Key result
Stroke-prone hypertensive rats show ~2-fold greater endothelin-1 binding across major organs versus normotensive controls.
Why the study?
The mechanism by which severe hypertension and stroke develop in salt-loaded stroke-prone spontaneously hypertensive rats remains unclear, particularly regarding endothelin-1 binding.
Effect estimate: 1.5- to 2.1-fold greater Bmax
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Upregulated ET-1 binding in SHRsp tissues may implicate the pathway in salt-loaded hypertension and stroke; leaves open therapeutic relevance pending prospective studies.
Savage et al. (2002) studied Hypertension and stroke (animal model). Stroke-prone spontaneously hypertensive rat (SHRsp) strain vs. Normotensive Wistar-Kyoto rats (WKY) was evaluated on [125I]ET-1 binding (Bmax and KD values) in brain, heart, kidney, liver, and spleen (1.5- to 2.1-fold greater Bmax). Endothelin-1 binding (Bmax) in the brain, heart, kidney, and liver of stroke-prone spontaneously hypertensive rats was 1.5- to 2.1-fold greater than in normotensive Wistar-Kyoto rats.
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