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)

A double-blind study of Phanurane and placebo was conducted on 61 patients with mild essential hypertension. Each patient received 2 gelules daily (2 X 50 mg of canrenone) during a 2 month period. Statistical analysis has shown that patients on Phanurane experienced a significant decrease in systolic and diastolic blood pressure compared with patients on placebo. Clinical tolerance of canrenone was excellent. Uric acid and triglyceride levels remained normal.
 ...
PMID:[Effect and tolerance of Phanurane in the treatment of essential hypertension. (Double blind study) (author's transl)]. 23 24

A double-blind study of hydrochlorothiazide and spironolactone, alone and in combination, was conducted in 49 patients with mild-to-moderate essential hypertension after a 4-wk placebo washout period. In the whole group mean arterial blood pressure fell to levels of less than or equal to 107 mm Hg or declined by more than 15 mm Hg in 78% of the patients after twelve weeks of treatment. Sixty-nine percent of patients receiving hydrochlorothiazide alone developed serum potassium levels lower than 3.5 mEq/L; serum potassium levels were above 5.5 mEq/L in 2 patients (5.5%) receiving spironolactone 400 mg/day. Uric acid levels rose in all patients, more in those on hydrochlorothiazide, but clinical gout did not develop in any subject. Hydrochlorothiazide, spironolactone, and the combination of the two are effective antihypertensives. Spironolactone in doses of 200 and 400 mg/day was associated with side effects but did not induce a greater antihypertensive effect than doses of 100 mg/day. Our data suggest that when hydrochlorothiazide is associated with potassium loss, when gout or elevated uric acid levels are of concern, or when carbohydrate tolerance is abnormal, supplementation or replacement with spironolactone (up to 100 mg/day) may be useful in controlling blood pressure while reducing side effects.
 ...
PMID:Hydrochlorothiazide and spironolactone in hypertension. 36 34

A new hypouricemic diuretic (tienilic acid) was compared with hydrochlorothiazide in a double-blind study in 8 patients with mild essential hypertension. After a two-week placebo period the patients received either 250 mg tienilic acid or 50 mg hydrochlorothiazide in a single daily dose for 3 weeks. After a second placebo period of 2 weeks the patients received, in a crossover design, either tienilic acid or hydrochlorothiazide for a further 3 weeks. The reduction of blood pressure and of body weight was similar for both drugs. When treatment was started diuresis and natriuresis increased with tienilic acid and with hydrochlorothiazide. Whereas serum sodium levels showed only minor variations, serum potassium levels fell with both diuretics and urinary potassium excretion increased. Urinary calcium excretion decreased and serum calcium levels slightly increased under both treatments. Both diuretics induced similar increases of plasma renin activity, plasma aldosterone concentration and aldosterone-18-glucuronide excretion. Blood urea nitrogen and, to a lesser extent, serum creatinine levels were raised slightly under both drug regimens. Whereas the serum uric acid level rose and remained elevated for the duration of hydrochlorothiazide treatment, it fell significantly and remained lowered during treatment with tienilic acid. Uric acid clearance was about twice as high with tienilic acid as with hydrochlorothiazide. Tienilic acid therefore appears to be a therapeutic alternative to thiazides and other hyperuricemic diuretics in hypertensive patients in whom hyperuricemia should be avoided or corrected.
 ...
PMID:[Experiences with a new hypouricemic diuretic (tienilic acid): comparison with hydrochlorothiazide]. 37

The tubular transport of urate was studied in 40 hypertensive patients and in 20 normal subjects by means of pyrazinamide and benzbromarone tests. There was a marked decrease in urate excretion per nephron in hyperuricemic patients with essential hypertension. Serum uric acid correlated inversely with fractional excretion of urate (r = -0.7450, p less than 0.001). Presecretory and postsecretory reabsorption of urate did not significantly differ between hypertensive patients with high uric acid levels and control subjects. Urate secretion was significantly reduced in hypertensive patients and in those with hyperuricemia showed a twofold decrease. Serum uric acid correlated inversely with tubular secretion of urate (r = -0.7091, p less than 0.001) in hypertensive patients. These findings indicate that impaired tubular secretion of urate is a potential mechanism of hyperuricemia in essential hypertension.
 ...
PMID:Evaluation of renal handling of uric acid in essential hypertension: hyperuricemia related to decreased urate secretion. 175 23

