Reference

Antihypertensive effects of temocapril hydrochloride (CS-622), a novel angiotensin converting enzyme inhibitor

Antihypertensive effects of temocapril hydrochloride (CS-622), a novel angiotensin converting enzyme inhibitor. Nishino, Hiroshi; Oizumi, Kiyoshi; Ikeda, Keiko; Miyamoto, Masaaki; Koike, Hiroyuki (Biol. Res. Lab., Sankyo Co., Ltd., Japan). Yakuri to Chiryo, 20(1), 21-9 (Japanese) 1992. CODEN: YACHDS. ISSN: 0386-3603. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The purpose of this study was to examine and compare the antihypertensive effect of temocapril hydrochloride (temocapril, CS-622) with that of enalapril in renal hypertensive (RHR), spontaneously hypertensive (SHR), DOCA-salt hypertensive (DOCA) and normotensive rats. Temocapril and enalapril were orally administered to these rats and mean blood pressure was monitored for 24 h by a direct method. The antihypertensive effect of temocapril was, as compared with enalapril, more potent in RHR, SHR and normotensive rats. In RHR, temocapril was 2-3 times more potent than enalapril and the onset of action was rapid. Temocapril produced a slight decrease of blood pressure in DOCA rat. These results suggest that the agent can be used on a once day regime in clin. settings.Except for chemicals metioned above, 111902-57-9 and 75847-73-3 are also used. .

Temocapril treatment upregulated cardiomyocyte thioredoxin expression and improved autoimmune myocarditis

Temocapril treatment upregulated cardiomyocyte thioredoxin expression and improved autoimmune myocarditis. Yuan, Zuyi; Liu, Yan; Kishimoto, Chiharu; Shioji, Keisuke; Yodoi, Junji; Liu, Zhiquan (The First Hospital, Xian Jiaotong University, Xian, Shanxi Province 710061, Peop. Rep. China). Zhonghua Neike Zazhi (Beijing, China), 42(5), 309-312 (Chinese) 2003 Zhonghua Yixuehui Zazhishe. 111902-57-9 and 9015-82-1 are cas registry numbers. These chemicals are also mentioned in this article. CODEN: CHHNAB. ISSN: 0578-1426. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) This study was carried out to investigate whether temocapril, a novel non-sulfhydryl contg. Angiotensin-converting enzyme inhibitor (ACEI), reduces the severity of myocarditis via redox regulation mechanisms involving t thioredoxin (TRX). The up-regulation of TRX by temocapril treatment was checked by Western blot in normal rat myocytes in vitro and in vivo, as well as in rats with exptl. autoimmune myocarditis (EAM). Results showed that temocapril enhanced cytosolic redox regulatory protein TRX expression, but neither mitochondrial TRX2 nor antioxidant enzymes, such as copper-zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) expression, was up-regulated by the preconditioning treatment. In rats with EAM, the severity of myocarditis and the protein carbonyl contents were less increased with temocapril treatment (10 mgkg-1d-1, orally) from day 1 to day 21, but not in temocapril treatment from day 15 to day 21. If the characteristics of this model that myocardial inflammation begins around day 15 and keeps on until day 21 is considered, temocapril treatment for 3 wk might be thought as a preconditioning treatment. It was conclusion that TRX and the redox state modified by TRX may play a crucial role in the pathophysiol. of EAM. Temocapril ameliorates myocarditis with inducing TRX up-regulation in a preconditioning manner, although the mechanism of TRX up-regulation by temocapril remains to be elucidated. .