Why the study?
Does spontaneous hypertension alter renal vascular resistance and reactivity in rats?
Does spontaneous hypertension alter renal vascular resistance and reactivity in rats?
Spontaneously hypertensive rats exhibit higher renal vascular resistance and enhanced reactivity to vasoactive substances even in the prehypertensive stage, suggesting primary structural and functional alterations.
May indicate primary renal vascular defects in SHRSP models; leaves open translation to human hypertension.
Vascular resistance and reactivity were investigated in isolated, constant flow perfused kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) and age- and sex-matched normotensive Wistar-Kyoto control rats (WKY rats). Stroke-prone spontaneously hypertensive rats were studied at 4 wk, 2 mo, and 4 mo of age representing different stages of development of hypertension. Resistance in maximally vasodilated vascular beds was greater and the pressure-flow relationship was significantly shifted to the left in kidneys of SHRSP as compared to WKY rats. Responses to norepinephrine, vasopressin, serotonin, and angiotensin II were enhanced in the renal vascular bed of SHRSP. Dose-response curves were shifted to the left, had steeper slopes, decreased thresholds, and increased maximal responses. With longer duration of hypertension, resistance increased, the slopes of the dose-response curves were steeper, and maximum responses greater. The higher resistance and enhanced reactivity in the renal vasculature of SHRSP, already demonstrable in the prehypertensive stage appear to be due to primary structural and functional alterations of the resistance vessels.
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Berecek et al. (1980) studied this question.
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