The Bigenelli acid catalyzed condensation of 2-trifluoromethylbenzaldehyde (1), urea (2) and an alkyl acetoacetate (3) afforded the respective alkyl (Me, Et, i-Pr, i-Bu) 6-methyl-4-(2-trifluoromethylphenyl)-1,2,3,4-tetrahydro-2H-pyrimidine-2-one-5-carboxylate (4-7). Subsequent N 3 -nitration of the alkyl esters (4-7) using Cu(NO 3 ) 2 •3H 2 O and Ac 2 O furnished the target alkyl 6-methyl-3-nitro-4-(2-trifluoromethylphenyl)-1,2,3,4-tetrahydro-2H-pyrimidine-2-one-5-carboxylates (8-11). The N 3 -nitro compounds (8-11) were less potent calcium channel antagonists (IC 50 values in the 1.9 x 10 -7 to 3.9 x 10 -6 M range) on guinea pig ileal longitudinal smooth muscle than the reference drug nifedipine (Adalat®, IC 50 = 1.4 x 10 -8 M). In vitro calcium channel modulation studies on guinea pig left atrium (GPLA) showed that the methyl and ethyl esters (8-9) induced a weak-to-modest positive inotropic (agonist) effect, and that the inactive isopropyl (10) and isobutyl (11) esters did not alter the cardiac contractile force of GPLA.