nitrophenols and Cardiomyopathies

The T-type Ca2+ channel (TCC) is activated, and abnormalities of the TCC may be related to the pathogenesis of Ca2+ overload, in cardiomyopathic hamster hearts. The aims of the present study were to investigate the alteration in expression of the TCC and to examine the effects of a dual L-and T-type Ca2+ channel blocker, efonidipine (EFO), on cardiac function and TCC during development of heart failure in UM-X7.1 cardiomyopathic hamsters.. UM-X7.1 and golden hamsters were examined, and EFO was administered at the age of 20 weeks for 4 weeks. Cardiac function was examined, the expression of TCCalpha1G was measured, and ventricular myocytes were subjected to a patch-clamp study. At 24 weeks, vehicle-treated UM-X7.1 hamsters exhibited significant increases in left ventricular (LV) size, with marked decreases in ejection fraction (LVEF) compared with golden hamsters. In the UM-X7.1 group, the expression of TCCalpha1G increased during development of heart failure compared with the golden hamster group. In the UM-X7.1 group, EFO treatment significantly attenuated the decrease of LVEF without affecting blood pressure compared with the vehicle group. EFO treatment decreased heart rate (by approximately 10%) in both groups. In the golden hamster group, EFO treatment did not affect LV function. The TCC current in ventricular myocytes was significantly increased in UM-X7.1, and was inhibited by EFO in a dose-dependent manner.. In cardiomyopathic hamster hearts, abnormalities in the TCC may be at least in part related to the pathogenesis of abnormal Ca2+ homeostasis, and TCC-blocker treatment may decrease the TCC current, resulting in an improvement of cardiac function. TCC blocker therapy might be a new strategy for certain types of heart failure.

Topics: Animals; Blood Pressure; Calcium Channel Blockers; Calcium Channels, L-Type; Calcium Channels, T-Type; Cardiomyopathies; Cricetinae; Dihydropyridines; Disease Models, Animal; Dose-Response Relationship, Drug; Electrophysiology; Female; Heart Rate; Male; Mesocricetus; Myocytes, Cardiac; Natriuretic Peptide, Brain; Nitrophenols; Organophosphorus Compounds; Patch-Clamp Techniques

The cardiovascular effects of porins were evaluated using porins isolated from Salmonella typhimurium SH5014. In dogs porins depress arterial systemic pressure, vasomotor reactivity of norepinephrine and peripheral vagal stimulation. They are capable of modifying the sinocarotidal baroreceptor reactivity. In mice porins increase the cardiotoxic effects of isoprenaline, thyroxine, emetine and of p-nitrophenol. In rats porins increase the arrhythmogenic and lethal effects of BaCl2 and also give rise to renal lesions, probably at the tubular level.

Topics: Animals; Bacterial Outer Membrane Proteins; Barium; Barium Compounds; Blood Pressure; Cardiomyopathies; Chlorides; Dogs; Drug Synergism; Electrocardiography; Emetine; Heart Rate; Isoproterenol; Kidney; Male; Mice; Nitrophenols; Porins; Rats; Respiration; Salmonella typhimurium; Thyroxine