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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood pressure lowering effects of spironolactone have been studied in 40 subjects with benign essential hypertension in an attempt to determine the optimum starting dose for the drug. The trial was carried out by the double blind method. In almost all patients 100-400 mg spironolactone caused a signnificant decrease in diastolic and systolic arterial pressure. Present findings indicate that 100-200 mg spironolactone represents the optimum attack dose. The medication caused a significant rise in serum potassium. Other parameters were not affected by the treatment. In conclusion, it would appear that spironolactone--in association with other antihypertensive regiments--may improve the treatment of essential hypertension, especially in patients showing a tendency to hypokalemia and uricemia, and may offer an additional possibility or alternative in the therapy of hypertensive diseases.
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PMID:[Detection of the optimal dose of spironolactone for the treatment of benign essential hypertension]. 33 98

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.
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PMID:[Experiences with a new hypouricemic diuretic (tienilic acid): comparison with hydrochlorothiazide]. 37

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.
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PMID:Serum uric acid and the renin-angiotensin system in hypertension. 65 66

Available clinical evidence indicates a high prevalence of hyperuricemia in patients with essential hypertension; this becomes accentuated with diuretic therapy. Since there is an association of hyperlipidemia with hyperuricuria and hypertension and since hyperuricemia is a feature of diuretic therapy, we explored whether these relationships might be provoked by prolonged diuretic therapy. Eighteen male patients with uncomplicated essential hypertension of mild severity were treated for 9 months with hydrochlorothiazide and supplemental potassium chloride, 100 mg and 45 mEq/day, respectively. Arterial pressure, renal function, and serum electrolyte, uric acid, blood glucose, and lipid concentrations were measured several times before and during therapy. Arterial pressure remained significantly reduced during therapy (P less than 0.001); this was associated with reduced serum potassium (P less than 0.01) and increased blood glucose and serum uric acid concentrations (P less than 0.005, P less than .025, respectively). Blood urea nitrogen, serum creatinine, sodium, cholesterol and triglyceride levels did not significantly change with treatment. Thus, although diuretics increase serum uric acid and blood glucose, their effect on serum lipid concentration is negligible.
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PMID:Effects of diuretics on lipid metabolism in patients with essential hypertension. 107 5

The aim of the study was to evaluate the antihypertensive effect of K-canrenoate, alone or in combination with butizide, in mild to moderate essential hypertensives. Fifteen patients (supine diastolic blood pressure ranging from 95 to 114 mmHg) received K-canrenoate 50mg/die (step 1). In patients with supine diastolic blood pressure greater than 90 mmHg therapeutic regimen was modified at two-week intervals according to the following design: K-canrenoate 100 mg/die (step 2), K-canrenoate 50 mg + butizide 5 mg/die (step 3), K-canrenoate 100 mg + butizide 10 mg/die (step 4). Blood pressure control was achieved in 2 patients treated with K-canrenoate alone (step 2) and in 8 patients on a combined regimen (step 3), and it was maintained throughout the whole trial period (12 weeks); step 4 did not achieve the goal of therapy in the remaining 5 subjects. A statistically significant increase in triglyceridemia (123.2 +/- 42.1 vs 158.3 +/- 62 mg/dl) and uricemia (4.6 +/- 0.9 vs 5 +/- 0.9 mg/dl) was observed at the end of the follow-up period. Serum potassium levels remained stable in all patients. Therefore, K-canrenoate in combination with butizide is an effective and well tolerated drug in the treatment of mild to moderate essential hypertension.
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PMID:[Potassium canrenoate and the combination of potassium canrenoate-butizide in the therapy of light to moderate arterial hypertension]. 150 73

Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

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.
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PMID:Evaluation of renal handling of uric acid in essential hypertension: hyperuricemia related to decreased urate secretion. 175 23

Evidence of old cerebral infarction of magnetic resonance imaging (MRI) is common in acute stroke patients without a prior history of stroke. This experience led us to investigate the incidence of silent cerebral infarction (SCI) in the patients with essential hypertension, as well-known major predisposing factor for stroke. The incidence, number, size and localization of SCI on MRI (MARK-J, 0.1 T) and the prevalence of risk factors for stroke were investigated both in 66 hypertensive patients (WHO stage I or II; 63 +/- 9 (mean +/- S.D.) years old) and in 42 age-matched normotensive patients (61 +/- 9 years old). Risk factors selected were as follows: diabetes mellitus, hypercholesterolemia, daily alcohol intake, cigarette smoking, obesity, cardiac disease (arrhythmia and ischemic heart disease), hyperuricemia and high hematocrit. In hypertensive patients, the relationships between the incidence of SCI and hypertensive damages in major organs were also investigated. SCI was found in 45 out of the 108 subjects studied and a total of 216 SCI lesions were detected. All of the SCI lesions were localized in the subcortical white matter or in the basal ganglia. All SCI lesions were smaller than 3 cm in diameter and 201 lesions (93%) were smaller than 1 cm. The incidence of SCI tended to be higher in hypertensive patients (47%) than that in normotensives (33%) and increased significantly with advancing age in hypertensives from 26.9% in the 50s to 86.7% in the 70s, while no significant increase was noted in normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Silent cerebral infarction in the patients with essential hypertension]. 179 35

In forty patients with mild to moderate essential hypertension and in twenty healthy subjects serum uric acid was measured and parameters of renal excretion of urate were evaluated. Serum uric acid concentration and prevalence of hyperuricemia were significantly higher in hypertensive patients. Patients with essential hypertension and concomitant hyperuricemia showed significantly decreased clearance and fractional excretion of uric acid in comparison with normotensive subjects. Adverse correlation between serum uric acid and clearance as well as fractional excretion of urate found in hypertensive patients indicates that high prevalence of hyperuricemia in essential hypertension is caused by impaired renal excretion of uric acid.
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PMID:[Uric acid and arterial hypertension. I. Relation between serum uric acid level and its renal excretion in primary arterial hypertension]. 180

In forty patients with mild to moderate essential hypertension correlation between serum uric acid as well as renal excretion of urate and the transport of uric acid in nephron was evaluated. Quantity of the separate phases of uric acid transport in nephron was calculated based upon pharmacological tests with pyrazinamide and benzbromarone. The results obtained in twenty normotensive subjects were assumed to be a normal values. Positive correlation between serum uric acid and presecretory reabsorption of urate was found in hypertensive patients. However presecretory reabsorption of urate did not significantly differ between hypertensive patients with concomitant hyperuricemia and normotensive subjects. Tubular secretion of uric acid was significantly lower in hypertensive patients in comparison with normotensive subjects. Plasma uric acid correlated inversely++ with tubular secretion of urate in patients with essential hypertension. There was no difference in postsecretory reabsorption of uric acid between the groups. Plasma uric acid did not correlate with postsecretory reabsorption of urate in hypertensive patients. These findings suggest that decreased uric acid clearance in hypertension with concomitant hyperuricemia is connected with impaired tubular secretion of urate.
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PMID:[Uric acid and arterial hypertension. II. Evaluation of uric acid transport in the nephrons in primary arterial hypertension]. 180 1


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