Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific features of antihypertensive action of two new isoprenoid compounds, i.e. 5-nicotinooxymethyl -gamma - tocopherylnicotinate (NNT) and decaprenoic ethylester (EDP) were studied in rats. NNT and EDP were very similar to each other in their pharmacological features as far as we studied. Both NNT and EDP did not affect blood pressure in normotensive animals but significantly reduced blood pressure in SHR and DOCA/salt hypertensive animals in the acute studies with single dosing of 1 to 10 mg/kg (p.o.). Their antihypertensive action was mild but long-lasting and cumulated by the repeated administration. The chronic administration of NNT and EDP at oral doses of 0.2 and 2 mg/kg once a day completely suppressed the development of hypertension in rats unilaterally nephrectomized and treated with DOCA/salt and in SHR which were unilaterally ureter-ligated to accelerate the progress of their genetic hypertension. The mechanism of their antihypertensive action remains to be solved.
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PMID:Antihypertensive actions of isoprenoids. 707 84

Tubular cell damage is an important mediator of interstitial fibrosis in chronic renal diseases. Glomerular and tubular damage in genetic hypertension was therefore studied. Tubular and glomerular damage was investigated in 10-, 40-, and 70-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and compared with glomerular capillary pressure (P(GC)) and glomerulosclerosis in superficial (OC) and juxtamedullary (JMC). Tubular vimentin was used as criterion of tubular damage. Variation in tubular diameter was measured during change in perfusion pressure, and ureter ligation was used to demonstrate the relationship between tubular pressure and appearance of vimentin-positive cells. Tubular and glomerular damage was most pronounced in JMC and greater in SHR than in WKY. It was absent in 10-wk-old WKY and significantly higher in JMC of SHR compared with WKY at 70 wk of age. Numbers of vimentin-positive segments were 18 +/- 9 vs. 38 +/- 7% in JMC of 70-wk-old WKY and SHR (P < 0.02), and glomerulosclerosis was seen in 8 +/- 3 vs. 19 +/- 5% of glomeruli in JMC of 70-wk-old WKY and SHR, respectively (P < 0.01). P(GC) was 45 +/- 3 mmHg in JMC of WKY and 57 +/- 3 mmHg in JMC of 70-wk-old SHR (P < 0.001). Tubular diameter variation was greatest in SHR (P < 0.05) during pressure variation. Proteinuria was present only in 40- and 70-wk-old SHR and did not correlate with tissue damage. Tubular and glomerular damage in both strains develops in parallel and may be caused by a common mechanism, which may be glomerular capillary and tubular wall stretch during acute blood pressure variation which is greatest in JMC in SHR.
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PMID:Glomerular and tubular damage in normotensive and hypertensive rats. 1553 68