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

18-hydroxy 11-deoxycorticosterone (18-OH DOC), a weak mineralocorticoid, was estimated by a radioimmunoassay procedure after purification in 49 patients with hypertension and 38 normal control subjects. The sensitivity of the method was 2-4 pg; there was no detectable blank, and the precision was 9-10%. In normal subjects the absolute plasma levels were similar to those of aldosterone. ACTH administration produced a 23-fold increase, and sodium restriction resulted in a 4-fold increase (5.4+/-0.7-20.5+/-3.0 ng/dl). On the other hand, the plasma levels of 18-OH DOC declined by nearly 50% with upright posture or angiotensin II infusion. During both of these procedures, plasma aldosterone levels significantly increased. Patients with normal and low renin hypertension had similar changes in plasma 18-OH DOC levels with sodium restriction. However, the mean high sodium level in the normal renin essential hypertension group (11.6+/-1.6 ng/dl) was significantly greater (P is less than 0.001) than in the control group (5.4+/-0.7 ng/dl). In addition, at least 22% and perhaps as high as 37% of the hypertensive subjects had levels greater than the upper limits of normal on a high sodium intake. Differences between the groups were less impressive in the sodium-restricted studies. There were no significant differences in age, duration of hypertension, sodium balance, serum sodium, potassium, or blood urea nitrogen in those patients who had elevated levels of plasma 18-OH DOC. Patients with primary aldosteronism had levels within the normal range on both dietary intake. However, in contrast to the other groups there were no significant changes in the plasma levels with sodium restriction. Thus, a significant number of patients with essential hypertension presumably have an alteration in 18-OH DOC secretion.
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PMID:The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man. 18 59

Endocrine activity in patients with essential hypertension was studied by measuring the urinary excretion of catecholamines, prostaglandin E (PGE) and cyclic adenosine monophosphate (cAMP). Simultaneously, plasma renin activity, concentrations of serum sodium, potassium, blood urea nitrogen (BUN) and creatinine were determined. Systolic blood pressure and BUN increased progressively with age until the sixth decade. Urinary excretion of norepinephrine was correlated with the systolic blood pressure. In contrast, plasma renin activity and urinary excretion of PGE decreased progressively with the increase in systolic blood pressure. Although the cause of essential hypertension is not known, it is suggested that hypertension accelerates the aging process in the kidney and thus decreases renal PGE synthesis. This decrease of PGE in turn causes a reduction of plasma renin activity, possibly either by accelerating the retention of sodium and water or by failing to stimulate renin synthesis. A decrease of PGE may also potentiate the vasopressor action of norepinephrine.
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PMID:Changes in hormonal activities relative to the severity of essential hypertension. 21 51

In a double-blind study, 28 patients having mild to moderate essential hypertension were randomly assigned to a 6-week regimen of ticrynafen, hydrochlorothiazide, or placebo. Blood pressure fell after ticrynafen and hydrochlorothiazide. Serum uric acid fell strikingly with ticrynafen whereas it rose with hydrochlorothiazide. Serum potassium declined very little with ticrynafen; much less than with hydrochlorothiazide. Serum creatinine and blood urea nitrogen rose slightly more with ticrynafen than with hydrochlorothiazide. There were no clinical adverse effects to either of the medications. Ticrynafen appears to be an effective antihypertensive with a substantial hypouricemic effect.
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PMID:Ticrynafen and hydrochlorothiazide in hypertension. 34 80

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

526 patients with essential hypertension or congestive cardiac failure were treated with ticrynafen (250--500 mg/day) or hydrochlorothiazide (50--100 mg/day) for 6 weeks to 6 months. There was no appreciable effect on renal function, as measured by changes in blood urea nitrogen and serum creatinine levels. Both drugs exhibited similar antihypertensive activity and ability to control signs and symptoms of congestive cardiac failure. Side effects were mild and reversible. A notable difference is the marked reduction in serum uric acid in patients treated with ticrynafen, unlike the elevated urate levels occurring after treatment with hydrochlorothiazide.
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PMID:Renal function during ticrynafen therapy. 38 57

In a double-blind study, thirty patients having mild to moderate essential hypertension were randomly assigned to a six week regimen of either tienilic acid, hydrochlorothiazide, or placebo. Blood pressure was significantly reduced with tienilic acid and hydrochlorothiazide although more so with tienilic acid. Serum uric acid declined strikingly with tienilic acid and increased significantly with hydrochlorothiazide. Serum potassium declined slightly with tienilic acid but more so with hydrochlorothiazide. Serum creatinine and blood urea nitrogen increased slightly more with tienilic acid than with hydrochlorothiazide. There were no clinical adverse effects to any of the medications during this study. Twenty-four months of continuous administration of tienilic acid revealed maintenance of blood pressure effect, but with slight increases in blood urea nitrogen, serum creatinine and uric acid and slight decreases in serum potassium as compared to six weeks administration. Tienilic acid appears to be a useful new antihypertensive agent. The hypouricaemic effect is profound and strongly suggests the need for continuing evaluation of this compound because of its unique combination of diuretic, antihypertensive and hypouricaemic properties.
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PMID:A double-blind study of tienilic acid with two year follow-up of patients with mild to moderate essential hypertension. 38 95

