Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.3 (HSD)
3,464 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to examine the role of endothelin-A (ET(A)) receptors in mediating the hypertension and renal injury associated with high salt intake in Dahl salt-sensitive (DS) rats. To achieve this goal, we examined the effects of chronic selective ET(A) antagonist (A-127722) treatment at a dose of 10 mg/kg/d on arterial pressure, renal function, and morphology in DS and Dahl salt-resistant (DR) rats placed on a high sodium (8% NaCl) diet (HSD) for 3 weeks. Placement of DS rats (n=13) on HSD for 3 weeks caused a progressive increase in systolic pressure (from 118+/-3 to 186+/-15 mm Hg). The increase in systolic pressure was significantly attenuated (from 125+/-4 to 167+/-12 mm Hg) in DS rats treated with A-127722 (n=13). Mean arterial pressure (MAP) measured directly at the end of the study was also significantly lower by 18 mm Hg (P<.02) in the DS rats treated with A-127722. The slope of the chronic pressure-natriuresis curve was shifted to the right in DS rats and to the left by chronic ET(A) receptor blockade in DS rats. The hypertension in DS rats was associated with marked proteinuria (from 4.1+/-1.1 to 74.3+/-5.3 mg/24 h/100 g body weight) that was significantly attenuated (from 5.7+/-1.2 to 55.2+/-6.5 mg/24 h/100 g body weight) in DS rats treated with A-127722. The percentage of glomeruli displaying fibrosis, hypercellularity, and hyalinization was also significantly reduced after treatment with A-127722 in DS rats. Arterial pressure, protein excretion, renal hemodynamics, and morphologic structure were not significantly changed in response to ET(A) receptor blockade in DR rats placed on HSD. These data indicate that endothelin-A receptor activation may play a role in the exacerbation of hypertension and development of renal injury in DS rats.
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PMID:Endothelin-A receptor antagonism attenuates the hypertension and renal injury in Dahl salt-sensitive rats. 945 35

Conventional parameters are often inadequate to describe the dynamic flow changes in microcirculation. We used a novel approach to characterize oscillatory flow conditions in a canine model of hemorrhagic shock. Microcirculation in the ileal mucosal villi was visualized using intravital microscopy with the orthogonal polarization spectral imaging technique. The distribution of red blood cell velocity (RBCV) was estimated from the relative time periods of observed RBCV, and the average RBCV (A-RBCV) and its SD were then computed from the first and second moments of the RBCV distribution, respectively. Hemorrhagic shock (for 60 min) was followed by resuscitation with saline, hypertonic saline-Dextran solution (HSD, 7.2% NaCl-10% Dextran, 4 mL/kg), or HSD supplemented with the selective endothelin-A receptor antagonist ETR-p1/fl peptide (100 nmol/kg), respectively. The macrohemodynamic derangement (70% decrease in cardiac index and ileal blood flow) during shock was associated with the appearance of flow motion in the villi and an enhanced endothelin-1 release. The calculated A-RBCV was decreased by 40%. At resuscitation onset, continuous flow periods were transiently seen in 33%, 40%, and 50% of the experiments after saline, HSD, and HSD + ETR p1/fl treatment, respectively. HSD with or without endothelin-A antagonist treatment resulted in an increased relative duration of high-flow periods (by 20%) and a significant, 20% to 40% rise in A-RBCV. These results demonstrate that time-wise variability of RBCV should be used for the analysis of oscillatory flow conditions. The probabilistic estimation of A-RBCV provides a quantitative basis for comparison of the effectiveness of different resuscitation or vasoactive strategies.
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PMID:Flow motion in the intestinal villi during hemorrhagic shock: a new method to characterize the microcirculatory changes. 1517 32