Effects of Systolic Atrial Function on Plasma Renin Activity and Natriuretic Peptide Secretion after High Rate Atrial and Ventricular Pacing in Dogs

Abstract

Rapid atrial rates cause electrical, structural remodeling, and neuro-humoral changes. This study compares the effects of mechanical remodeling on plasma renin activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA-E) were assessed by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP enlarged significantly (2.16 +/- 0.21 cm vs 2.41 +/- 0.23 cm, P = 0.002). Compared with baseline, LAA-E velocities were significantly reduced (0.65 +/- 0.12 m/s vs 0.26 +/- 0.16 m/s, P = 0.001) after AP only. AP caused a significant elevation of PRA in right atrial (9.28 +/- 4.23 nmol/L per hour) and peripheral samples compared with baseline values (4.82 +/- 2.53 nmol/L per hour, P = 0.04). ANP levels increased after AP (1117.12 +/- 252.21 fmol/L) with respect to baseline values (824.37 +/- 159.08 fmol/L, P = 0.001). There was no difference in PRA and ANP levels between atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and ANP. Both neuro-humoral pathways may be therapeutic targets in the treatment of patients with AF.

Plasma renin activity and pro-B-type natriuretic peptide levels in different atrial fibrillation types

“…Angiotensin II can induce the proliferation of fibroblasts and hypertrophy of cardiomyocytes through the mitogen-activated protein kinase pathway (2-4). Subsequently, atrial remodeling consisting of atrial hypertrophy, fibrosis and electrophysiological abnormalities may develop, which facilitates the occurrence of AF (1)(2)(3)(4)(5)(6)(7)(8). The inhibition of RAS may prevent this remodeling in experimental models (2)(3)(4)(5).…”

“…The growing evidence suggests that activation of RAS may contribute to the development and recurrence of AF (1)(2)(3)(4)(5)(6)(7)(8). Angiotensin II can induce the proliferation of fibroblasts and hypertrophy of cardiomyocytes through the mitogen-activated protein kinase pathway (2-4).…”

“…Accordingly, RAS contributes to atrial electrical and structural remodeling in the AF setting (2)(3)(4)(5)(6)(7)(8). In animal model, rapid atrial pacing has been reported to elevate plasma renin activity (PRA) (8). In a recent study, however, rapid atrial depolarization has reduced the expression of renin in cellular and animal model of AF (2).…”

“…Renin-angiotensin system (RAS) can play an important role in the pathophysiology of AF, and seems to be one of the popular mechanisms (1)(2)(3)(4)(5)(6)(7)(8). Previous studies have showed the changes in atrial expression/activity of angiotensin converting-enzyme (ACE) (3) and angiotensin II receptors (6,7) in persistent AF patients with normal left ventricular (LV) function.…”

“…Previous studies have showed the changes in atrial expression/activity of angiotensin converting-enzyme (ACE) (3) and angiotensin II receptors (6,7) in persistent AF patients with normal left ventricular (LV) function. Accordingly, RAS contributes to atrial electrical and structural remodeling in the AF setting (2)(3)(4)(5)(6)(7)(8). In animal model, rapid atrial pacing has been reported to elevate plasma renin activity (PRA) (8).…”