Add time:07/11/2019         Source:sciencedirect.com

We investigated noncholinergic actions of 2-sec-butylphenyl N-methylcarbamate (BPMC) on the isolated rabbit thoracic aorta to help determine the mechanisms responsible for its unique toxicological properties, which are characterized by cardiovascular collapse and low lethality compared to its anticholinesterase (anti-ChE) activity. BPMC inhibited K+-induced contraction more effectively than it did norepinephrine (NE)-induced contraction. The inhibitory effect on K+-induced contraction was not altered by changing the external K+ concentration, but it was decreased by adding an L-type Ca2+ channel agonist, BAY K 8644. Simultaneous measurement of tension and cytosolic Ca2+ levels elevated by K+ stimulation revealed that BPMC decreased the Ca2+ levels prior to and parallel to the tension. The magnitude of the inhibitory effect on Ca2+ levels was increased by treating BPMC before Ca2+ application in the depolarized preparation. However, BPMC did not inhibit caffeine- or NE-induced transient contraction in Ca2+-free medium. On the other hand, BPMC produced tonic contraction in the resting aorta. The contraction to BPMC did not develop after removing the adventitia. The contraction was inhibited by phentolamine or guanethidine but not by atropine or tetrodotoxin. These results suggest that BPMC inhibits depolarization- or agonist-induced contraction by inhibiting Ca2+ entry through L-type Ca2+ channels, whereas it produces vascular contraction in the resting state by releasing NE from sympathetic nerve terminals. These apparently opposing mechanisms may contribute to the unique noncholinergic toxicological properties of BPMC.

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