The results of this study demonstrate that the spontaneously hypertensive rat is sensitive to salt excess. The hypertensinogenic effect of salt was mediated through elevation of peripheral vascular resistance. The addition of DOCA aggravated the hypertension, mainly be elevating the cardiac output without appreciably decreasing peripheral vascular resistance. SHR'S EXPOSED TO 1% NaCl consumed more fluids and excreted more sodium and urine than control rats. Those exposed to 1% NaCl and DOCA had higher fluid consumptions and excreted more sodium than the other two groups. These effects of sodium in a neurogenic strain of hypertensive rats suggest a possible interplay between the neurogenic and salt-dependent components in the development and maintenance of hypertension. They also suggest that SHRs, like other hypertensive rat models, are salt sensitive.