Key result
Human vertebral arteries from treated hypertensive patients contract in response to high concentrations of acetylcholine, whereas those from normotensive patients remain maximally dilated.
Why the study?
Does acetylcholine induce contraction rather than dilatation in vertebral arteries from treated hypertensive patients, and is this mediated by endothelin?
Observational
Does acetylcholine induce contraction rather than dilatation in vertebral arteries from treated hypertensive patients, and is this mediated by endothelin?
The normal dilator response to acetylcholine is abrogated and replaced by contraction in vertebral arteries from treated hypertensive patients, a mechanism independent of endothelin-1.
Answers are grounded in this paper and cite their sources.
Paradoxical contraction to acetylcholine signals persistent endothelial dysfunction in treated hypertension; leaves open its cerebrovascular impact and endothelin-independent mechanisms.
Endothelium-dependent vasodilatation to acetylcholine is abnormal in animal models of hypertension. This abnormality reflects a change in the balance of relaxing and contracting factors produced in the vascular wall. In human cerebral arteries, endothelin has been implicated in the abnormal vasoconstrictor response following subarachnoid hemorrhage. This study tests the hypothesis that cerebral arteriolar dilatation to acetylcholine reduced in clinical hypertension due to an overproduction of endothelin. Our results show that at high concentrations of muscarinic agonist (0.3-3 microM), human vertebral arteries from hypertensive patients contract whereas those from normotensive patients remain maximally dilated. We conclude that the normal dilator response to acetylcholine is abrogated in vertebral arteries from treated hypertensive patients but endothelin-1 does not contribute to the abnormal responsiveness.
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Charpie et al. (1996) conducted an observational in Hypertension. Treated hypertension vs. Normotension was evaluated on Arterial contraction/dilatation response to acetylcholine. Human vertebral arteries from treated hypertensive patients contract in response to high concentrations of acetylcholine, whereas those from normotensive patients remain maximally dilated.
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