Search

Objective: The objective of this article is to investigate the possible role of atrial natriuretic peptide (ANP) in Angiotensin-(1-7) (Ang-(1-7)) signaling pathway on atrial electrical and structural remodeling in a chronic rapid atrial pacing canine model., Methods: Twenty-four dogs were randomly assigned to four groups: a sham group, paced control group, a paced + Ang-(1-7) group and a paced + Ang-(1-7) + A-71915 group. Atrial rapid pacing (ARP) at 600 bpm was maintained for 14 days except in the animals from the sham group. During the pacing, Ang-(1-7) (6 μg•kg-1•h-1) or Ang-(1-7) (6 μg•kg-1•h-1) + A-71915 (ANP receptor antagonist, 0.30 μg•kg-1•h-1) were given intravenously, respectively. After pacing, it was measured that electrophysiological parameters including atrial effective refractory periods (ERPs), inducibility and duration of atrial fibrillation (AF), ICaL and INa changed, where ICaL refers to voltage-dependent L-type Ca(2+) current and INa refers to cardiac sodium current. Then, the fibrosis and the expression of Cav1.2, INav1.5α subunit, TGF-β1 and ANP in atria were assessed., Results: After ARP, compared with the sham group, the atrial ERPs at six sites in each dog were shortened with the increasing in inducibility and duration of AF in the paced control group. The density of ICaL, INa and the expression of Cav1.2, INav1.5α subunit mRNA were decreased. Atrial tissue from the paced dogs showed significant interstitial fibrosis. The expression of TGF-β1 and ANP in mRNA and protein levels were increased. Compared with the paced control group, the shortening of atrial ERPs, and the increasing of inducibility and duration of AF induced by ARP were alleviated by Ang-(1-7) treatment (p < 0.05). The density of ICaL and INa and the expression of Cav1.2 and INav1.5α subunit mRNA were slightly decreased. Atrial tissue showed less interstitial fibrosis after Ang-(1-7) treatment. The increasing of ANP expression was improved by Ang-(1-7), while the increasing of TGF-β1 expression was alleviated by Ang-(1-7) (p < 0.05). A-71915 treatment blocked the beneficial effects of Ang-(1-7) on the aforementioned electrophysiological parameters and atrial fibrosis. And A-71915 treatment blocked Ang-(1-7), improving the expression of TGF-β1., Conclusion: Ang-(1-7) prevented atrial structural and electrical remodeling induced by ARP. Furthermore, Ang-(1-7) promoted ANP secretion, and ANP played a crucial role in the cardiac protection of the former., (© The Author(s) 2016.)

Objective: To investigate the effects of the angiotensin-(1-7) signaling pathway and the possible role of atrial natriuretic peptide (ANP) on atrial electrical remodeling in canines with acute atrial tachycardia., Methods: Forty dogs were randomly assigned to eight groups (five dogs/group): sham, paced control, paced + angiotensin-(1-7), paced + angiotensin-(1-7) + Mas inhibitor, paced + angiotensin-(1-7) + Akt inhibitor, paced + angiotensin-(1-7) + PI3K inhibitor, paced + angiotensin-(1-7) + nitric oxide (NO) inhibitor, and paced + angiotensin-(1-7) + A-71915 (ANP receptor antagonist). Rapid atrial pacing was maintained at 600 bpm for 2 h for all groups, except the sham group, and angiotensin-(1-7) (6 μg kg(-1) h(-1)), Mas inhibitor (5.83 μg kg(-1) h(-1)), Akt inhibitor (2.14 μg kg(-1) h(-1)), PI3K inhibitor (2.86 μg kg(-1) h(-1)), NO synthase inhibitor (180 μg kg(-1)h(-1)), or A-71915 (0.30 μg kg(-1) h(-1)) were administered intravenously. Atrial effective refractory periods, inducibility, and duration of atrial fibrillation (pacing cycle lengths: 300, 250, and 200 ms), and left atrial ANP concentrations were measured., Results: After pacing, the atrial effective refractory periods at the six sites shortened with increased inducibility and duration of atrial fibrillation, which was attenuated by angiotensin-(1-7), and increased ANP concentrations, which was promoted by angiotensin-(1-7) (paced control vs. sham; P < 0.05). All inhibitors and A-71915 blocked the electrophysiological effects of angiotensin-(1-7). ANP secretion induced by angiotensin-(1-7) was also blocked by all inhibitors., Conclusion: Angiotensin-(1-7) prevented acute electrical remodeling in canines with acute atrial tachycardia via the angiotensin-(1-7)/Mas/PI3K/Akt/NO signaling pathway. ANP was related to the anti-arrhythmic effects of angiotensin-(1-7)., (© The Author(s) 2014.)

