Mechanism of vascular hyperresponsiveness in the spontaneously hypertensive rat

Hyperresponsiveness of resistance vessels has been described in various vascular beds of spontaneously hypertensive rats perfused with artificial medium. This change has been attributed to altered vascular dimensions secondary to the development of hypertension. To test the possibility that true changes in sensitivity might contribute independently to vasoconstrictor hyperresponsiveness in spontaneously hypertensive rats, threshold vasoconstrictor doses of norepinephrine and barium chloride were determined in denervated hindquarters of rats perfused at constant flow with autologous blood. Threshold constrictor responses to norepinephrine were elicited in the hypertensive rats at concentrations averaging less than one-third that required in controls. Threshold vasoconstrictor concentrations of barium were not significantly different between the two groups. The ratio of norepinephrine/barium sensitivity was also significantly elevated in the hypertensive group. These data suggest that in the presence of a full humoral complement, excitability (barium sensitivity) in resistance vessels of spontaneously hypertensive rats is not altered, whereas the smooth muscle is hypersensitive to norepinephrine. Thus, it appears that changes in sensitivity as well as altered vascular geometry are important in the production of vascular hyperresponsiveness in the spontaneously hypertensive rat.