Disease relevance of SA 466

• Spironolactone (25 mg/kg/day, p.o.) and kallidinogenase (25 KU/day, i.m.) also showed beneficial effects on glomerular histopathological changes and hypertension, although both drugs were not as effective as SA-446 [1].
• Reproductive toxicity studies of rentiapril [2].
• An i.v. administration of SA-446 at a dose of 1 mg/kg induced a considerable hypotension in both types of hypertensive rats and increased the flow rates in most organs, along with an increase of cardiac output [3].

High impact information on SA 466

• In the patients with RVH, blood pressure was significantly reduced more quickly and for longer periods by rentiapril than by captopril or alacepril; in the patients with EH, alacepril was the most potent antihypertensive agent [4].
• The renal excretory mechanism of an orally active inhibitor of angiotensin converting enzyme (SA-446) was examined in anesthetized dogs [5].
• These results suggest that the antinephritic effect of SA-446 may be related to the antihypertensive action and the increase in renal blood flow through activation of the kallikrein-kinin and prostaglandins systems [1].
• Intrarenal infusion of the larger dose of SA-446 (0.1 mg/min) caused an increase in RBF, urine flow and renin release and caused a fall in blood pressure [6].
• Effects of angiotensin I-converting enzyme inhibitor (SA-446) on renal function in dogs [6].

Chemical compound and disease context of SA 466

• Toxicity study of the angiotensin converting enzyme inhibitor rentiapril in rats [7].

Biological context of SA 466

• Administration of indomethacin (13 mg/kg i.v.) suppressed natriuresis and, to some extent, the renal vasodilation caused by SA-446 [8].
• The blood pressure dropped after i.v. injection of SA-446, while the regional blood flow increased [9].

Anatomical context of SA 466

• Rentiapril at the highest dose of 1000 mg/kg caused low food consumption and death of some animals with signs of bloody feces and anemia [7].
• The haemodynamics of the inner ear and other organs and the effects of a converting-enzyme inhibitor (SA-446) on the regional blood flow were compared among NR, SHR, and RHR, the blood pressure being 107, 152, and 185 mm Hg, respectively [9].

Associations of SA 466 with other chemical compounds

• The magnitude of falls in plasma angiotensin II and aldosterone concentration induced by MK 421, SA 446 and captopril was not significantly different between both regular and low sodium diets [10].
• Comparison of the acute effects of three structurally different converting enzyme inhibitors (captopril, SA-446 and MK-421) on blood pressure, the renin-angiotensin system and the kallikrein-kinin system [11].
• Pharmacological properties of (2R,4R)-2-(o-hydroxyphenyl)-3-(3-mercaptopropionyl)-4- thiazolidinecarboxylic acid (rentiapril, SA 446), a potent inhibitor of angiotensin converting enzyme, were examined [12].
• The bullfrog renal HHL hydrolyzing activity was completely inhibited by typical ACE inhibitors, ethylenediamine tetraacetic acid (10(-3) M), captopril (10(-5) M), SA-466 (10(-5) M) and MK-422 (10(-6) M) [13].

Gene context of SA 466

• The effects of an orally active inhibitor of angiotensin-converting enzyme (SA-446) on systemic arterial pressure, renal function and renin release were examined in anesthetized dogs [6].

Analytical, diagnostic and therapeutic context of SA 466

• Pretreatment with SA 446 plus nephrectomy did not cause any further change in irAng II release as compared with that with SA 446 alone [14].
• Determination of SA-446 in human whole blood and urine by electron capture-gas liquid chromatography [15].
• Intravenous infusion of SA-446 (1 mg/min) decreased systemic blood pressure and increased renal blood flow in anesthetized dogs [8].
• These results indicate that the no-effect dose of rentiapril in rats by three months oral administration is 30 mg/kg in female and 125 mg/kg in male, and suggest that, like other ACE-inhibitors, this compound also has a toxic potential to affect renal tissues [7].

References