One possible explanation for the salt sensitivity of blood pressure (BP) in certain hypertensive individuals is that neural mechanisms which normally counteract the pressor effect of a high dietary sodium intake are defective. We have tested this possibility in normotensive Wistar-Kyoto rats (WKY) by surgically ablating the arterial baroreflex mechanism. This manoeuvre, by itself, conferred substantial salt-sensitivity on the WKY rats whose BP is normally relatively insensitive to dietary sodium intake. The treated rats responded to a high sodium diet with a significant rise in systolic BP which was reversed by substituting a low sodium diet. Thus, impaired baroreflex function which has been observed in essential hypertension and in hypertensive animals, may be responsible for the hypertensive effect of sodium.