The unchanged sensitivity to endothelin-1 and unspecifically increased reactivity in the mesenteric vascular beds of spontaneously hypertensive rats suggest that hyperreactivity to endothelin-1 may not be a primary mechanism in genetic hypertension.
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ET-1 hyperreactivity without sensitivity change in SHR MVBs suggests it is not primary in genetic hypertension; leaves open its role in human disease.
Criscione et al. (1992) studied this question.
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