The increased vascular reactivity in spontaneously hypertensive rats appears to be related to a membrane or cellular defect facilitating Ca2+ availability, rather than being secondary to elevated peripheral resistance and hypertrophy.
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Intrinsic Ca2+ defect may drive SHR vascular reactivity; leaves open relevance to human hypertension or beta-blocker therapy.
Goldberg et al. (1978) studied this question.
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