angiotensin-i has been researched along with Tachycardia--Supraventricular* in 1 studies
1 other study(ies) available for angiotensin-i and Tachycardia--Supraventricular
Article | Year |
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Angiotensin-(1-7) prevent atrial tachycardia induced sodium channel remodeling.
Activation of the renin-angiotensin system plays an important role in atrial electrical remodeling; angiotensin-(1-7) (Ang-(1-7)) counterbalances the actions of angiotensin II. The aim of this study was to determine the effects of Ang-(1-7) on cardiac sodium current (INa ) in a canine model of atrial tachycardia.. Eighteen dogs were randomly assigned to sham, pacing, or pacing + Ang-(1-7) groups (n = 6 in each group). Rapid atrial pacing (500 beats/min) was maintained for 2 weeks, while the dogs in the sham group were not paced. Ang-(1-7) (6 μg/kg/h) was administered intravenously during pacing. Whole-cell patch clamp techniques were utilized to record INa from canine atrial myocytes. Reverse transcription-polymerase chain reaction was used to assess possible underlying changes in cardiac Na(+) channels (Nav1.5).. Our results showed that INa density and expression of the Nav1.5 mRNA significantly decreased following pacing (P < 0.05 vs sham); however, the half-activation voltage (V1/2act ) and half-inactivation voltage (V1/2inact ) of INa were not significantly altered (P > 0.05 vs sham). Ang-(1-7) treatment significantly increased INa densities and hyperpolarized V1/2act without concomitant changes in V1/2inact but have no effect on the expression of the Nav1.5 gene.. Ang-(1-7) significantly increased INa densities, which contributed to improving intraatrial conduction and decreasing the likelihood of atrial fibrillation maintenance. Topics: Angiotensin I; Animals; Atrial Remodeling; Dogs; Female; Gene Expression; Male; NAV1.5 Voltage-Gated Sodium Channel; Peptide Fragments; Tachycardia, Supraventricular | 2014 |