Reference

Inhibition of cardiac phosphodiesterases by amiloride and its N-chlorobenzyl analogs

Inhibition of cardiac phosphodiesterases by amiloride and its N-chlorobenzyl analogs. Carpenedo, Francesca; Debetto, Patrizia; Floreani, Maura; Guarnieri, Adriano; Luciani, Sisto (Dep. Pharmacol., Univ. Padova, Padua 35131, Italy). Biochem. Pharmacol., 36(5), 778-80 (English) 1987. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 7 The o-chlorobenzyl [1163-44-6] and 3',4'-dichlorobenzyl [1166-01-4] derivs. 2609-46-3 and 9068-52-4 are cas registry numbers of chemicals which are used as reagents here. of amiloride [2609-46-3] were good inhibitors of bovine heart cAMP phosphodiesterase [9036-21-9] and cGMP phosphodiesterase [9068-52-4]; whereas millimolar concns. of amiloride inhibited the enzymes, only micromolar amts. of the derivs. were required for inhibition. The cAMP-hydrolyzing enzyme was more sensitive to the inhibitors than the cGMP enzyme; the kinetics of cAMP phosphodiesterase inhibition were non-competitive. .

Mechanism of ouabain-induced contractions in guinea-pig tracheal rings

Mechanism of ouabain-induced contractions in guinea-pig tracheal rings. Espinosa-Tanguma, R.; Valle-Aguilera, J. R.; Zarazua-Garcia, O.; Navarro-Huerta, M. P.; Pecina, C.; Sanchez-Armass, S.Some commonly used reagents like 1166-01-4 and 7440-70-2 are used in this experiment. ( Departamentos of Fisiologia y Farmacologia, Facultad de Medicina, Universidad Autonoma de San Luis Potosi, San Luis Potosi, Mex.). Clinical and Experimental Pharmacology and Physiology, 31(10), 710-715 (English) 2004 Blackwell Publishing Asia Pty Ltd. CODEN: CEXPB9. ISSN: 0305-1870. DOCUMENT TYPE: Journal CA Section: 13 (Mammalian Biochemistry) Section cross-reference(s): 1 The aim of the present study was to analyze the mechanism that underlies the force development induced by ouabain (ED100 = 100 mmol/L) in guinea-pig tracheal rings. The dose-response curve showed that concns. of ouabain above 100 mmol/L evoked smaller contractions. Ouabain, at 100 mmol/L, produced two long-lasting consecutive transient contractions. The peak of the first contraction was 750 ± 75 mg, whereas the peak of the second contraction was 280 ± 46 mg. Both contractions induced by ouabain were dependent on extracellular Ca2+. Consistent with this, verapamil (10 mmol/L) inhibited the first and second contractions by 77 and 59%, resp. 3,4-Dichlorobenzamil (20 mmol/L) inhibited the first and second contractions by 68 and 97%, resp. Simultaneous exposure to 15 mmol/L sodium soln. and 100 mmol/L ouabain evoked only one transient contraction, larger (987 ± 135 mg) than either of the ouabain-induced contractions. Inhibition of the sarco-endoplasmic reticulum Ca-ATPase with cyclopiazonic acid potentiated the first and second ouabain-induced contractions by 47 and 300%, resp. Atropine (1 mmol/L) inhibited the first and second contractions by 44 and 76%, resp. In conclusion, the results of the present study are relevant to the understanding of the mechanisms by which ouabain (100 mmol/L) contracts guinea-pig tracheal rings. At the muscular level, ouabain induces Ca2+ influx through L-type Ca2+ channels and the reverse mode of the sodium-calcium exchanger. At the nerve terminals, ouabain promotes the release of acetylcholine secondary to the increase in Ca2+ influx mediated by the reverse mode of the sodium-calcium exchanger. .