N-Acetylprocainamide

Name: N-Acetylprocainamide
SKU: ACM32795441
Rating: 5 (1 reviews)

CAS

32795-44-1

Catalog Number

ACM32795441

Category

Other Products

Molecular Weight

277.36

Molecular Formula

C₁₅H₂₃N₃O₂

COA MSDS SDS Spec Sheet

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N-Acetylprocainamide in the Relaxation of Bovine Tracheal Smooth Muscle via K⁺ Channel Modulation

Role of K+ channels in N-acetylprocainamide-induced relaxation of bovine tracheal smooth muscle

Nakahara T, et al. European Journal of Pharmacology, 2001, 415(1), 73-78.

N-Acetylprocainamide, the primary hepatic metabolite of procainamide, has been investigated for its ability to induce relaxation in bovine tracheal smooth muscle, with emphasis on the involvement of K⁺ channels. Experimental evaluation utilized methacholine (0.3-1 μM) and high-K⁺ (40 mM) to elicit stable contractile responses. Upon reaching plateau tension, cumulative additions of N-acetylprocainamide (0.1-10 mM) were introduced into the bath medium, and concentration-response relationships were recorded. Comparative assays with procainamide confirmed reduced potency of the metabolite against methacholine-induced contractions, though N-acetylprocainamide more effectively inhibited high-K⁺-induced contraction.
To delineate channel-specific mechanisms, pharmacological blockers were applied prior to metabolite exposure. Iberiotoxin (30 nM) and Ba²⁺ (1 mM), individually or combined, significantly attenuated the relaxant effects, implicating large-conductance Ca²⁺-activated and inward rectifier K⁺ channels. In contrast, apamin (100 nM), 4-aminopyridine (300 μM), and glibenclamide (10 μM) produced no effect. These findings establish N-acetylprocainamide as a K⁺ channel-dependent modulator of airway smooth muscle tone, highlighting its experimental value in dissecting ion channel pharmacology and respiratory pharmacotherapeutics.

N-Acetylprocainamide for the Experimental Interruption of Atrial Flutter in a Sterile Pericarditis Dog Model

Effects of N-acetylprocainamide on experimental atrial flutter and atrial electrophysiologic properties in conscious dogs with sterile pericarditis

Okumura K, et al. Journal of the American College of Cardiology, 1987, 9(6), 1332-1338.

In a controlled investigation of antiarrhythmic mechanisms, N-acetylprocainamide (NAPA) was evaluated in conscious dogs with sterile pericarditis to assess its class III activity against reentrant atrial flutter. Twelve subjects underwent reproducible induction of sustained flutter, followed by intravenous NAPA administration (25 mg/kg). Electrophysiologic monitoring included atrial flutter cycle length, atrial effective refractory period (ERP), and intraatrial conduction time during programmed atrial pacing at sinus rhythm and rapid rates (150-400 beats/min). NAPA significantly prolonged cycle length (118 ± 15 to 141 ± 18 ms) and ERP (138 ± 17 to 168 ± 20 ms), effectively terminating flutter in 11/12 trials. Unlike quinidine, NAPA selectively increased conduction delay only at high pacing frequencies, suggesting rate-dependent modulation. These findings highlight its experimental utility as a class III antiarrhythmic agent capable of disrupting reentrant activity via refractory prolongation and conduction modification.

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