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)

Hypertension-associated growth of vascular smooth muscle cells might be mediated in vivo by platelet-derived growth factor (PDGF). Our previous investigations in hypertensive rats failed to demonstrate changes in aortic steady-state mRNA levels of PDGF A or B chains. The current studies were performed to determine whether hypertension might affect the expression of PDGF receptors. We studied PDGF alpha- and beta-receptor gene expression by Northern analysis using human and rat cDNA probes. Studies of tissue distribution revealed that PDGF beta-receptor mRNA was most abundant in total aorta and aortic media, whereas the PDGF alpha-receptor mRNA was most abundant in the lung and was expressed at low levels in aortic tissue. Deoxycorticosterone acetate (DOCA)-salt hypertension induced a threefold increase in aortic steady-state PDGF beta-receptor mRNA levels. Aortic PDGF beta-receptor expression also was higher in spontaneously hypertensive rats (SHRs) when compared with age-matched normotensive Wistar-Kyoto (WKY) controls. Aortic PDGF alpha-receptor steady-state mRNA levels were unchanged in DOCA-salt hypertension and were expressed at similar levels in WKY rats and SHRs. Unlike the findings with aorta, cardiac PDGF beta- and alpha-receptor and PDGF B-chain expressions were unchanged in the DOCA-salt model and were decreased in SHRs. These findings indicate that hypertension can increase aortic steady-state mRNA levels for PDGF beta-receptor. They also indicate that tissue-specific expression of the genes of the PDGF ligand/receptor system are differentially regulated in hypertension.
Hypertension 1991 Jun
PMID:Hypertension-induced changes of platelet-derived growth factor receptor expression in rat aorta and heart. 164 70

There is evidence that platelet derived growth factor (PDGF) is a mediator of proliferative changes in renal arteries and mesangium in human disease, in the mesangium in experimental mesangial proliferative glomerulonephritis, and in the interstitium in a rodent model of angiotensin II mediated hypertension. We utilized a monoclonal antibody to the beta-subunit of the PDGF-receptor to localize constitutive expression of this receptor in human and nonhuman primate tissues. Tissues were fixed in cold 2 or 4% paraformaldehyde, and immunohistochemical techniques both at the light microscopic level and immunoelectron microscopy were employed. In the glomerulus, there is widespread expression of this molecule by mesangial cells, and there is frequent expression on the apical and lateral surface of parietal epithelial cells. There is also widespread expression of this molecule by cortical and medullary peritubular interstitial cells, but not by glomerular or peritubular capillary endothelium or other renal parenchymal structures. The identification of receptors capable of binding PDGF B-chain at each of these sites: (1) provides a basis for PDGF mediated mesangial proliferation in human disease; (2) provides a basis for PDGF mediated interstitial cell migration and/or proliferation and/or activation at sites of tubulointerstitial injury; and (3) suggests that glomerular parietal epithelial cells may be responsive to stimulation by PDGF.
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PMID:PDGF-receptor localizes to mesangial, parietal epithelial, and interstitial cells in human and primate kidneys. 844 Dec 24

1. The present study was conducted to analyse the release and production of mitogen in cultured aortic endothelial cells of stroke-prone spontaneously hypertensive rats (SHRSP), for the further understanding of the role of arterial endothelial cells in the genesis of vascular lesions in hypertension. 2. The cultured aortic endothelial cells derived from SHRSP increased released mitogens were compared with those from control Wistar-Kyoto rats (WKY) with respect to cultured vascular medial smooth muscle cells and fibroblasts. 3. Biochemical analyses determined that the major part of mitogen released from aortic endothelial cells of both SHRSP and controls was the platelet-derived growth factor B-chain. 4. Further northern analyses revealed that the transcripts of PDGF B-chain were constitutively accumulated three- to four-fold in quiescent aortic endothelial cells from SHRSP, compared with those from WKY through passages 2 to 5. 5. However, the half-lives of the transcripts after actinomycin D treatment were 1.12 h (s.d. = 0.14, n = 4) and 1.28 h (s.d. = 0.08, n = 3), in SHRSP and in WKY, respectively, showing no significant difference. 6. These suggest that the increased accumulated transcripts of PDGF B-chain in SHRSP are due to an enhanced transcriptional rate. These enhanced release and production of PDGF-B chain in arterial endothelial cells, which may be induced under chronic hypertensive conditions, is suggested to contribute to the genesis of vascular lesion in hypertension, through the stimulation of vascular smooth muscle cell proliferation and hypertrophy.
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PMID:Platelet-derived growth factor B-chain comprises the major part of enhanced released mitogen from aortic endothelial cells of stroke-prone spontaneously hypertensive rats. 907 22

To assess the chronic in vivo effects of OPC-21268, a vasopressin-V1 receptor antagonist, on renal injury, we investigated the mRNA expressions of platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-beta1 and proliferating cell nuclear antigen (PCNA) in the glomeruli of spontaneously hypertensive rats (SHR) treated with OPC-21268 for 3 weeks. SHR aged 10 weeks were given 2% NaCl in drinking water for 3 weeks. The OPC group was fed a 0.5% OPC-21268-containing diet for 3 weeks and the control group was given a normal diet. There were no significant changes in the time course of systolic blood pressure, heart rate, urine volume, or urinary sodium, protein and N-acetyl-beta-glucosaminidase (NAG) excretion between the two groups. Serum electrolytes, protein and creatinine levels also did not differ between the groups. The mRNA expressions of PDGF B-chain, TGF-beta1 and PCNA in the glomerulus were examined using reverse transcriptase-polymerase chain reaction (RT-PCR) methods. The mRNA expressions of PDGF B-chain and PCNA among these were significantly suppressed in the OPC group. No significant differences in renal histology including the organ weights were found between the two groups; however, the glomerular size tended to be enlarged in the OPC group. These findings suggest that chronic V1-receptor blockade directly inhibits the glomerular proliferative injury of salt-loaded SHR at the established hypertension stage.
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PMID:Effects of OPC-21268, a vasopressin V1-receptor antagonist, on expression of growth factors from glomeruli in spontaneously hypertensive rats. 965 81