Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate how blocking functional endothelin-converting enzyme activity may offer a new approach to inhibition of changes in pulmonary vessels reactivity due to development of hypoxia-induced pulmonary arterial hypertension in rats. This data shows that treatment with endothelin-converting enzyme blocker PP36 significantly reduced pathological changes due to hypoxia-induced pulmonary hypertension. One of the reasons may be the increased production and role of nitric oxide in pulmonary artery tone.
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PMID:[Chronic theatment with an endothelin-converting enzyme inhibitor reduces the development of hypoxia-induced pulmonary hypertension in rat]. 1876 89

The aim of the study was to evaluate the effect of chronic inhibition of endothelin-1 (ET-1) synthesis on renovascular hypertension development. Male Wistar rats were subjected to an operation, according to the "1 kidney, 1 clip" method and were given an endothelin-converting enzyme inhibitor PP36 per os with drinking water for 4 weeks. Serum urea rose by 21% in hypertensive rats and by 44% in PP36 treated hypertensive rats. PP36 treatment resulted in blood pressure rise both in the Sham group (compared to the initial blood pressure level) and in hypertensive rats (compared to hypertensive control group). Significant reduction of circulating ET-1 after chronic PP36 administration by 28% was obtained only in normotensive, but not hypertensive rats. Circulating ET-1 was not altered in hypertensive rats, but ET-1 excretion rate was significantly enhanced by 90%, which was abolished by PP36. We suggest that chronic reduction of ET-1 synthesis in the kidney might lead to water and salt retention.
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PMID:[Protective effect of endothelin-1 in goldblatt "one-kidney, one-clip" hypertension]. 2307 31