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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a prospective study in residents of a small farming community in southwestern Japan to determine whether elevated serum N-acetyl-beta-D-glucosaminidase (NAG) activity would predict future hypertension. The 505 normotensive subjects (blood pressure, < 140/90 mm Hg; mean age, 52 +/- 12 years) were reexamined after 7 years; 111 (22%) had become hypertensive (defined as blood pressure > or = 140/90 mm Hg and/or taking antihypertensive medication at follow-up). After adjustment for age and sex, the development of hypertension was significantly related to body mass index (P < .002), the sum of skinfolds (P < .001), baseline blood pressure (P < .0001), serum cholesterol (P < .01), serum uric acid level (P < .0001), and serum NAG activity (P < .005). Elevated NAG activity showed an independent relationship to future hypertension (P < .005) after adjustments for age, sex, baseline blood pressure (systolic, diastolic, or mean), uric acid level, and the sum of skinfolds. Therefore, elevated serum NAG activity was an effective indicator of future hypertension, and it might therefore be related to functional and/or structural changes in the cardiovascular system.
Hypertension 1995 Jun
PMID:Serum N-acetyl-beta-D-glucosaminidase activity in predicting the development of hypertension. 776 79

Renal effects of mild hypertension and therapy have not been established. Since urinary albumin and N-acetyl-beta-D-glucosaminidase excretions reflect renal effects of hypertension, they were related to blood pressure, other cardiovascular risk factors, cardiac target organ effects, and response to therapy in mild hypertension (diastolic blood pressure 85-99 mm Hg). Participants were from two clinics of the Treatment of Mild Hypertension Study (TOMHS), a multicenter randomized, double-blind, controlled trial. Participants received nutritional-hygienic therapy and one of five active drugs or placebo. Urinary albumin and N-acetyl-beta-D-glucosaminidase excretions were assessed prospectively using office "spot" collections from one clinic (n = 213) and retrospectively using overnight collections from the other clinic (n = 210). Relationships were determined between protein excretions and blood pressure, age, gender, race, blood glucose, cholesterol concentrations, and indices of body mass and left ventricular mass and function at baseline. Treatment effects were assessed after 3 to 12 months. Spot and overnight albumin excretions related positively to baseline systolic blood pressure by univariate analyses. Spot albumin excretion related positively to systolic blood pressure, age, creatinine clearance, and left ventricular function while overnight albumin excretion related positively to left ventricular mass and female gender by multiple regression analyses. Spot, but not overnight, albumin excretion declined significantly with active drug therapy. N-acetyl-beta-D-glucosaminidase excretion did not relate to blood pressure or decline with therapy. The combined results suggest albumin excretion correlates with blood pressure, decreases with antihypertensive drug therapy, and is associated with greater left ventricular function and mass, as well as glomerular filtration rate, even at mild levels of hypertension.
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PMID:Urinary albumin and N-acetyl-beta-D-glucosaminidase excretions in mild hypertension. 784 23

Urinary N-acetyl-beta-D-glucosaminidase was estimated in 109 primigravidas and the level correlated with the subsequent development of preeclampsia and pregnancy-induced hypertension in these women. The enzyme value was significantly higher in those who developed preeclampsia. Its sensitivity and specificity for the prediction of the disorder were 80% and 78% respectively. The positive predictive value was 21% while the negative predictive value was 98%.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase in the prediction of preeclampsia and pregnancy-induced hypertension. 817 51

In order to elucidate the diagnostic significance of urinary apolipoprotein H (apo H), known as beta 2-glycoprotein I, urinary apo H levels were measured by a non-competitive enzyme immunoassay in diabetics without hypertension and Albustix-positive proteinuria. The relationships between urinary apo H levels and urinary albumin (Alb) levels as well as clinical profiles in diabetics were investigated. The mean urinary apo H level in 45 diabetics was 264.2 +/- 189.5 micrograms/g.cr, and significantly higher than that in 41 healthy subjects (120.6 +/- 84.8 micrograms/g.cr, p < 0.01). Diabetics were classified into three groups based on urinary Alb levels; 17 group I patients with normoalbuminuria (U-Alb < 15mg/g.cr), 12 group II patients, whose urinary Alb levels were in between normo- and microalbuminuria (15 < or = U-Alb < 30mg/g.cr) and 16 group III patients with microalbuminuria (30 < U-Alb < or = 300mg/g.cr). The mean urinary apo H level in group I patients, who were regarded as without nephropathy, was 199.2 +/- 109.0 micrograms/g.cr, significantly higher than that in normal subjects (p < 0.01). The mean urinary apo H levels in group II and III were 271.4 +/- 177.1 and 327.8 +/- 246.1 micrograms/g.cr, respectively. These values were also higher than in normal subjects (both of p < 0.01). Urinary apo H levels correlated positively with urinary levels of glycosaminoglycan (r = 0.382, n = 45, p < 0.01), which was regarded as an indicator of the anion loss from glomerular basement membrane to urine, and with urinary N-acetyl-beta-D-glucosaminidase activities (r = 0.378, n = 37, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on urinary apolipoprotein H in diabetics]. 850 49

