Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacological interruption or genetic disruption of the renin-angiotensin system before completion of nephrogenesis produces papillary atrophy and an impaired urinary concentrating ability. The mechanisms involved are yet to be elucidated, but renal hypoperfusion and subsequent ischemia, particularly to the immature renal medulla, may be hypothesized. The acute intrarenal responses to angiotensin-converting enzyme (ACE) inhibition in the newborn piglet were thus investigated by means of regional blood flow distribution, renal interstitial hydrostatic pressure (RIHP), and medullary oxygen tension (PO2) in the anesthetised 4- to 5-day-old piglet. Moreover, the calcium antagonist nifedipine and the nitric oxide synthesis inhibitor L-NAME were also given in order to reduce renal blood flow by other means. The drugs were given intravenously in equipotent pressor doses, mimicking intraperitoneal injections in neonatal rats. Enalaprilat (200 microg/kg) reduced mean arterial pressure (MAP) by 14+/-10% (mean+/-SD, P=0.006) and RIHP by 18+/-18% (P=0.001), whereas total renal blood flow and medullary PO2 remained unchanged. In contrast, nifedipine (0.5 mg/kg) reduced MAP and RIHP by 39+/-8% and 38+/-14%, respectively, total and regional blood flows by 30%-60%, and medullary PO, by 46+/-29% (P=0.001). Acute administration of L-NAME (15 mg/kg) increased MAP by 27+/-10% (P=0.0005), whereas RIHP and renal blood flow decreased by 20%-50%, resulting in a reduction of the medullary PO2 by 10+/-12% (P=0.05). We conclude that the renal abnormalities observed after neonatal ACE inhibition are not likely to be caused by renal ischemia.
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PMID:Acute renal responses to angiotensin-converting enzyme inhibition in the neonatal pig. 1104 89

Exposure to mercury at nanomolar level affects cardiac function but its effects on vascular reactivity have yet to be investigated. Pressor responses to phenylephrine (PHE) were investigated in perfused rat tail arteries before and after treatment with 6 nM HgCl2 during 1 h, in the presence (E+) and absence (E-) of endothelium, after L-NAME (10(-4) M), indomethacin (10(-5 )M), enalaprilate (1 microM), tempol (1 microM) and deferoxamine (300 microM) treatments. HgCl2 increased sensitivity (pD2) without modifying the maximum response (Emax) to PHE, but the pD2 increase was abolished after endothelial damage. L-NAME treatment increased pD2 and Emax. However, in the presence of HgCl2, this increase was smaller, and it did not modify Emax. After indomethacin treatment, the increase of pD2 induced by HgCl2 was maintained. Enalaprilate, tempol and deferoxamine reversed the increase of pD2 evoked by HgCl2. HgCl2 increased the angiotensin converting enzyme (ACE) activity explaining the result obtained with enalaprilate. Results suggest that at nanomolar concentrations HgCl2 increase the vascular reactivity to PHE. This response is endothelium mediated and involves the reduction of NO bioavailability and the action of reactive oxygen species. The local ACE participates in mercury actions and depends on the angiotensin II generation.
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PMID:Low nanomolar concentration of mercury chloride increases vascular reactivity to phenylephrine and local angiotensin production in rats. 1809 79