Increased reactivity to endothelin-1 in the mesenteric vascular beds of spontaneously hypertensive rats is likely due to structural vascular changes rather than a primary hypertensive mechanism, and is only partially dependent on voltage-operated calcium channels.
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Supports structural vascular changes as driver of endothelin hyperreactivity in SHR; leaves open relevance to human hypertension.
Criscione et al. (1990) studied this question.
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