Atrial regulation of intravascular volume: Observations on the tachycardia-polyuria syndrome

Abstract The atria, strategically located at the junction of the venous and arterial circulation, contain a network of neural and humoral structures by which they sense and regulate intravascular volume. Atrial receptors, most commonly consisting of complex unencapsulated nerve endings discharging into myelinated vagal fibers, are located in the intrapericardial portions of the caval and pulmonary veins and the adjacent atrial walls. Receptor activation by atrial distension results in increased afferent vagal fiber discharge, which in turn leads to tachycardia (Bainbridge's reflex) and decreased renal sympathetic nerve activity, renal vasomotor tone, and antidiuretic hormone activity. In addition, atrial distension also releases ANF, a peptide with potent diuretic, natriuretic, and vasorelaxant actions. The combined effect of these neurohumoral changes is the production of a large hypotonic diuresis. In the clinical setting the volume-regulating role of the atria is demonstrated by the tachycardia-polyuria syndrome. Laboratory and clinical evidence points to the activation of atrial neurohumoral mechanisms in response to atrial distension as the mediators of the polyuria that often accompanies paroxysmal tachycardias. The involvement of these mechanisms in other forms of cardiac congestion and the capability to easily measure in the blood an index of atrial distension, namely ANF, provide the opportunity to elucidate the pathophysiology and hence to open new therapeutic avenues in many cardiac disorders.