:41 EDT 2024 Thu Oct 03 16:51:25 EDT 2024
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	9
Keywords	atrial remodeling atrial fibrillation chronic volume overload aldosterone
Language	English
LinkModel	OpenURL
MergedId	FETCHMERGED-LOGICAL-c429t-eb0c82c58475104736c7b8c36ead7d998f258a2d463d51b1ac0526e2b43b711e3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
OpenAccessLink	https://www.jstage.jst.go.jp/article/bpb/47/9/47_b24-00445/_article/-char/en
PMID	39284736
PQID	3116496570
PQPubID	1966364
PageCount	7
ParticipantIDs	proquest_miscellaneous_3106046165 proquest_journals_3116496570 crossref_primary_10_1248_bpb_b24_00445 pubmed_primary_39284736 jstage_primary_article_bpb_47_9_47_b24_00445_article_char_en
PublicationCentury	2000
PublicationDate	2024/09/13
PublicationDateYYYYMMDD	2024-09-13
PublicationDate_xml	– month: 09 year: 2024 text: 2024/09/13 day: 13
PublicationDecade	2020
PublicationPlace	Japan
PublicationPlace_xml	– name: Japan – name: Tokyo
PublicationTitle	Biological & pharmaceutical bulletin
PublicationTitleAlternate	Biol Pharm Bull
PublicationYear	2024
Publisher	The Pharmaceutical Society of Japan Japan Science and Technology Agency
Publisher_xml	– name: The Pharmaceutical Society of Japan – name: Japan Science and Technology Agency
References	13) Hiram R, Naud P, Xiong F, Al-u’datt D, Algalarrondo V, Sirois MG, Tanguay JF, Tardif JC, Nattel S. Right atrial mechanisms of atrial fibrillation in a rat model of right heart disease. J. Am. Coll. Cardiol., 74, 1332–1347 (2019). 10) Tanabe A, Naruse M, Takagi S, Tsuchiya K, Imaki T, Takano K. Variability in the renin/aldosterone profile under random and standardized sampling conditions in primary aldosteronism. J. Clin. Endocrinol. Metab., 88, 2489–2494 (2003). 21) Gómez AM, Rueda L, Sainte-Marie Y, Pereira L, Zissimopoulos S, Zhu X, Schaub R, Perrier E, Perrier R, Latouche L, Richard S, Picot MC, Jaisser F, Lai FA, Valdivia HH, Benitah JP. Mineralocorticoid modulation of cardiac ryanodine receptor activity is associated with downregulation of FK506-binding proteins. Circulation, 119, 2179–2187 (2009). 18) Boixel C, Gavillet B, Rougier J, Abriel H. Aldosterone increases voltage-gated sodium current in ventricular myocytes. Am. J. Physiol. Heart Circ. Physiol., 290, H2257–H2266 (2006). 2) Nattel S, Burstein B, Dobrev D. Atrial remodeling and atrial fibrillation: mechanisms and implications. Circ. Arrhythm. Electrophysiol., 1, 62–73 (2008). 14) Inoue K, Kurotobi T, Kimura R, Toyoshima Y, Itoh N, Masuda M, Higuchi Y, Date M, Koyama Y, Okamura A, Iwakura K, Fujii K. Trigger-based mechanism of the persistence of atrial fibrillation and its impact on the efficacy of catheter ablation. Circ. Arrhythm. Electrophysiol., 5, 295–301 (2012). 5) Milliez P, Girerd X, Plouin PF, Blacher J, Safar ME, Mourad JJ. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. J. Am. Coll. Cardiol., 45, 1243–1248 (2005). 8) Curione M, Petramala L, Savoriti C, Verrenti M, Baiocco E, Salvatore S, Zinnamosca L, Iannucci G, Sciomer S, Letizia C. Electrical and myocardial remodeling in primary aldosteronism. Front. Cardiovasc. Med., 1, 7 (2014). 12) Liu M, Li W, Wang H, Yin L, Ye B, Tang Y, Huang C. CTRP9 ameliorates atrial inflammation, fibrosis, and vulnerability to atrial fibrillation in post-myocardial infarction rats. J. Am. Heart Assoc., 8, e013133 (2019). 20) Perrier R, Richard S, Sainte-Marie Y, Rossier BC, Jaisser F, Hummler E, Bénitah JP. A direct relationship between plasma aldosterone and cardiac L-type Ca2+ current in mice. J. Physiol., 569, 153–162 (2005). 