Reticuline is an anti-inflammatory and antihypertensive natural product that reduces JAK2/STAT3 and NF-κB phosphorylation levels, inhibits TNF-α and IL-6 mRNA expression, thereby alleviating oedema in rats.

In intact endothelium aortic rings, reticuline (3 μM-1.5 mM) concentration-dependently inhibited phenylephrine- and KCl (80 mM and 30 mM)-induced contractions, with IC50 values of 40±10, 240±40, and 300±40 μM, respectively [2].
After endothelium removal, the inhibitory effect of reticuline on phenylephrine-induced contraction was significantly attenuated, with an IC50 value of 250±70 μM [2].
In the presence of L-NAME (100 or 300 μM) or atropine (1 μM), the vasorelaxant effect of reticuline was also markedly reduced [2].
Reticuline further suppressed CaCl2-induced contraction and calcium transients triggered by the release of intracellular calcium stores sensitive to depolarizing agents such as phenylephrine, but did not affect caffeine-sensitive calcium stores [2].

Reticuline (5, 10, and 20 mg/kg, intravenous injection) induced significant hypotensive responses in normotensive Wistar rats, accompanied by increased heart rate. After pretreatment with L-NAME or atropine, the hypotensive effect and tachycardia caused by reticuline were markedly attenuated or even completely abolished [2].