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)

HBP-1 is a sequence-specific DNA-binding protein that interacts with the hexameric sequence ACGTCA, the putative cis-acting element of the wheat histone H3 gene. Gel mobility shift and DNase I footprint analyses showed that this protein interacts with homologous sequences in the regulatory regions for the transcription of the cauliflower mosaic virus (CaMV) 35S RNA and nopaline synthase (NOS) genes, evidence that HBP-1 may bind to hexameric sequences in the regulatory regions of various genes. An HBP-1-like protein, indistinguishable from wheat HBP-1 in its the DNA-binding specificity, is present in sunflower nuclear extract, an indication that HBP-1-like DNA-binding proteins also exist in dicots.
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PMID:Wheat nuclear protein HBP-1 binds to the hexameric sequence in the promoter of various plant genes. 260 42

A novel DNA-binding protein that specifically interacts with the hexameric sequence ACGTCA in the regulatory region of the wheat histone H3 gene has been identified in wheat nuclear extract and designated HBP-1a. The nuclear protein HBP-1 previously identified as a DNA-binding protein that interacts with hexameric sequences in the H3, cauliflower mosaic virus (CaMV) 35 S RNA, and nopaline synthase (NOS) promoter regions therefore has been renamed HBP-1b. The flanking sequences that surround the hexameric sequence may account for the difference in the binding properties of HBP-1a and HBP-1b.
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PMID:Multiplicity of the DNA-binding protein HBP-1 specific to the conserved hexameric sequence ACGTCA in various plant gene promoters. 268 Jun 1

Using the Reverse Transcription (RT)-Polymerase Chain Reaction (PCR) method of Martin (1993) for semiquantitation determinating of NOS gene, it was found that NOS mRNA is not only existed in brain, but also distributed extensively in heart, kidney, lung and liver. Among of them, NOS mRNA levels were highest in the brain, followed in descending order by kidney, heart. In addition to endothelial cell, NOS gene was also highly expressed in smooth muscle cells, suggesting that they may be an important site of NOS in organism. Furthermore, NOS mRNA levels were found to decrease significantly in brain, kidney, liver and smooth muscle cell in spontaneous hypertensive rat. These data suggest that pathogeny of hypertension may be related to low expression of NOS gene in these tissues.
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PMID:[Semiquantitative detection and application about the expression of nitric oxide synthase gene]. 752 70

Nitric oxide (NO) generated from arginine exerts a variety of renal and extrarenal physiological and pathophysiological effects. NO is generated by two types of nitric oxide synthases: acutely responsive, constitutive NOS and slower, more persistent inducible NOS (iNOS). The latter is transcriptionally dependent, often stimulated by cytokines. NO regulates glomerular ultrafiltration, tubular reabsorption, and intrarenal renin secretion; many of these renal effects are mediated by interactions with angiotensin II and adrenergic (alpha 2) activity. Decreased NO activity also enhances tubuloglomerular feedback activity, which could contribute to renal vasoconstriction, NaCl retention, and elevated blood pressure. Loss of renal function could influence NO activity via: (1) endothelial dysfunction; (2) decreased arginine synthesis by kidney; (3) responses to arginine analogs that act as NOS inhibitors; (4) increased cytokine activity; and (5) altered oxidation:reduction status of cells, etc. For example, platelet dysfunction in uremia may be caused by cytokine-induced iNOS activation. Moreover, acutely responsive, constitutive NOS activity may be depressed in progressive loss of renal function. Decreased NO activity might contribute to baroreceptor dysfunction observed in hypertension and progressive renal disease. Studies of the impact of uremia suggest that iNOS may be chronically stimulated by cytokines, whereas acutely responsive, constitutive NOS activity may be concurrently depressed.
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PMID:Activities of nitric oxide in normal physiology and uremia. 873 57

The kidney vasculature is under tonic control by nitric oxide (NO) and in cortex, NO controls RA and Kf. Systemic NO inhibition leads to systemic hypertension, increases in RE, mediated by Ang II and ET, and direct effects on RA and Kf. The relationship between NO and other vasoconstrictor systems is variable. In the conscious relaxed animal, vasoconstrictor activity is low, yet acute NO inhibition leads to pressor and renal vasoconstrictor responses. At physiologic levels, ET unexpectedly is a renal vasodilator, possibly via NO generation at RA. When vasoconstrictor activity is high, NO is very important in maintenance of renal perfusion. Chronic L-NAME produces dose dependent systemic and glomerular capillary hypertension and eventual proteinuria and glomerular damage. NO deficiency is key in this process, although the hypertension becomes refractory to L-arginine administration and dependent on Ang II and the SNS, by mechanisms not yet defined. In contrast, the renal vasculature remains fully responsive to L-arginine, suggesting that pressor and renal vascular responses to chronic NO inhibition are separately regulated. NO generated from iNOS does not normally control BP or renal hemodynamics. The relative contributions of NO from bNOS and eNOS, and importance of NOS in different locations in the kidney, remain to be determined.
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PMID:Importance of nitric oxide in the control of renal hemodynamics. 874 86

