Population
Cultured spontaneously hypertensive rat-derived vascular smooth muscle cells or aortic adventitial fibroblasts
Design
Review
Authors
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Excludes early receptor/signaling defects in SHR vascular hyperplasia; leaves open distal events as focus for hypertension mechanism studies.
The abnormal hyperproliferation of vascular cells in spontaneously hypertensive rats is likely driven by distal events in cell growth signaling rather than early receptor-mediated pathways.
Marche et al. (1995) studied this question.
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