Article date: August 1996
By: Rajamma Mathew, Hatim A. Omar, Raisa Fayngersh, Weiqun Shen, Jie Wang, Michael H. Gewitz, Thomas H. Hintze, Michael S. Wolin, in Volume 118, Issue 8, pages 1886-1890
Pacing‐induced congestive heart failure (CHF) in dogs is associated with increased plasma levels of atrial natriuretic factor (ANF) and inhibiton of receptor‐mediated cyclic AMP‐dependent relaxation in isolated pulmonary arteries (PA). Since ANF is known to be negatively coupled to adenylate cyclase, we studied cyclic AMP‐mediated relaxation to isoprenaline (Iso) and arachidonic acid (AA) in PA from control dogs (C), dogs with pacing‐induced CHF (CHF) and dogs with bilateral atrial appendectomy and CHF (ATR APP + CHF).
In CHF, plasma ANF levels increased from a baseline of 80±8 pg ml−1 to 283±64 pg ml−1 (P<0.05), but the ATR APP + CHF group failed to show this increase (67±7 pg ml−1 vs 94±15 pg ml−1, P = NS). Plasma ANF levels, however, did not influence myocardial dysfunction in CHF.
The relaxation of 49±5% to 1 μm Iso in C was reduced to 23±4% in CHF (P<0.05), but relaxation of 49±12% was observed in the ATR APP+CHF group (P = NS vs C). Relaxation responses to 10 μm AA were as follows: 77±5% (C, n = 8), 27±8% (CHF, n = 10, P<0.05 vs C), and 93±5% (ATR APP + CHF, n = 5). The presence of CHF, or the plasma ANF levels, did not affect responses to cyclic GMP‐mediated relaxing agents in PA.
These data indicate that the myocardial performance in CHF is not influenced by plasma ANF levels. However, altered cyclic AMP‐mediated relaxation in PA during CHF is, in part, modulated by circulating ANF levels.
Pacing‐induced congestive heart failure (CHF) in dogs is associated with increased plasma levels of atrial natriuretic factor (ANF) and inhibiton of receptor‐mediated cyclic AMP‐dependent relaxation in isolated pulmonary arteries (PA). Since ANF is known to be negatively coupled to adenylate cyclase, we studied cyclic AMP‐mediated relaxation to isoprenaline (Iso) and arachidonic acid (AA) in PA from control dogs (C), dogs with pacing‐induced CHF (CHF) and dogs with bilateral atrial appendectomy and CHF (ATR APP + CHF).
In CHF, plasma ANF levels increased from a baseline of 80±8 pg ml−1 to 283±64 pg ml−1 (P<0.05), but the ATR APP + CHF group failed to show this increase (67±7 pg ml−1 vs 94±15 pg ml−1, P = NS). Plasma ANF levels, however, did not influence myocardial dysfunction in CHF.
The relaxation of 49±5% to 1 μm Iso in C was reduced to 23±4% in CHF (P<0.05), but relaxation of 49±12% was observed in the ATR APP+CHF group (P = NS vs C). Relaxation responses to 10 μm AA were as follows: 77±5% (C, n = 8), 27±8% (CHF, n = 10, P<0.05 vs C), and 93±5% (ATR APP + CHF, n = 5). The presence of CHF, or the plasma ANF levels, did not affect responses to cyclic GMP‐mediated relaxing agents in PA.
These data indicate that the myocardial performance in CHF is not influenced by plasma ANF levels. However, altered cyclic AMP‐mediated relaxation in PA during CHF is, in part, modulated by circulating ANF levels.
DOI: 10.1111/j.1476-5381.1996.tb15620.x
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