The essential feature of left ventricular dysfunction is an increase in left atrial pressure and pulmonary venous congestion leading to a fluid flux across the pulmonary microvasculature. Small acute increases (< 10 mmHg) in left atrial pressure enhance the extravascular fluid volume in the airways and activate the rapidly adapting receptors (RAR). With larger increases in left atrial pressure (approximately 25 mmHg) both the RAR and the C-fiber receptors in the airways and the alveoli are activated. Activation of RAR causes a reflex increase in respiratory rate, tracheal tone and mucus secretion from the airways. It appears that small increases in extravascular fluid volume of the airways also cause a reflex diuresis which is mediated by activation of neuronal nitric oxide synthase in the renal medulla. In contrast, when left atrial pressure is elevated chronically, further small increments in extravascular fluid volume of the airways no longer stimulate the RAR. The reflex diuresis is also not evident under these circumstances. However, the RAR continue to be activated by increments in left atrial pressure in excess of 25 mmHg. It is suggested that the RAR of the airways play a significant role in monitoring changes in the extravascular fluid volume of the airways and mediate the reflexes which are associated with the symptomatology of acute left ventricular dysfunction.