Increased sympathetic nervous system activity in the kidney has been postulated as a possible etiologic factor in some forms of hypertension. The present investigation sought to document the possibility of a chronic increase in neurogenic renal vasoconstriction in an experimental model in which increased nervous activity would be expected--neurogenic hypertension resulting from partial baroreceptor deafferentation. In anesthetized rats with chronic neurogenic hypertension, renal vascular resistance was significantly higher than in sham-operated rats. After acute renal denervation, there was no statistically significant difference in renal vascular resistance between the two groups. Thus, a chronic increase in neurogenic renal vascular resistance was apparent in the hypertensive rats. Since renal vascular responses to direct renal nerve activation, norepinephrine, and other exogenous vasoactive hormones were not altered in the hypertensive rats, the increased neurogenic vasoconstriction was probably the result of increased renal nerve discharge. Unaltered neurotransmission and reactivity further indicated a failure of the renal nerves or blood vessels to "adapt" to increased nervous activity. These results support previous suggestions that increased renal sympathetic nerve activity could result in sustained neurogenic renal vasoconstriction and thereby contribute to the development of hypertension.