Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

78 patients with essential hypertension (17 with borderline hypertension and 61 with hypertension) and 13 normal controls were examined to evaluate the relation between the urinary excretion rate of guanidinoacetic acid/creatinine (U-GAA/Cr), beta 2-microglobulin/creatinine (U-BMG/Cr), radio-sensitive microalbumin excretion rate/creatinine (U-AER/Cr), N-acetyl-D-glucosaminidase/creatinine (U-NAG/Cr) and renal function. There was no significant difference among these groups in creatinine clearance (Ccr), serum creatinine (Cr) or in U-BMG/Cr, U-NAG/Cr and U-AER/Cr. In hypertensive patients U-GAA/Cr was 49.2 +/- 16.7 mg/gCr, which was much lower than in controls (78.1 +/- 13.4) (p less than 0.001). The Ccr has a significant relation with U-GAA/Cr (r = 0.29, p less than 0.01) but not with U-AER/Cr, U-BMG/Cr nor U-NAG/Cr. In 44 patients, all of the above factors were investigated for 24 weeks during 4 kinds of anti-hypertensive treatment (10 with an angiotensin-converting enzyme inhibitor: A group, 11 with a beta-adrenergic blocker: B group, 12 with a Ca entry blocker: C group and 12 with diuretics: D group). In A and C group, U-GAA/Cr was elevated during therapeutic course. However, in B and D group it declined during treatment. These findings suggested that urinary excretion of GAA may be a more sensitive marker than AER, BMG or NAG in hypertension and angiotensin-converting enzyme inhibitor and Ca entry blocker can be useful in the treatment of patients with essential hypertension with renal damage.
 ...
PMID:[Estimation of urinary excretion rate of guanidinoacetic acid in essential hypertension]. 269 98

To evaluate the humoral and hemodynamic (both systemic and renal) effects of chronic treatment with celiprolol, six out-patients with mild to moderate uncomplicated essential hypertension received placebo for 1 month and celiprolol (400 mg qid) for 6 months. At the end of placebo and of the first and sixth month of treatment, blood pressure (BP), heart rate (HR), renal plasma flow (RPF), glomerular filtration rate (GFR), plasma renin activity (PRA), aldosterone (ALD) and noradrenaline (NA), urinary enzymes (NAG: N-acetyl-beta glucosaminidase, AAP: alanine aminopeptidase) were measured. Compared to placebo, celiprolol significantly and steadily reduced BP and HR. However, although the systemic hemodynamic effect was constant during the whole period of the study, the reduction of renovascular resistance and of plasma noradrenaline, detectable at the first month of therapy, disappeared at the sixth month. However, PRA, plasma aldosterone, GFR, and urinary enzymes did not change. These findings suggest that the antihypertensive effect of celiprolol is well maintained over the 6-month period; the drug did not exert any adverse effect on the kidney, and chronic celiprolol treatment does not influence renal hemodynamics.
 ...
PMID:Long-term humoral and hemodynamic effects of celiprolol. 297 Aug 52

Interest in the cardiovascular protective effects of calcium channel antagonists has increased in the past decade. We investigated prevention of vascular wall remodeling by the long-acting calcium channel antagonist pranidipine in 12-week-old Dahl salt-sensitive (SS) rats with high-salt-induced (4% NaCl) hypertension. Six-week pranidipine treatment (60 mg/kg chow) decreased systolic blood pressure (SBP) by 22% in SS rats. This BP reduction was associated with decreases in cardiac mass and weight of the aortic wall. Glomerular filtration rate (GFR) was increased by 33%, but this did not lead to a decrease in urinary protein or NAG excretion. Morphologic investigation demonstrated striking resolution of arterial injury (medial necrosis and/or hyperplasia, inflammatory cell infiltration, and thrombus formation) by 87% after pranidipine treatment. Glomerular sclerosis was also attenuated by 61%, whereas tubular injury was improved by only 28%. These morphologic changes were reflected in the findings that the capacity of kidney homogenate for generating lipid peroxides was significantly decreased and that collagen levels and pattern type became similar to those of normotensive salt-resistant (SR) rats. Pranidipine also attenuated hypertensive vasculopathy in small arteries of the middle cerebral arteries. Thus, the calcium channel antagonist pranidipine can attenuate the vascular injury that occurs in salt-induced hypertension, a promising property that implicates its clinical usage, particularly in essential hypertension with cardiovascular complications.
 ...
PMID:New dihydropyridine calcium channel antagonist, pranidipine, attenuates hypertensive renal injury in Dahl salt-sensitive rats. 752 90