In an in-depth examination to better define the renal effects of mild hypertension, we used urinary proteins to indicate damage to the glomerulus (albumin), tubular reabsorption capability (retinol-binding protein), and turnover of tubular tissue (alanine aminopeptidase and N-acetyl-beta-D-glucosaminidase) in a group of 18 people with mild hypertension not associated with diabetes and a control group (n = 12). The participants' activity was controlled on a high normal salt diet for 3 days followed by a low salt diet for 4 days. Two distinct patterns of albumin excretion were evident in the hypertensive group: 22% had elevated, highly variable excretion patterns, and the rest had tightly grouped values below 16 mg/g creatinine, 16 micrograms/min, or 16 mg/L, with the lowest within-person biological variability given by albumin calculated as a ratio to creatinine. Albumin and NAG excretion primarily correlated with systolic blood pressure and the best correlations were given by ratios to creatinine. A marked decrease in salt excretion of 71% (to 50.8 mEq/day) resulted in significant (P < .0005) decreases in systolic (13.9 mm Hg), diastolic (6.4 mm Hg), and mean arterial pressures (8.9 mm Hg) only in the group with mild hypertension. However, albumin excretion did not decrease when dietary salt content was lowered. The group with hypertension also had higher urinary excretion of lysosomal N-acetyl-beta-D-glucosaminidase (P < .01), and whites in the group had a higher excretion of retinol-binding protein than did whites in the control group (P < .02). Retinol-binding protein values, however, were within the normal range, indicating that the elevated albumin values were the result of changes in selectivity of the glomerulus.
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PMID:An in-depth examination of the excretion of albumin and other sensitive markers of renal damage in mild hypertension. 855 30

In rapidly growing male Sprague-Dawley rats with an initial body weight of 100 +/- 10 g, we investigated how alimentary magnesium (Mg) supply, Mg metabolism and ciclosporine (Ci)-associated nephrotoxicity are interrelated. Food with 100 ppm Mg (1Mg) or 1,000 ppm Mg (stMg) or 10,000 ppm Mg (rMg), Ci 20 mg/kg body weight daily or olive oil were applied for 3 months (n = 10/group). Mg concentrations in various compartments were measured by atomic absorption spectrophotometry. Creatinine clearance (Jaffe), urinary N-acetyl-beta-D-glucosaminidase (NAG) activity (fluorometrically), urinary sodium excretion (flame photometry) and osmolality were measured. Histomorphological examination was done and renal renin expression was studied by monoclonal antibodies. Ci reduced the Mg concentration of the femur under 1Mg (72.6 +/- 9.7 vs. 112.6 +/- 14.3 mmol/kg dry substance, p < 0.05) and under stMg (150.6 +/- 16.6 vs. 194.1 +/- 10.2 mmol/kg dry substance, p < 0.05), thus indicating Ci-related Mg deficiency. This was due to a significant increase in Mg excretion in Ci treatment compared to dietary controls. Under rMg, there was no difference between Ci-treated and control animals. Ci treatment lowered creatinine clearance in 1Mg (1.42 +/- 0.05 vs. 3.02 +/- 0.58 ml/min) and in stMg (1.04 +/- 0.45 vs. 2.18 +/- 0.51 ml/min), NAG/creatinine and urinary sodium excretion were negatively affected by Ci under 1Mg and stMg. Histomorphology showed macrocalcifications due to Mg deficiency and Ci-specific findings, which were markedly enhanced in 1Mg and stMg. Animals with plentiful Mg supply had no functional alterations due to Ci and no or weakly expressed histomorphological lesions. Renin-positive stained cells were higher in Ci-treated animals. This seems to be functionally relevant under 1Mg and stMg, since it was associated with sodium retention and elevated relative heart weight, indicating hypertension. Alimentary or drug-induced Mg deficiency plays a relevant role in the pathophysiology of chronic Ci nephrotoxicity. Our data suggest that Mg supplementation is helpful to reduce Ci toxicity, even if there is 'normal' alimentary Mg intake.
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PMID:Magnesium metabolism: basic aspects and implications of ciclosporine toxicity in rats. 890 62

Increased urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) has been reported in many clinical conditions, including essential hypertension. Since hypertension is increasingly recognized as beginning in childhood, we hypothesized that urinary NAG changes with increasing blood pressure may start early in life and may also be the evidence of the existence of early hypertensive disease. We analyzed the urinary NAG changes in 980 young adults, ages between 18 to 32, in relation to age, race, sex, and systolic and diastolic blood pressure. We observed that black women had the highest level of NAG, with or without adjustment for creatinine. With aging, urinary NAG significantly increased in men. As blood pressure increased, urinary NAG excretion appeared to increase, and this was more apparent in black women (P < .05). Significant correlations between NAG excretion and systolic (r = 0.12, P = .04) and diastolic (r = 0.18, P = .003) blood pressures existed in the oldest age group, 28 to 32 years old. These findings show that a significant association between urinary NAG and blood pressure exists in normal young adults and changes in urinary NAG may be evidence of early hypertensive disease.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase changes in relation to age, sex, race, and diastolic and systolic blood pressure in a young adult biracial population. The Bogalusa Heart Study. 892 65