Background: Atrial fibrillation (AF) is associated with activation of the renin-angiotensin system (RAS) in the atria. Angiotensin-(1-7) [Ang-(1-7)] is a biologically active component of the RAS, it not only counterbalances the actions of angiotensin II (Ang II) but also is a potential inhibitor of angiotensin-converting enzyme (ACE). The purpose of this study was to investigate the effects of the ACE inhibitor enalapril, the angiotensin-receptor blocker (ARB) irbesartan, and Ang-(1-7) on the chronic atrial ionic remodeling., Methods: Thirty dogs were assigned to sham, paced, paced + enalapril, paced + irbesartan or paced + Ang-(1-7) group, 6 dogs in each group. Rapid atrial pacing at 500 beats per minute was maintained for 14 days, but dogs in sham group were instrumented without pacing. During the pacing, enalapril (2 mg · Kg(-1) · d(-1)) and irbesartan (60 mg · Kg(-1) · d(-1)) were given orally and Ang-(1-7) (6 μg · Kg(-1) · h(-1)) was given intravenously. Whole-cell patch-clamp technique was used to record atrial ionic currents and action potential duration (APD). And RT-PCR was applied to assess atrial mRNA expression of I(TO) Kv4.3 and I(CaL)α1C subunits., Results: Compared with sham, rapid pacing shortened APD90 (P < 0.05) of atrial myocytes, and decreased APD90 rate adaptation (P<0.05). APD90 changes were prevented by irbesartan and Ang-(1-7), but not enalapril. In atria from paced group, the densities and gene expression of I(TO) and I(CaL) were reduced (P < 0.01 vs. sham). Enalapril increased the density and gene expression of I(TO) compared with sham (P < 0.01), Ang-(1-7) prevented the decrease of I(TO) and I(CaL) (P < 0.05 vs. control) and Kv4.3 mRNA expression (P < 0.01 vs. control). Irbesartan had no effect on I(TO) and I(CaL) densities or mRNA expression., Conclusions: These results suggest that enalapril, irbesartan, and Ang-(1-7) have differing influences on atrial tachycardia-induced atrial ionic remodeling., (Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.)

Renin-angiotensin system (RAS) is activated in the fibrillating atria. Angiotensin-(1-7) [Ang-(1-7)] counterbalances the actions of angiotensin II (Ang II). To investigate the effects of Ang-(1-7) on the long-term atrial tachycardia-induced atrial fibrosis and atrial fibrillation (AF) vulnerability, eighteen dogs were assigned to sham group, paced group, or paced+Ang-(1-7) group, 6 dogs in each group. Rapid atrial pacing at 500 bpm was maintained for 14 days, but dogs in the sham group were instrumented without pacing. During the pacing, Ang-(1-7) (6 microg x kg(-1) x h(-1)) was given intravenously. After pacing, atrial mRNA expression of ERK1/ERK2 and atrial fibrosis were assessed, the inducibility and duration of AF were measured. Compared with sham, ERK1/ERK2 mRNA expression was increased in the paced group (P<0.05). Atrial tissue from the paced dogs showed a large amount of interstitial fibrosis, and the inducible rate of AF was increased at various BCLs in paced dogs (P<0.01). Compared with the paced group, Ang-(1-7) prevented the increase of ERK1/ERK2 mRNA expression (P<0.01 and P<0.05, respectively), and attenuated the interstitial fibrosis (P<0.01). Inducibility and duration of AF were reduced by Ang-(1-7) at various BCLs. In conclusion, Ang-(1-7) reduced AF vulnerability in chronic paced atria, and antifibrotic actions contributed to its preventive effects on AF., (Copyright 2010 Elsevier B.V. All rights reserved.)

The article presents a case study of a previously healthy 25 year old man who presented with both narrow and wide QRS complex tachycardia documented by Holter monitor during a work-up for recurrent palpitations which resulted in emergency room visits. A discussion of the mechanisms which could have led to the two types of tachycardia is presented.

Abstract: Aims: To study atrial tachycardia-induced electrical remodeling in a canine model of sinus node dysfunction (SND). Materials and methods: A canine model of SND was established by contacting a cotton patch with 20% formaldehyde on the sinus node. Atrial effective refractory period (ERP), ERP dispersion, and inducibility of atrial fibrillation (AF) were recorded at multiple sites in the atrium, before and after SND induction as well as after rapid atrial pacing. The recovery of atrial ERP in the left and right atrium (LA and RA) after cessation of atrial pacing was also recorded. Results: Compared with baseline, the atrial ERPs were shortened after SND (P <0.05). After rapid atrial stimulation, the atrial ERPs were further decreased significantly (P <0.05), and the dispersion of atrial ERPs measured at different pacing cycle lengths (PCLs) showed significant variation. Seven sites were used to induce AF in each dog (56 sites in 8 dogs). The average duration and inducibility of AF after SND was increased compared with baseline (16.5±4.7 vs 2.3±1.2 s and 12/56 vs 4/56 sites, P <0.05). After rapid atrial stimulation, the average duration and inducibility of AF were further increased (16.5±4.7 vs 33.6±16.1 s and 12/56 vs 25/56 sites, P <0.05). The recovery of atrial ERP in LA was significantly delayed compared to the RA. Conclusion: SND induces atrial electrical remodeling which is further aggravated by atrial tachycardia. Therefore, SND creates an electrophysiological substrate that facilitates AF initiation and perpetuation. [ABSTRACT FROM AUTHOR]