LL. Water deprivation increases Fos expression in hypothalamic corticotropin-releasing factor neurons induced by right atrial distension in awake rats. Am J Physiol Regul Integr Comp Physiol 295: R1706 -R1712, 2008. First published September 10, 2008 doi:10.1152/ajpregu.00022.2008.-Atrial mechanoreceptors, sensitive to stretch, contribute in regulating heart rate and intravascular volume. The information from those receptors reaches the nucleus tractus solitarius and then the paraventricular nucleus (PVN), known to have a crucial role in the regulation of cardiovascular function. Neurons in the PVN synthesize CRF, AVP, and oxytocin (OT). Stimulation of atrial mechanoreceptors was performed in awake rats implanted with a balloon at the junction of the superior vena cava and right atrium. Plasma ACTH, AVP, and OT concentrations and Fos, CRF, AVP, and OT immunolabeling in the PVN were determined after balloon inflation in hydrated and water-deprived rats. The distension of the balloon increased the plasma ACTH concentrations, which were higher in water-deprived than in hydrated rats (P Ͻ 0.05). In addition, the distension in the water-deprived group decreased plasma AVP concentrations (P Ͻ 0.05), compared with the respective control group. The distension increased the number of Fos-and double-labeled Fos/CRF neurons in the parvocellular PVN, which was higher in the water-deprived than in the hydrated group (P Ͻ 0.01). There was no difference in the Fos expression in magnocellular PVN neurons after distension in hydrated and water-deprived groups, compared with respective controls. In conclusion, parvocellular CRF neurons showed an increase of Fos expression induced by stimulation of right atrial mechanoreceptors, suggesting that CRF participates in the cardiovascular reflex adjustments elicited by volume loading. Activation of CRF neurons in the PVN by cardiovascular reflex is affected by osmotic stimulation. cardiac reflex; paraventricular nucleus CHANGES IN BLOOD VOLUME OR arterial and venous pressure lead to activation of physiological responses to restore cardiovascular homeostasis. These responses involve regulatory adjustments that are detected by arterial baroreceptors and cardiopulmonary mechanoreceptors (19,53). Hemorrhage produces unloading of arterial baroreceptors that initiate a reflex response to increase the sympathetic vasomotor activity and vasopressin secretion (19,52). On the other side, blood volume expansion activates atrial mechanoreceptors, with an increase of heart rate, inhibition of renal sympathetic nerve activity, and a decrease of vasopressin release (5, 30). The reflex tachycardia in response to hypervolemia was first described by Bainbridge in dogs (9), and it was also described in other species, including humans (10, 12, 34, 62).The atrial mechanoreceptors are located at the venous-atrial junction of the heart, and it is continuously signaling the central venous volume to the brain. Through vagal afferent projections, the information from the atrial mechanoreceptors reaches the nuc...