Key result
In rat isolated renal arteries, acetylcholine and carbachol produced a non-NO/non-PGI2 relaxation mediated by an endothelium-derived hyperpolarizing factor, possibly involving Na+-K+ ATPase activation.
Population
Rat isolated renal artery segments contracted with 0.1 microM phenylephrine and in the presence of the NO…
Design
Preclinical
Authors
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Hypothesis-generating for EDHF in renal vasodilation; leaves open human relevance and therapeutic targeting.
This preclinical study demonstrates that acetylcholine and carbachol induce NO-independent relaxation in rat renal arteries via an EDHF, likely involving Na+-K+ ATPase activation.
Jiang et al. (2000) studied Nitric oxide-independent relaxations. Carbachol and acetylcholine was evaluated on Endothelium-dependent relaxations in the presence of L-NAME. In rat isolated renal arteries, acetylcholine and carbachol produced a non-NO/non-PGI2 relaxation mediated by an endothelium-derived hyperpolarizing factor, possibly involving Na+-K+ ATPase activation.
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