The inducible nitric oxide synthase (iNOS) present in vascular smooth muscle cells (VSMC) may play a role in the generation of nitric oxide (NO) in the vascular wall, regulating blood vessel tone in normotension and hypertension. In this study the effect of interleukin (IL)-1 beta, a cytokine that induces iNOS, on NO generation (measured as nitrite), cyclic guanosine monophosphate (cGMP) generation, and steady-state abundance of iNOS mRNA were examined in VSMC from 3 week old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, during the period preceding the elevation of blood pressure. With cell density dependent variations in nitrite production eliminated, VSMC from SHR and WKY did not differ in NO generation except after prolonged incubation (30 h), when SHR cells produced less NO. However, cGMP concentrations associated with IL-1 beta stimulation were significantly smaller in SHR VSMC than in cells from WKY. IL-1 beta stimulation resulted in increased abundance of iNOS mRNA to the same extent in both WKY and SHR VSMC. Inhibitors of NOS, NG-monomethyl-L-arginine (L-NMMA) and N omega-nitro-L-arginine methyl ester (L-NAME), did not block the induction of iNOS mRNA, although nitrite production and cGMP generation were inhibited. The protein synthesis inhibitor cycloheximide and the RNA synthesis inhibitor actinomycin-D almost completely blocked the production of nitrite in cells from both strains of rats. Actinomycin-D completely blocked the induction of iNOS mRNA by IL-1 beta in cells from both strains of rats, whereas cycloheximide partially blocked its synthesis in WKY, but had no significant effect on IL-1 beta induced expression of iNOS mRNA in SHR VSMC. Thus, IL-1 beta controls iNOS gene expression at the transcriptional level, and an intermediate labile protein, whose synthesis is inhibited by cycloheximide, is required for IL-1 beta stimulated induction of iNOS mRNA transcription in WKY cells but not in SHR. We conclude that although iNOS is expressed to similar extent in VSMC of prehypertensive SHR and WKY and similar amounts of NO are initially generated, there are differences between the VSMC of SHR and WKY in the regulation of the transcription of iNOS mRNA, there is a lower sustained production of NO, and there is a reduced generation of cGMP in response to IL-1 beta stimulated NO production. These differences between VSMC from prehypertensive SHR and WKY may indicate a pathophysiological role of iNOS in early blood pressure elevation in SHR.
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PMID:Inducible nitric oxide synthase in vascular smooth muscle cells from prehypertensive spontaneously hypertensive rats. 887 43

In patients with benign nephrosclerosis, the histologic changes are characterized by hyaline degeneration of afferent arterioles with reduced kidney size. Although the glomeruli are nearly intact in patients with adult essential hypertension, the greatest numbers of sclerotic glomeruli are seen in nephrosclerosis with the aging process. Aging undoubtedly plays a role. In the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of cholesterol, shows an increased mesangial matrix and hypertrophic vascular medial smooth muscle cells. Kidneys of elderly subjects also are associated with a large number of sclerotic glomeruli. Experimental evidence supports the notion that the pathogenesis of glomerulosclerosis with nephrosclerosis has been demonstrated as important factors: (1) the elevation of PG (glomerular hypertension); (2) mesangial dysfunction, such as mesangiolysis and increased mesangial matrix; and (3) genetic abnormalities (apoptosis) in mesangial cells with glomerular hypertension. Malignant nephrosclerosis is characterized histologically by vascular endothelial damage and fibrinoid necrosis of afferent and interlobular arteries. In an afferent arteriole or a glomerulus, NOS or endothelin produced in endothelial cells may play a role in the reduction or the maintenance of vascular tone. The frequency of malignant hypertension has decreased because of the effective treatment of essential hypertension with new antihypertensive agents: calcium antagonists, ACE inhibitors, and angiotensin II receptor antagonists. Therefore, the importance of the prevention of essential hypertension with these antihypertensive agents, by slowing and stopping the increase in blood pressure from mild hypertension, has received widespread recognition in the prevention of organ damage, such as cases of cardiovascular disease and ESRD. Thus, prevention of renal injuries is an important goal of antihypertensive therapy.
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PMID:Nephrosclerosis and hypertension. 935 98

