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 article deals with the effect of exogenic phospholipids of vegetative origin enriched with polyunsaturated fatty acids (EPL substance) on prostaglandin release and the activity of the isolated, perfused according to Langendorf , heart of Wistar and Okamoto-Aoki rats with congenital arterial hypertension. Exogenic essential phospholipids were shown to facilitate a significant enhancement of endogenic prostaglandin release and to induce a positive inotropic, negative chronotropic and marked coronarodilating effects. These EPL effects were inhibited by indometacin and were considerably altered in rats with spontaneous hypertension. It was concluded that the cardiac effects of essential phospholipids are modulated by elevated prostaglandin secretion. The role of essential phospholipids in the prostaglandin biosynthesis regulation and the cardiac activity of rats is discussed.
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PMID:[Cardiac effects of essential phospholipids and prostaglandin release by the heart in the rat]. 623 48

The pathophysiological consequences of excess mineralocorticoid for salt status include hypertension, vascular inflammation, and cardiac fibrosis. Mineralocorticoid receptor (MR) blockade can both prevent and reverse established inflammation and fibrosis due to exogenous mineralocorticoids or endogenous glucocorticoid activation of the MR. Glucocorticoids also exert potent antiinflammatory effects via glucocorticoid receptors (GR) in the vascular wall. We propose that GR signaling may ameliorate mineralocorticoid/salt-induced vascular inflammation and fibrosis in the mineralocorticoid/salt model. In the present study, the role of GR in the mineralocorticoid/salt model was explored in uninephrectomized rats that were maintained on 0.9% saline solution to drink and treated as follows: control (CON), no further treatment; deoxycorticosterone (DOC; 20 mg/wk) for 4 wk (DOC4); DOC for 8 wk (DOC8); DOC for 8 wk plus the GR antagonist RU486 (2 mg/d) wk 5-8 (DOC8/RU486); and DOC for 8 wk plus RU486 and the MR antagonist eplerenone (EPL; 50 mg/kg.d) for wk 5-8 (DOC8/RU486+EPL). DOC treatment significantly increased systolic blood pressure, cardiac fibrosis, inflammation (ED-1-positive macrophages and osteopontin), and mRNA for markers of oxidative stress (p22phox, gp91phox, and NAD(P)H-4). GR blockade reduced the DOC-mediated increase in systolic blood pressure and the number of infiltrating ED-1-positive macrophages but had no effect on fibrosis, oxidative stress, or osteopontin mRNA levels. EPL reversed DOC-induced pathology in the absence or presence of GR blockade. Thus, blocking agonist activity at the GR neither enhances nor attenuates the fibrotic response, although it may modulate systolic blood pressure and macrophage recruitment in the mineralocorticoid/salt model.
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PMID:The role of the glucocorticoid receptor in mineralocorticoid/salt-mediated cardiac fibrosis. 1699 Mar 42