Renal vascular resistance and reactivity in the neurogenic hypertensive rat

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Abstract
Increased sympathetic nervous system activity in the kidney was postulated as a possible etiologic factor in some forms of hypertension. The possibility of a chronic increase in neurogenic renal vasoconstriction in an experimental model with increased nervous activity would be expected; neurogenic hypertension resulting from partial baroreceptor deafferentation was studied. 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 2 groups. Chronic increase in neurogenic renal vascular resistance was apparent in hypertensive rats. Since renal vascular responses to direct renal nerve activation, norepinephrine and other exogenous vasoactive hormones were not altered in the hypertensive rats, and increased neurogenic vasoconstriction was probably the result of increased renal nerve discharge. Unaltered neurotransmission and reactivity indicated a failure of renal nerves or blood vessels to adapt to increased nervous activity. Increased renal sympathetic nerve activity could result in sustained neurogenic renal vasoconstriction and contribute to development of hypertension.