Key result
In rats, 15 nM ANG II blocked the PGE2-mediated increase in substance P release (from 7 to 19 pg/min) by suppressing adenylyl cyclase activation via a pertussis toxin-sensitive mechanism.
Population
Rats fed low- and high-sodium diets (renal pelvic tissue preparations and in vivo models)
Comparison
Pharmacological manipulation with PGE2, ANG II… vs Basal conditions or absence of specific…
Design
Preclinical
Authors
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Renal ANG II may inhibit sensory nerve activation in rats; leaves open its role in human hypertension or kidney disease.
Renal pelvic ANG II modulates the responsiveness of renal sensory nerves by suppressing PGE2-mediated activation of adenylyl cyclase via a pertussis toxin-sensitive mechanism.
Kopp et al. (2003) studied this question. Angiotensin II vs. Basal/Vehicle was evaluated on Substance P release. In rats, 15 nM ANG II blocked the PGE2-mediated increase in substance P release (from 7 to 19 pg/min) by suppressing adenylyl cyclase activation via a pertussis toxin-sensitive mechanism.
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