Stroke-prone spontaneously hypertensive rats exhibited enhanced renal vascular resistance and reactivity that was not prevented by neonatal sympathectomy, suggesting a primary pathogenic mechanism.
Alterations in vascular reactivity were assessed in isolated artificially perfused kidneys from stroke-prone spontaneously hypertensive (spSH) rats at different stages of hypertension and after neonatal sympathectomy with 6-hydroxydopamine (6-OHDA). 2. During the pre-hypertensive stage, and the early and chronic stages of hypertension, the responses to noradrenaline, vasopressin, serotonin and angiotensin II were enhanced in renal vascular beds from spSH animals compared with age- and sex-matched Wistar-Kyoto (WK) rats; dose-response curves were shifted to the left, had steeper slopes, greater maximal responses and decreased thresholds. 3. With increasing severity and duration of hypertension, renal vascular resistance at maximal vasodilatation increased, the slopes of the dose-response curves were steeper and maximal responses were greater. 4. Neonatal sympathectomy with 6-OHDA greatly attenuated but did not prevent the eventual development of hypertension; furthermore, this treatment had no effect on the enhanced resistance or reactivity in renal vascular beds from spSH rats. 5. The appearance of enhanced resistance and reactivity in the early stages of hypertension and the inability to prevent these vascular changes by neonatal sympathectomy suggest that these alterations are a primary pathogenic mechanism in spSH rats.
Berecek et al. (1979) studied Spontaneous hypertension. Neonatal sympathectomy with 6-hydroxydopamine (6-OHDA) vs. Untreated spSH rats and Wistar-Kyoto (WK) rats was evaluated on Vascular reactivity and renal vascular resistance. Stroke-prone spontaneously hypertensive rats exhibited enhanced renal vascular resistance and reactivity that was not prevented by neonatal sympathectomy, suggesting a primary pathogenic mechanism.