The purpose of this double-blind study was to compare the effects on blood pressure of tienilic acid and hydrochlorothiazide in patients with essential hypertension. The biochemical effects of tienilic acid in relation to those of hydrochlorothiazide were also determined over a long-term period of therapy. Sixty-six outpatients with mild to moderate essential hypertension were treated for seven months with either 250 mg of tienilic acid or 50 mg of hydrochlorothiazide after a 3 week placebo period. When warranted, dosage was increased to a maximum of 500 mg of tienilic acid and 100 mg of hydrochlorothiazide daily. Results indicate that tienilic acid reduced blood pressure significantly and to the same extent as hydrochlorothiazide. No significant side effects were observed. The effects on potassium, blood urea nitrogen and creatinine were comparable in both groups. However, serum uric acid rose with hydrochlorothiazide but fell with tienilic acid. In view of this effect, tienilic acid may have certain advantages over thiazide therapy in the treatment of hypertension.
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PMID:Long-term usage of tienilic acid in essential hypertension. 38 97

Endocrine and renal functions were studied in 149 patients with essential hypertension by measuring plasma electrolytes, renin activity, creatinine and aldoserone, as well as the urinary excretion of creatinine and sodium chloride, before and during treatment for hypertension. Half of the patients responded to trichlormethiazide (thiazide-responsive group) but the other half did not (thiazide-unresponsive group). Systolic and diastolic blood pressures increased progressively uith age in the thiazide-unresponsive group, but were lower and did not progress with age in the thiazide-responsive group. There was no consistent difference in plasma renin activity between the thiazide-responsive and the thiazide-unresponsive groups. The fluctuation of plasma renin activity in response to an excess of sodium chloride or to thiazide treatment was reduced progressively with age. Creatinine clearance decreased and the blood urea nitrogen level increased with age. The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water.
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PMID:Age-related changes in endocrine and renal function in patients with essential hypertension. 46 52

The effect of spironolactone (50 mg b.i.d.) in essential hypertension was studied by measurement of effective renal plasma flow (ERPF), blood urea nitrogen (Ur+), serum creatinine (Cr), cardiac index (CI), plasma volume (PV), body weight (BW), mean arterial blood pressure (MAP), total peripheral resistance index (TPRI), plasma renin activity (PRA) and plasma aldosterone (PA) in two groups of patients. Ten cases had determinations before, after 5 weeks and 4 months of treatment; fourteen cases who had been treated at an average of 18 months, had measurements while on treatment and 5 weeks after cessation of the drug. Among the ten patients ERPF fell in six and increased in four patients during treatment, but was statistically unchanged in the total group. Ur + and Cr were also unchanged by treatment. ERPF was unchanged after withdrawal of the drug. During treatment BW decreased 3.5%, PV decreased in nine and increased in one patient, while PRA and PA increased 426% and 202%, respectively. After cessation of the aldosterone blockade, BW increased 1.9%, PV 10.5% while PRA and PA fell 60% and 48.9%, respectively. MAP fell in eight out of ten patients during treatment. This fall was associated with a fall in CI or TPRI, or both. After withdrawal of the drug, MAP increased in nine and decreased in five of the patients. The data shows that this dosage of spironolactone gave minor adjustments of the systemic and renal circulation in spite of the consistent changes in BW, PV, PRA and PA.
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PMID:Haemodynamic effects of treatment and withdrawal of spironolactone in essential hypertension. 52 64

The antihypertensive effect of spironolactone was studied in 20 patients with essential hypertension and normal stimulated peripheral renin activity (PRA). Single-blind 8-wk treatment periods of placebo, 100, 200, and 400 mg spironolactone were used in consecutive order. Average supine and erect blood pressures were lower than placebo values at the end of each treatment. A prominent orthostatic effect was observed. Changes in blood pressure were not related to changes in body weight, PRA, or blood urea nitrogen. A larger proportion (50%) of patients had a more normal erect diastolic pressure at the end of 400 mg/day than at the end of 100 mg/day (20%), but the response to 400 mg/day could not be predicted from the responses to lower doses. Larger doses of spironolactone were predictably associated with rises in serum potassium, PRA, and aldosterone excretion. Adverse effects were absent during therapy with 100 mg/day but were frequent during 200--400 mg/day. Although there are no apparent advantages in increasing spironolactone from 100 to 200 mg/day in this group of patients with normal renin hypertension, increasing the dose to 400 mg/day resulted in better blood pressure control with more frequent adverse effects.
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PMID:Antihypertensive responses to spironolactone in normal renin hypertension. 69 76


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