Exploratory analyses were conducted in a nested case-control study of 1,031 incident cases of essential hypertension and 1,031 persistently normotensive controls from the Kaiser Permanente Multiphasic Health Checkup cohort in Northern California. Previous analyses have confirmed hypotheses that baseline weight, subsequent weight gain, alcohol consumption, parental history of hypertension, excessive use of salt, and centralized body fat distribution are predictive of developing hypertension. In the present study, pulmonary function tests, several serum chemistries, and heart rate were strongly predictive in univariate analyses. Adjusting for the risk factors mentioned above, forced vital capacity (p less than 0.001), serum uric acid (p = 0.003), serum cholesterol (p = 0.012), and heart rate (p = 0.014) remained independently predictive. Further adjustment for baseline blood pressure completely explained the association of heart rate with hypertension, and reduced the association with serum cholesterol to borderline significance. Forced vital capacity remained a strong, inverse predictor (odds ratio, fifth vs. first quintile = 0.22, 95% confidence interval (Cl) 0.11-0.46). Uric acid remained positively related to risk (odds ratio, fifth vs. first quintile = 2.19, 95% Cl 1.20-3.98). Although neither association is presently understood, both forced vital capacity and serum uric acid are closely linked to development of hypertension and may be markers of susceptibility or intermediate steps in pathways leading to hypertension.
 ...
PMID:Precursors of essential hypertension: pulmonary function, heart rate, uric acid, serum cholesterol, and other serum chemistries. 201 30

Twenty-four black men with mild to moderate essential hypertension were enrolled in an open-label trial comparing the efficacy of two doses of Capozide (captopril and hydrochlorothiazide). All antihypertensive drugs were discontinued and patients then received placebo for 2 weeks. Twenty-two patients, mean age 59.1 +/- 14.3 years, with sitting diastolic blood pressure (BP) 92 to 110 mm Hg, entered the 6-week active-drug phase. Eleven patients (Group A) were randomized to Capozide 25/15 and 11 (Group B) to Capozide 50/15. Baseline mean BPs were 151.0/100.7 mm Hg in Group A and 153.1/100.7 mm Hg in Group B. At week 6, mean BPs were 128.7/84.4 mm Hg in Group A and 126.8/82.7 mm Hg in Group B. Uric acid, blood urea nitrogen and creatinine levels rose slightly in both groups. There were no adverse events. Eighteen patients had normal BPs at study completion. Twice-daily Capozide treatment is effective and well tolerated in blacks; patients responded equally well to both doses.
 ...
PMID:Treating black hypertensives with capozide. 304 29

A new fixed-dose combination drug, Minotensin (1 film-coated tablet contains 120 mg bupranolol, 2.5 mg bendroflumethiazide and 25 mg triamterene) was tested in a long-term study. 20 patients with mild to moderate primary hypertension were treated for 6 months. Items of investigation were: influence on low range serum potassium, influence on serum magnesium concentration, blood pressure lowering effect, tolerance and side effects. Initial dosage of 1 tablet b.i.d. could be reduced to 1 tablet in the morning in 4 patients. The mean serum potassium concentration rose from 3.79 +/- 0.3 mmol/l to 4.15 +/- 0.55 mmol/l (p less than 0.01) after 4 weeks, and to 4.26 +/- 0.37 mmol/l (p less than 0.001) after 6 months of treatment, all single values remaining within normal limits. The serum magnesium concentration rose to a small, insignificant extent. Systolic and diastolic blood pressure were lowered highly significantly from 177 +/- 12/103 +/- 7 mm Hg by 19/11 mm Hg. The mean values were within normal limits (less than 160/95 mm Hg) after treatment. Heart rate fell simultaneously by 11 beats per minute, on average (p less than 0.01). Atrioventricular conduction time was slightly prolonged in 2 cases. Serum levels of sodium, BUN and creatinine rose slightly, but remained within the normal range during treatment. Uric acid and lipids were not influenced significantly. 1 patient complained of transient gastrointestinal discomfort. Generally the drug was tolerated very well.
 ...
PMID:[Potassium-sparing effect of triamterene in a 3-component combination preparation for the therapy of hypertension]. 396 10

The effects of propranolol and prazosin on plasma lipoproteins in patients with essential hypertension were evaluated according to a crossover protocol of two 8-week periods with a washout of 4 to 6 weeks. Eleven patients with moderate hypertension (greater than 90 but less than or equal to 144 mm Hg, diastolic) and slightly overweight (+10% to +/- +30%, according to Metropolitan Life Insurance tables) were selected. No dietary changes were prescribed. Plasma cholesterol, triglycerides (TG), and lipoprotein changes were monitored at the beginning of each sequence and at 2-, 4- and 8-week intervals. Prazosin, when given first, did not essentially modify any of the metabolic parameters, except for a slight elevation in plasma apoprotein AI levels, i.e., the main protein component of high density lipoprotein (HDL); propranolol caused a significant rise in total TG and very low density lipoprotein TG (VLDL-TG) levels (+37.3% and +23.9%, respectively). Somewhat lower total TG (+19.6%) and vLDL (17.8%) TG elevations were noted when propranolol was given first; plasma glucose was also significantly raised (+12.8%). Triglyceride and glucose levels returned to normal upon changing to prazosin. Total plasma- and lipoprotein-associated cholesterol levels were essentially unchanged with either drug; similarly, no significant changes were detected in total plasma apoprotein B (the main protein component of LDL and also VLDL), a component of apoprotein AI levels. Uric acid levels were slightly raised on propranolol. There was an 8.8% reduction in uric acid levels when the medication changed from propranolol to prazosin.
 ...
PMID:Plasma lipid and lipoprotein changes in hypertensive patients treated with propranolol and prazosin. 617 63

