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Controlled animal study reveals persistent structural vascular alterations in immunosympathectomized hypertensive rats, suggesting an innate genetic drive for vascular remodeling.
Newborn litters of spontaneously hypertensive rats (SHR) and normotensive control rats (NCR) were identically treated with sympathetic nerve growth factor antiserum (Wellcome) which markedly interferes with adrenergic cardiovascular control (Zaimis 1967). Blood pressure, measured intermittently during 8 months, was in treated SHR (SHR is ) about 25 % higher than in NCR is , their respective pressures being about 40 % and 25 % lower than those of sham‐treated SHR and NCR.–The hindquarters of one SHR is , or NCR is , were then perfused at constant flow in parallel with those of ordinary NCR. Starting from maximal vasodilatation, resistance increases were induced by graded noradrenaline (NA) infusions, from “threshold” to maximal pressor responses. Compared to NCR is , SHR is showed an increased resistance at maximal dilatation, an increased slope of the NA dose‐response curve and an increased maximal pressor response, while their NA “thresholds” did not differ significantly. Thus, the structurally determined hemodynamic differences between ordinary SHR and NCR (Folkow et al. 1970 b) characterize also SHR is and NCR is , though to a reduced extent. Even when comparing SHR is with ordinary‐ NCR, which exhibited similar “resting” pressures, these differences partly remain, suggesting that the SHR resistance vessels might, for genetic reasons, be more prone to adapt structurally to pressure loads than those of NCR.
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Folkow et al. (1972) studied this question.
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