Role of tachycardia and V wave wall stress in the release of ANF during volume loading.

Heart rate is believed to be a primary determinant of atrial natriuretic factor (ANF) release; however, we postulated that V wave wall stress is the main signal for ANF release during volume loading. Conscious dogs were volume loaded with 1,000 ml of saline while the heart rate was allowed to vary and on another day while the heart was paced at 240 beats/min. During volume loading, plasma ANF increased from 58 +/- 10 to 221 +/- 31 pg/ml (P < 0.05), and heart rate increased from 97 +/- 3 to 182 +/- 9 beats/min. During pacing, plasma ANF increased from 42 +/- 8 to 85 +/- 10 pg/ml. A wave atrial pressures were increased during pacing and were fixed due to contraction against a closed atrioventricular valve. Volume loading increased plasma ANF to 180 +/- 25 pg/ml. V wave atrial pressure increased markedly, and V wave atrial wall stress increased from 25 +/- 10 to 131 +/- 44 and from 7 +/- 4 to 116 +/- 25 g/cm2, respectively. A wave pressure and wall stress were not increased by volume loading. V wave wall stress and ANF were significantly correlated. V wave atrial wall stress accounts for the majority of change in plasma ANF (60%), while tachycardia and A wave wall stress account for a smaller fraction (40%) of change.

Dynamics of atrial peptide secretion in the coronary circulation of the conscious dog.

The secretion of atrial natriuretic peptide by the heart is not simply the arterial-coronary sinus concentration difference times coronary blood flow, because only a small fraction of total coronary blood flow passes through the atria. We measured coronary sinus and arterial plasma atrial natriuretic factor (ANF) concentrations and blood flow to each part of the heart using the radioactive microsphere technique. Before acute volume expansion, the arterial-coronary sinus ANF difference was 305 +/- 23 pg/ml and rose to 1,009 +/- 220 pg/ml during volume expansion, whereas total coronary blood flow rose from 167 to 465 ml/min. Atrial blood flow rose from 2.9% to 4.6% of total coronary blood flow during volume expansion. ANF secretion rate increased from 51 to 469 ng/min. When divided by atrial weight, ANF secretion rate increased from 4.0 +/- 0.3 to 56 +/- 12 ng/min/g atrial tissue-in other words, from 0.3% to 3.7% of tissue ANF content each minute. Dividing by atrial blood flow indicated that the concentration of ANF leaving atrial tissue was 10,000 to 29,651 pg/ml, and the additional secretion of ANF was determined by the increase in coronary blood flow. Therefore, at least two mechanisms are responsible for altering coronary sinus ANF and circulating ANF: the release rate from atrial myocytes and the washout via changes in atrial blood flow.

Bilateral atrial appendectomy abolishes increased plasma atrial natriuretic peptide release and blunts sodium and water excretion during volume loading in conscious dogs.

The atrial appendages contain most of the atrial natriuretic factor (ANF) in the mammalian heart, and atrial appendage mechanical function predicts ANF secretion during volume loading. To demonstrate the crucial role of the atrial appendages in ANF release, we first measured hemodynamics and changes in plasma ANF after injection of 1,000 ml i.v. normal saline in conscious dogs and again after bilateral atrial appendectomy; we next measured changes in renal function using infusions of atriopeptin 24 to achieve plasma levels corresponding to levels achieved during volume loading; and we lastly measured renal function during acute volume expansion and also after atrial appendectomy. Plasma ANF increased from 65 +/- 11 to 246 +/- 54 pg/ml after volume loading but did not increase after atrial appendectomy. Atrial appendectomy did not alter the tachycardia or hemodynamic effects of volume loading. Infusion of 10 ng/kg/min atriopeptin 24 increased plasma ANF from 50 +/- 9 to 234 +/- 54 pg/ml, increased urine output 34 +/- 10%, and increased sodium excretion 62 +/- 10% in dogs with intact atrial appendages. Renal function was compared in dogs before atrial appendectomy: 20, 40, and 60 minutes after volume loading, urine flow rate increased by 5.9 +/- 0.5, 6.9 +/- 0.4, and 4.4 +/- 0.8 ml/min, while sodium excretion increased by 717 +/- 60, 839 +/- 84, and 582 +/- 57 mueq/min. After atrial appendectomy urine flow rate increased 2.1 +/- 0.7, 2.7 +/- 0.7, and 2.0 +/- 0.6 ml/min, and sodium excretion increased only by 327 +/- 110, 324 +/- 77, and 340 +/- 92 mueq/min (p less than 0.01) during volume loading.(ABSTRACT TRUNCATED AT 250 WORDS)