ABSTRACT
The ability of atrial receptors to influence renal function was first recognized by Henry, Gauer, and Reeves who reported that an increase in left atrial pressure produced by partially obstructing the mitral orifice in an anesthetized dog usually elicited a diuresis. The cardiac-denervated animals also provided a model to test the validity of the opinion, held in some quarters at that time, that the diuresis evoked by intravascular volume expansion is mediated primarily via a reflex originating from atrial receptors. The evidence that cardiac receptors elicit reflex responses when cardiac filling pressure is elevated implied that reductions in filling pressure might elicit opposite reflex effects. Receptors in the carotid sinus and aortic arch also are capable of stimulating the secretion of vasopressin during hemorrhage. Sinoaortic baroreceptors are known to be important short-term regulators of arterial blood pressure; they efficiently buffer acute changes in blood pressure.
