The high-pressure or arterial baroreceptors and low-pressure or atrial receptors are believed to participate in the reflex control of arginine vasopressin (AVP) and renin secretion. The current concept of the control system is that at normal blood volume and pressure, afferent impulses from the receptors tonically inhibit central mechanisms controlling secretion of AVP and renin. Thus, a reduction in blood volume or pressure causes a decrease in receptor activity and a reflex increase in hormone secretion; conversely an increase in blood volume causes the opposite sequence of events. Furthermore, it is widely believed that cardiac atrial receptors are more important than arterial baroreceptors in the reflex control of AVP and renin secretion. Evidence presented in this review challenges the traditional view that cardiac receptors are importantly involved in the reflex control of AVP secretion. Recent evidence indicates that plasma AVP does not increase during progressive hypovolemia until volume loss causes a frank fall in arterial pressure. Furthermore, the evidence suggests that it is the sudden unloading of arterial baroreceptors that triggers the surge in AVP secretion and not signals from cardiac receptors. There is also very little evidence that increasing the load on cardiac receptors inhibits AVP secretion. In contrast, there is considerable evidence that renal sympathetic nerve activity, and hence reflex control of renin secretion, is tightly and inversely coupled to changes in blood volume. Furthermore, the evidence supports the concept that atrial receptors are the mediators of the fine reflex control of renin secretion in response to changes in blood volume.