The purpose of the present study was to examine renal functional changes caused by chronic blockade of nitric oxide (NO) synthesis in young rats. Two types of NO synthase inhibitor were used: NG-nitro-L-arginine methyl ester (L-NAME) as a non-selective inhibitor and aminoguanidine (AG) as a selective inhibitor of the inducible isoform. Oral administration of L-NAME (20-80 mg/dL of drinking water), not AG (400 mg/dL), for 4 weeks induced systemic hypertension in the treated rats. Both inhibitors caused a significant reduction in urinary excretion of NO2-/NO3-. Rats treated with L-NAME developed proteinuria and tubular enzymuria (high excretion of N-acetyl-beta-D-glucosaminidase) in a dose-dependent fashion, with normal serum levels of creatinine, albumin and cholesterol. Chronic AG administration did not alter the urinary levels of protein and N-acetyl-beta-D-glucosaminidase or serum laboratory values. Overall, these observations highlight the importance of the continuous generation of NO by the constitutive isoform in the control of vascular tone and the maintenance of renal glomerular and tubular function. Oral administration of L-NAME may serve as a model of chronic NO-deficient hypertension with renal injury in young rats.
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PMID:Renal functional measurements in young rats with chronic inhibition of nitric oxide synthase. 900 96

1. The protective effect of ME3221, a surmountable AT1 antagonist, on the hypertension and its concomitant complications in aged (32 week old) stroke-prone spontaneously hypertensive rats (SHRSP) was studied following long-term (32 weeks) oral administration, and compared with those of losartan (metabolite EXP3174 is an insurmountable AT1 antagonist) and enalapril. 2. During the treatment period, ME3221, at a dose of 10 mg/kg per day steadily reduced the systolic blood pressure, and no tolerance was developed to the fall in blood pressure. The reference drugs showed similar activity, but the antihypertensive effect of ME3221 was more potent. 3. In the control group, rats began to die from 52 weeks of age and all rats had died by 64 weeks of age. In contrast, no rats treated with ME3221, losartan or enalapril died before 64 weeks of age. 4. ME3221, losartan and enalapril suppressed the hypertensive complications observed in control SHRSP, that is, cerebral apoplexy (stroke and cerebral oedema), renal injury (increased proteinuria, total N-acetyl-beta-D-glucosaminidase activity and ascites) and heart failure (cardiac hypertrophy and pleural effusion). 5. These results indicate that ME3221 has a stable anti-hypertensive effect, prevents hypertensive complications and prolongs survival in aged SHRSP equally as well as losartan and enalapril.
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PMID:Effect of chronic treatment with ME3221 on blood pressure and mortality in aged stroke-prone spontaneously hypertensive rats. 907 29

Serum N-acetyl-beta-D-glucosaminidase activity (NAG) is a possible predictor of vascular injury in hypertension. We assessed whether the activity of this enzyme reflects vascular damage in a genetic rat model of non-insulin-dependent diabetes mellitus (NIDDM) in humans. Otsuka Long-Evans Tokushima Fatty (OLETF) rats fed a regular chow were treated with the angiotensin converting enzyme (ACE) inhibitor imidapril for 16 wk. Systolic blood pressure increased in a time-dependent manner in the untreated OLETF rats as compared with that in the control Long-Evans Tokushima (LET) rats. The blood pressure elevation was associated with increases in cardiac and aortic weight. Imidapril treatment significantly attenuated the blood pressure elevation and reduced the increases in cardiac and aortic weight. The untreated OLETF rats had higher plasma glucose and insulin concentrations than did the LET rats and presented with glucosuria at the age of 22 wk. Imidapril treatment strikingly decreased plasma glucose levels and the glucosuria. Plasma insulin concentrations decreased, approaching those of the non-diabetic control LET rats. ACE inhibitor treatment attenuated the nodular lesions in the glomeruli of OLETF rats and improved the kidney function. Serum NAG activity increased significantly by 35% in the untreated rats; this increase was attenuated significantly by imidapril treatment. The reduction in serum NAG activity correlated with improvement in cardiovascular injury. In contrast, there were no changes in urinary NAG excretion in the three OLETF rat groups. In addition, NAG excretion did not correlate with indices of cardiovascular injury. These data suggest that serum NAG activity is useful in predicting injury in the cardiovascular system in rats with diabetes mellitus.
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PMID:Serum N-acetyl-beta-D-glucosaminidase activity in a genetic rat model of non-insulin-dependent diabetes mellitus. 932


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