Nitric oxide (NO), an L-arginine derivative, is implicated in neuronal transmission, immune response and vasodilation, and acts as a modulator of platelet function. Recent studies in the experimental model of renal mass reduction (RMR) in rats have generated the hypothesis that abnormalities in the NO synthetic pathway could play a key role in mediating the complex hemodynamic and hemostatic disorders associated with the progression of renal disease. Thus, renal NO generation is lower than normal in rats with RMR 7 days after surgery and progressively worsens with time in close correlation with signs of renal injury. This abnormality is due to a major defect in inducible NO synthase (iNOS) content in the kidney. In the same model, administration of either the NO precursor, L-arginine, or a NO-releasing compound reduces proteinuria, slows renal disease progression, and prolongs survival. In contrast, in the systemic circulation of uremic rats, NO is formed in excessive amounts, possibly caused by higher release from systemic vessels due to the augmented expression of both iNOS and endothelial NOS. Up-regulation of systemic NO synthesis might be a defense mechanism against uremic hypertension. On the other hand, a greater availability of NO to circulating cells may sustain the bleeding tendency, a well-known complication of uremia.
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PMID:Nitric oxide synthesis and L-arginine in uremia. 938 6

To compare the expression of endothelial nitrous oxide synthase (e-NOS), which plays a major role in vasoconstriction, in preeclampsia with that in the normotensive placenta and to identify whether or not e-NOS actually influences the pathogenesis of preeclampsia, we have studied the distribution and intensity of the endothelial isoform of NOS expression in preeclampsia (n = 121) and normal (n = 14) pregnancies. Archival paraffin-embedded tissues were immunostained with a polyclonal e-NOS antibody. E-NOS was stained predominantly in the endothelial cells of the umbilical cord and along the surface of the villi, especially within the cytoplasms of the syncytiotrophoblasts with a granular and punctuated pattern, but not in the trophoblastic island or in the intravillous capillaries. The degree of e-NOS expression in pregnancy-induced hypertension (PIH) was significantly lower than in normotensive placenta, and moreover in the patients lacking abruptio. The expression of e-NOS in preeclampsia has some correlation with patient age. In conclusion, the degree of e-NOS expression in cotyledon from PIH is far less than from control, it means a kind of hemodynamic alteration of the fetoplacental circulation in preeclampsia.
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PMID:Nitrous oxide synthase expression in placenta of preeclampsia. 944 92

Nitric oxide (NO) is an endogenous vasodilator synthesized in the endothelium by constitutive NO synthase (cNOS). We have shown that upregulation of cNOS activity in hypertension may contribute to forestalling left ventricular and aortic hypertrophy (Hypertension. 29: 235, 1997). NO has been shown to inhibit growth-related responses affecting vascular smooth muscle, and mesangial cells, as well as reduce production of extracellular matrix in response to injury. Here, we investigated the relationship between renal cNOS activity (conversion of [14C] L-arginine to [14C] L-citrulline) and glomerular (GIS) and tubulointerstitial (TIS) injury scores and urinary protein excretion, indices of renal injury, in age and blood pressure matched spontaneously hypertensive rats (SHR, SBP 220+/-9 mm Hg) fed 0.5% NaCl diet and Dahl salt-sensitive (DS) rats fed 4% NaCl diet (DS-4%, SBP 228+/-8 mm Hg) as well as their normotensive counterparts Wistar Kyoto rats fed 0.5% NaCl diet (WKY, 137+/-3 mm Hg) and DS rats fed 0.5% NaCl diet (DS-0.5%, SBP 135+/-4 mm Hg). In SHR, renal medullary cNOS activity was 89% higher than in WKY (8.91+/-0.98 vs 4.71+/-0.37 nmol/min/g protein, P<0.05) whereas, in hypertensive DS-4% rats cNOS activity was 43% lower than in DS-0.5% rats (1.98+/-0.16 vs 3.48+/-0.29 nmol/min/g protein, P<0.05). Renal cortical cNOS was lower than in medulla but similar in all groups; inducible NOS activity was not detected. Despite hypertension of similar severity and duration, hypertensive DS-4% developed 9 fold more GIS (190+/-42 vs 21+/-11), 20 fold more TIS (4.0+/-0.7 vs 0.2+/-0.3), and 5 fold more proteinuria (54+/-11 vs 8.5+/-3.0 mg/day), all P<0.05. The current studies, in conjunction with our recent studies in heart and aorta, strongly suggest that in hypertension, increased cNOS activity may provide a protective homeostatic role in all the end-organs that are targets of hypertensive injury.
Hypertension 1998 Jan
PMID:Nitric oxide synthase activity and renal injury in genetic hypertension. 945 14


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