In normal subjects, insulin decreases the urinary excretion of sodium, potassium, and uric acid. We tested whether these renal effects of insulin are altered in insulin resistant hypertension. In 37 patients with essential hypertension, we measured the changes in urinary excretion of sodium, potassium, and uric acid in response to physiological euglycemic hyperinsulinemia (by using the insulin clamp technique at an insulin infusion rate of 6 pmol/min/kg). Glucose disposal rate averaged 26.6 +/- 1.5 mumol/min/kg, i.e., 20% lower than in normotensive controls (33.1 +/- 2.1 mumol/min/kg, P = .015) In the basal state, fasting plasma uric acid concentrations were higher in men than women (P < .001), were positively related to body mass index (r = 0.38, P = .02), waist/hip ratio (r = 0.35, P < .05), and serum triglyceride levels (r = 0.59, P = .0001), and negatively related to HDL cholesterol concentrations (r = -0.59, P = .0001) and glucose disposal rate (r = 0.42, P < .01). Uric acid clearance, on the other hand, was inversely related to body mass index (r = 0.41, P = .01), plasma uric acid (r = 0.65, P < .0001) and triglyceride concentrations (r = 0.39, P < .02), and directly related to HDL cholesterol levels (r = 0.52, P < .001). During insulin infusion, blood pressure, plasma uric acid and sodium concentration, and creatinine clearance did not change. In contrast, hyperinsulinemia caused a significant decrease in the urinary excretion of uric acid (2.67 +/- 0.12 to 1.86 +/- .14 mumol/min/1.73 m2, P = .0001), sodium (184 +/- 12 to 137 +/- 14 mumol/min/1.73 m2, P = .0001), and potassium (81 +/- 7 to 48 +/- 4 mumol/ min/1.73 m2, P = .0001). Both in absolute terms (clearance and fractional excretion rates) and percentagewise, these changes were similar to those found in normotensive subjects. Insulin-induced changes in urate excretion were coupled (r = 0.55, P < .0001) to the respective changes in sodium excretion. In hypertensive patients, higher uric acid levels and lower renal urate clearance rates cluster with insulin resistance and dyslipidemia. Despite insulin resistance of glucose metabolism, acute physiological hyperinsulinemia causes normal antinatriuresis, antikaliuresis, and antiuricosuria in these patients.
 ...
PMID:Effect of insulin on renal sodium and uric acid handling in essential hypertension. 886 20

Experimental animal models suggest that uric acid might have a pathogenic role in the early development of primary hypertension. We hypothesized that serum uric acid is correlated with blood pressure in children with new-onset, untreated, primary hypertension. We evaluated 125 consecutive children referred to the Baylor Pediatric Renal Program for evaluation of hypertension. None of the subjects had previously been evaluated or treated for hypertension. The children ranged in age from 6 to 18 years (mean, 13.4+/-3.3) and had normal renal function (creatinine clearance >80 mL x min(-1) x 1.73 m(-2)). Sixty-three children had primary hypertension, 40 had secondary hypertension, and 22 had white-coat hypertension. Forty controls with normal blood pressure were recruited from the renal clinic. Uric acid levels were directly correlated with systolic (r=0.80, P=0.0002) and diastolic (r=0.66, P=0.0006) blood pressure in controls and in subjects with primary hypertension and were independent of renal function. Serum uric acid concentrations >5.5 mg/dL were found in 89% of subjects with primary hypertension, in 30% with secondary hypertension, in 0% with white-coat hypertension, and in 0% of controls. We conclude that serum uric acid is directly correlated with blood pressure in untreated children and that a serum uric acid value >5.5 mg/dL in an adolescent being evaluated for hypertension strongly suggests primary hypertension as opposed to white-coat or secondary hypertension. These results are consistent with the hypothesis that uric acid might have a role in the early pathogenesis of primary hypertension.
 ...
PMID:Hyperuricemia in childhood primary hypertension. 1290 Apr 31


1 2 3 Next >>