Edwards, B.S.

To address the role of atrial natriuretic factor (ANF) in hypothyroidism in the control of cardiorenal-endocrine function during volume loading, the relationships between atrial pressure, ANF, the renin-angiotensin-aldosterone system, and renal hemodynamic and excretory function were examined during and after acute 10% body wt saline volume infusion in pentobarbital-anesthetized hypothyroid dogs (n = 8). Hormonal changes before and after thyroidectomy were also evaluated. Four to 6 wk after thyroidectomy, ANF decreased and arginine vasopressin (AVP) and plasma renin activity (PRA) increased. Acute saline volume expansion caused an increase in ANF and decreases in AVP and PRA. Atrial pressure increased throughout volume expansion. Despite the absence of an increase in glomerular filtration rate (GFR) during volume expansion, urinary sodium excretion increased due to a marked rise in fractional excretion of sodium. These studies demonstrate that in hypothyroidism 1) ANF is decreased; 2) despite the decrease in basal ANF, increases in atrial pressure can stimulate relase of ANF; 3) despite the absence of an increase in GFR during volume expansion, fractional excretion of sodium increases associated with an increase in ANF; and 4) a lack of an increase in GFR during volume expansion is not related to an inability to increase ANF.

Atrial pressure, atrial natriuretic factor (ANF), the renin-angiotensin-aldosterone system, and renal hemodynamic functions were examined during and after right ventricular pacing in anesthetized dogs (n = 9). Mean arterial pressure, cardiac output, and renal blood flow decreased during tachycardia while right and left atrial pressures increased. ANF markedly increased during tachycardia but urinary and fractional excretion of sodium were unchanged from control. Plasma renin activity was not increased during pacing despite the decrease in renal perfusion pressure. After tachycardia and restoration of mean arterial pressure to control, ANF declined but remained elevated above control despite a return of atrial pressure to control level. After tachycardia, urinary and fractional sodium excretion increased significantly in the absence of an increase in glomerular filtration rate. These findings support the following conclusions: 1) tachycardia increases ANF in association with increased atrial pressure; however, an elevation of ANF persists following tachycardia despite the absence of the persistent stimulus of elevated atrial pressures; 2) the increase in ANF during tachycardia may contribute to the absence of a decrease in sodium excretion and activation of the renin-angiotensin system that occurs with reduction in renal perfusion pressure; and 3) tachycardia-induced natriuresis may be dependent on an increase in ANF and the maintenance of renal perfusion pressure.