The purpose of the study was to measure the urinary excretion of N-acetyl-beta-glucosaminidase (U-NAG) in patients suspected of having renovascular hypertension and to compare the enzyme excretion before and after active intervention with operation or percutaneous transluminal renal angioplasty (PTRA). Eighty-one patients with severe, therapy-resistant hypertension were examined with regard to renal artery stenosis (RAS). At least one significant renal artery stenosis was found in 61 patients, whilst the remaining 20 patients were classified as having essential hypertension. Enzyme levels were found to be significantly higher in RAS patients as compared with patients with severe hypertension lacking significant renal artery stenosis, 0.66 (0.41-0.91, median value, 1st and 3rd quartiles) versus 0.35 (0.27-0.54); P < 0.01. Both groups of patients had significantly higher U-NAG values than a healthy reference population (0.2, 0.13-0.27; P < 0.01). Forty of the RAS patients were randomized to surgery or PTRA and followed prospectively for 2 years. After either renal vascular surgery or PTRA a significant rise in U-NAG excretion was observed 7-10 days after treatment. Urinary NAG excretion remained elevated during long-term follow-up. It is suggested that U-NAG should be determined in patients with therapy-resistant hypertension with suspicion of renal artery stenosis.
 ...
PMID:Determination of urinary N-acetyl-beta-glucosaminidase in patients with hypertension and renal artery stenosis. 835 78

Arterial hypertension-related renal damage is an increasingly common problem recently, because approximately 25% of patients currently treated with dialysis were hypertensive before renal replacement therapy was started. Hypertension is also known as a metabolic disease, while carbohydrate, purine and lipid disturbances are the features of this syndrome. On the other hand, the progression of renal disease depends on the extent of tubulointerstitial injury. For this reason, we undertook a study to evaluate the relationship between excretion of the markers of tubular damage (NAG) and some parameters of carbohydrate, purine and lipid metabolism in untreated essential hypertension. Both healthy volunteers (n = 15) aged 32. 6+/-7.8 and essential hypertensives (n = 25) aged 37.24+/-11.39 underwent the same tests. These tests were performed at 2-day intervals: intravenous glucose tolerance test with 0.5 g/kg b.w. as 40% glucose solution and oral fructose load test with 1.0 g/kg b.w. Area under glucose curve (GA) and serum uric acid post-fructose (PUAA) were calculated. Fasting: insulin, total cholesterol and LDL, triglycerides, free fatty acids (FFA) and urine excretion of NAG, albumin were determined. Glomerular filtration rate was estimated as creatinine clearance. Hypertensives showed statistically higher BMI (p<0.007), NAG (p<0.02), total cholesterol (p<0.01), LDL (p<0.007), FFA (p<0.007), insulin (p<0.01), PGA (p<0.01) and PUAA (p<0.03). NAG excretion correlated positively with WHR (r = 0.40), MAP (r = 0.47) and PUAA (r = 0.47) in hypertensives only. We presume that tubular injury at an early stage of renal damage in patients with essential hypertension could be a part of metabolic syndrome X.
 ...
PMID:Hypertensive nephropathy - an increasing clinical problem. 1020 62

Arotinolol hydrochloride with alpha-and beta-receptor blocking action, developed in Japan, is mainly used for the treatment of hypertension. The study population consisted of 42 outpatients with essential hypertension with a blood pressure greater or equal to 160/96 mmHg. 10 men and 32 women, with a mean age of 77.5 year. The patients received 10 mg arotinolol hydrochloride daily for 24 weeks which was taken orally twice a day. We evaluated the changes of blood pressure, heart rate and chief complaints of patients before and every 4 weeks during treatment and the renal function before, 12 weeks after and 24 weeks after, the administration of arotinolol hydrochloride. Blood pressure and heart rate decreased significantly after 4 weeks of treatment with arotinolol hydrochloride (p < 0.05). However, no significant changes were found in blood urea nitrogen, serum creatinine, serum albumin, beta2-microglobuline, NAG or creatinine clearance during the 24 weeks of treatment. These results indicate that arotinolol hydrochloride has antihypertensive effects without renal dysfunction in elderly patients with essential hypertension.
 ...
PMID:[Clinical effect of arotinolol hydrochloride and its influence on renal function in elderly patients with essential hypertension]. 1055 61

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).
 ...
PMID:[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. 1139 62