17) Lalevée N, Rebsamen M, Barrerelemaire S, Perrier E, Nargeot J, Benitah J, Rossier M. Aldosterone increases T-type calcium channel expression and in vitro beating frequency in neonatal rat cardiomyocytes. Cardiovasc. Res., 67, 216–224 (2005). 19) Ouvrard-Pascaud A, Sainte-Marie Y, Bénitah JP, Perrier R, Soukaseum C, Nguyen Dinh Cat A, Royer A, Le Quang K, Charpentier F, Demolombe S, Mechta-Grigoriou F, Beggah AT, Maison-Blanche P, Oblin ME, Delcayre C, Fishman GI, Farman N, Escoubet B, Jaisser F. Conditional mineralocorticoid receptor expression in the heart leads to life-threatening arrhythmias. Circulation, 111, 3025–3033 (2005). 16) Bénitah JP, Perrier E, Gómez AM, Vassort G. Effects of aldosterone on transient outward K+ current density in rat ventricular myocytes. J. Physiol., 537, 151–160 (2001). 1) Schnabel RB, Yin XY, Gona P, Larson MG, Beiser AS, McManus DD, Newton-Cheh C, Lubitz SA, Magnani JW, Ellinor PT, Seshadri S, Wolf PA, Vasan RS, Benjamin EJ, Levy D. 50 year trends in atrial fibrillation prevalence, incidence, risk factors, and mortality in the Framingham Heart Study: a cohort study. Lancet, 386, 154–162 (2015). 3) Lau DH, Nattel S, Kalman JM, Sanders P. Modifiable risk factors and atrial fibrillation. Circulation, 136, 583–596 (2017). 7) Aimoto M, Yagi K, Ezawa A, Tsuneoka Y, Kumada K, Hasegawa T, Kuze T, Chiba T, Nagasawa Y, Tanaka H, Takahara A. Chronic volume overload caused by abdominal aorto-venocaval shunt provides arrhythmogenic substrates in the rat atrium. Biol. Pharm. Bull., 45, 635–642 (2022). 11) Haugan K, Lam HR, Knudsen CB, Petersen JS. Atrial fibrillation in rats induced by rapid transesophageal atrial pacing during brief episodes of asphyxia: a new in vivo model. J. Cardiovasc. Pharmacol., 44, 125–135 (2004). 4) Manolis AA, Manolis TA, Manolis AS. Neurohumoral activation in heart failure. Int. J. Mol. Sci., 24, 15472 (2023). 15) Bénitah JP, Vassort G. Aldosterone upregulates Ca2+ current in adult rat cardiomyocytes. Circ. Res., 85, 1139–1145 (1999). 6) Cao X, Aimoto M, Fukumoto M, Nagasawa Y, Tanaka H, Takahara A. Influence of chronic volume overload-induced atrial remodeling on electrophysiological responses to cholinergic receptor stimulation in the isolated rat atria. J. Pharmacol. Sci., 136, 73–78 (2018). 9) Reil JC, Hohl M, Selejan S, Lipp P, Drautz F, Kazakow A, Münz BM, Müller P, Steendijk P, Reil GH, Allessie MA, Böhm M, Neuberger HR. Aldosterone promotes atrial fibrillation. Eur. Heart J., 33, 2098–2108 (2012). 11 12 13 14 15 16 17 18 19 1 2 3 4 5 6 7 8 9 20 10 21
References_xml	– ident: 4 doi: 10.3390/ijms242015472 – ident: 19 doi: 10.1161/CIRCULATIONAHA.104.503706 – ident: 9 doi: 10.1093/eurheartj/ehr266 – ident: 8 doi: 10.3389/fcvm.2014.00007 – ident: 18 doi: 10.1152/ajpheart.01060.2005 – ident: 2 doi: 10.1161/CIRCEP.107.754564 – ident: 1 doi: 10.1016/S0140-6736(14)61774-8 – ident: 10 doi: 10.1210/jc.2002-021476 – ident: 3 doi: 10.1161/CIRCULATIONAHA.116.023163 – ident: 7 doi: 10.1248/bpb.b22-00031 – ident: 6 doi: 10.1016/j.jphs.2017.12.009 – ident: 5 doi: 10.1016/j.jacc.2005.01.015 – ident: 17 doi: 10.1016/j.cardiores.2005.05.009 – ident: 16 doi: 10.1111/j.1469-7793.2001.0151k.x – ident: 13 doi: 10.1016/j.jacc.2019.06.066 – ident: 14 doi: 10.1161/CIRCEP.111.964080 – ident: 20 doi: 10.1113/jphysiol.2005.092692 – ident: 15 doi: 10.1161/01.RES.85.12.1139 – ident: 11 doi: 10.1097/00005344-200407000-00017 – ident: 21 doi: 10.1161/CIRCULATIONAHA.108.805804 – ident: 12 doi: 10.1161/JAHA.119.013133
SSID	ssj0007023
Score	2.4700732
Snippet	We investigated the modulatory effects of aldosterone on atrial remodeling induced by an abdominal aorto-venocaval shunt (AVS) in rats, as patients with...
