Amlodipine has been shown to prevent decrease in vascular responsiveness induced by injection of Salmonella typhosa lipopolysaccharide (LPS); however, there is no study reporting if this protection by amlodipine extends to ventricular contractility. Therefore, we have investigated in rat isolated right ventricle strips contracted by electrical stimulation (1 and 3 Hz and subsequently 1 Hz) whether pre-treatment with amlodipine (15 mg/kg orally for 1 week) precludes the decrease in ventricular contractility related to the induction of nitric oxide synthase stimulated by LPS injection (4 mg/kg intraperitoneally). The induction of septic shock was confirmed in isolated aortic rings from LPS-injected rats by verifying that the contractile response to 1 microM noradrenaline had been (i) decreased after LPS injection and (ii) markedly potentiated by the addition of 10 microM l-arginine. The injection of saline to untreated and amlodipine-treated rats produced a non-significant effect on right ventricular contractility during 180 min. at 3 Hz; the recovery of the contractile response was improved when the stimulation frequency was subsequently returned to 1 Hz after 30 min. In contrast, injection of LPS to untreated and amlodipine-treated rats (amlodipine + LPS) produced a decrease in right ventricular contractility during 180 min. at 3 Hz, an effect that was more pronounced in LPS than in amlodipine-treated rats. These ex vivo results obtained after LPS injection suggest that amlodipine may have inhibited, at least in part, the induction of nitric oxide synthase with a resulting preclusion of the cardiovascular failure produced by septic shock.