SourceID	proquest crossref pubmed jstage
SourceType	Aggregation Database Index Database Publisher
StartPage	1525
SubjectTerms	Aldosterone Aldosterone - blood Animals atrial fibrillation Atrial Fibrillation - etiology Atrial Fibrillation - physiopathology atrial remodeling Atrial Remodeling - drug effects Cardiac arrhythmia chronic volume overload Fibrillation Fibrosis Heart Atria - drug effects Heart Atria - pathology Heart Atria - physiopathology Hypertrophy Male Rats Rats, Sprague-Dawley Surgery
Title	Aldosterone Robustly Promotes Atrial Fibrillation in the Presence of Chronic Volume Overload in Rats
URI	https://www.jstage.jst.go.jp/article/bpb/47/9/47_b24-00445/_article/-char/en https://www.ncbi.nlm.nih.gov/pubmed/39284736 https://www.proquest.com/docview/3116496570 https://www.proquest.com/docview/3106046165
Volume	47
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
ispartofPNX	Biological and Pharmaceutical Bulletin, 2024/09/13, Vol.47(9), pp.1525-1531
link	http://sdu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9NAEF6lBQkuCFIegYIWCeWSuvixfklcopIIREmrkqJysrz2JnWTxlEcC4Vfz8yuvU4kQHDgYkX2ZrXZ78t4ZnYehLzxeeqCVpAaQWL6Bpu4EyMArcFgTDBzgmIzka0Tvvijq-D9gA1arbprWXPvvyIN9wBrzJz9B7T1pHADPgPmcAXU4fpXuPfnKeZtrHLQHi9yXhbrOSYBYtCdKHp91aVjiIH-cxUGV0c6nstEpESoAA3VGeerlF29M9iFeR5jmabeRaxqP-mT4EyLT2TR8nrHR863q3sjr5Aa0jv7WUzL20zjnf0oZxnI-sZBMIqncRF_l8rttxw9ZfBrGkfDLMZS01K0zbJVvO29sBmGWqjkU_VmAY2gEWN4VNCcKPT6Mvt022VpBWDqqlLvx0IJbIf5YEyrlNBaoqsanhVzw1--KGyGyQ98yY85LspkqqjlbkHu0Vk0vDw9jcaDq_EeuWODLJNW-8dP-mXvm7KDoF5aVcYVpn-7M_mO2nP3BjT_qfi9USOVm_FD8qCySmhf0ekRaYlFmxz0F_E6v93QLpVxwnK72uTeSd0jsE265wruzREdN4l8xZH8iq6Jvjkg6RYtaU1LWtOSKlrSbVrSbEGBlrSmJc0ntKIlVbSkNS1xKNLyMbkcDsYnH4yqwYeRgBq0NgQ3k8BO8KTexZIhjpf4PEgcD8Sbn4ZhMLHdILZT5jmpa3ErTrA6kbA5c7hvWcJ5QvYXsO5nhGK2WWi7PE3dhAnOQ9-1BZg-DtjXtsOcDunW-x8tVR2XCO1fACoCoCIAKpJAdcg7hY4eVv2V5TDmRyFe9HD9FJMkQf50yGGNaVRJhSJyLMvDvgy-2SGv9WOACg_n4oXISxyDZaw8y4MVPFVc0CsAGybA3Xn-58lfkPvNX-yQ7K9XpXhJ9oq0fCVJ-xMtxsbi
link.rule.ids	315,782,786,27933,27934
linkProvider	Flying Publisher
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Aldosterone+Robustly+Promotes+Atrial+Fibrillation+in+the+Presence+of+Chronic+Volume+Overload+in+Rats&rft.jtitle=Biological+%26+pharmaceutical+bulletin&rft.au=Aimoto%2C+Megumi&rft.au=Mizuki+Nada&rft.au=Nagasawa%2C+Yoshinobu&rft.au=Takahara%2C+Akira&rft.date=2024-09-13&rft.pub=Japan+Science+and+Technology+Agency&rft.issn=0918-6158&rft.eissn=1347-5215&rft.volume=47&rft.issue=9&rft_id=info:doi/10.1248%2Fbpb.b24-00445&rft.externalDBID=NO_FULL_TEXT
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0918-6158&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0918-6158&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0918-6158&client=summon