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)

Forty-five patients with mild to moderate essential hypertension were randomly assigned to receive 10 to 40 mg of manidipine HCl or 15 to 60 mg of delapril daily for 12 months. In the manidipine-treated group were 13 women and 5 men (mean age, 48.2 years) and in the delapril-treated group 11 women and 11 men (mean age, 53.7 years). Blood samples were taken at baseline and after 6 and 12 months of treatment and again at 2 months after treatment discontinuation. Significant reductions in blood pressure were observed in both treatment groups. The reduction in diastolic blood pressure was significantly greater in the manidipine-treated patients than in the delapril-treated patients; no significant between-groups differences in systolic blood pressure were noted. Heart rate increased significantly in the manidipine group. No changes in serum levels of total cholesterol, triglycerides, and high-density and low-density lipoprotein cholesterol were noted during or after treatment. In the manidipine group, a small but significant decrease in apolipoprotein (apo) A-I and an increase in lipoprotein(a) were found at 6 months and a significant increase in apo A-II and apo E at 12 months; in the delapril group a significant decrease in apo A-I was found at 6 months. The results indicate that both manidipine and delapril are lipid-neutral antihypertensive drugs, since neither drug greatly affected serum lipid metabolism.
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PMID:Effects of manidipine and delapril on serum lipids, lipoproteins, and apolipoproteins in patients with mild to moderate essential hypertension: a randomized trial with one-year follow-up. 128 88

We administered diltiazem HCl i.v. (0.05 mg/kg in bolus followed by 0.01 mg/kg/min for 45 min), and determined the changes in blood pressure (BP), glomerular filtration rate (GFR), renal blood flow (RBF), total renal resistance, urinary volume (UV), urinary sodium (UNa) and potassium excretion, urea and osmolar clearance, and tubular reabsorption ratio of sodium (TRNa%). The serum concentration of diltiazem achieved was similar to the maximum level after a single oral dose of 120 mg. GFR and RBF were measured by i.v. infusion of sodium thiosulfate and sodium rho-amino-hippurate, respectively, as indicators. The subjects included 12 cases of essential hypertension (EH), 10 of chronic glomerular nephritis (CGN) with hypertension, 12 of CGN without hypertension, 12 of ischemic heart disease (IHD), and 10 of normotensive controls. BP decreased in hypertensives but not in normotensives. In patients with EH, GFR and RBF increased markedly (by 25.3 +/- 33.8% and 30.7 +/- 39.5%, respectively). In patients with IHD, GFR increased slightly by 9.8 +/- 17.6%, whereas in patients with CGN with hypertension, GFR decreased by -4.3 +/- 14.3%. No significant change of these indices was observed in normal subjects and in patients with CGN without hypertension. UV and UNa increased and TRNa% decreased in all groups. Urea and osmolar clearance increased in almost every group.
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PMID:Clinical effects of intravenous diltiazem hydrochloride on renal hemodynamics. 243 98

Myocardial contractility of normotensive and spontaneously hypertensive rabbits was determined following an iv bolus injection of propranolol HCl. Left ventricular pressure and dimension were used to calculate the contractility parameters of (dP/dt)max, maximum fiber shortening velocity (Vcf), and the slope of the end systolic pressure-end systolic volume line (ESP-ESV line). Hypertension was induced by a methoxamine HCl iv infusion which mimicked the cardiac effects seen in essential hypertension. Propranolol caused a significant decrease in all contractility parameters (p less than 0.05) within 15 min after administration, with a peak effect occurring after 30-35 mins. The pharmacokinetics and pharmacodynamics of propranolol were fit using Hill's equation in conjunction with the concentration of drug in the theoretical effect compartment. The normotensive group of rabbits had a calculated EC(50) of 12.7 ng/ml, while the hypertensive group had an EC(50) of 6.9 ng/ml, indicating that the hypertensive rabbits were much more sensitive to the propranolol than the normotensive group. In addition, the normotensive group of rabbits demonstrated a much different pharmacokinetic-pharmacodynamic relationship than that of the hypertensive group, indicating that the hypertensive state of the animal has a significant effect upon the concentration-effect relationship.
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PMID:Effect of propranolol on the myocardial contractility of normotensive and spontaneously hypertensive rabbits: relationship of pharmacokinetics and pharmacodynamics. 261 85

Quinapril HCl is a novel, nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor. The Study Group evaluated its efficacy (20, 40, 80 mg daily with forced dose titration determination at trough blood pressure) once daily versus twice daily versus placebo, as well as its tolerability and safety, in 270 patients with mild to moderate essential hypertension (WHO Stages I and II, sitting diastolic blood pressure [DPB] greater than or equal to 95 mm Hg), for twelve weeks. Reductions in DBP of up to 13 mm Hg were obtained, and in full dosage more than 65% of patients achieved a reduction in DBP of 10 mm Hg or more from baseline or reduced their DBP to 90 mm Hg or less. Quinapril was well tolerated, and reported adverse effects were scarcely more frequent than in the placebo group. Once daily doses of quinapril were as safe and effective as twice-daily doses. Quinapril is likely to exhibit good therapeutic utility in the management of essential hypertension.
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PMID:Quinapril: a double-blind, placebo-controlled trial in essential hypertension. 265 May 81

A 20-week double-blind randomised study of 50 black hypertensive patients was designed to compare the efficacy and safety of indoramin (Baratol; Wyeth/Ayerst) and propranolol in patients who did not respond to diuretic therapy alone. Indoramin (initial dose 50 mg/d) or propranolol (initial dose 80 mg/d) was added to the regimen of patients whose supine diastolic blood pressure (SDBP) remained elevated at 100- 200 mmHg after 2 weeks' treatment with a combination diuretic tablet (hydrochlorothiazide 50 mg plus amiloride HCl 5 mg). Supine systolic blood pressure (SSBP) and SDBP of all patients was successfully controlled (SDBP lowered to less than 95 mmHg) by daily doses that did not exceed 100 mg of indoramin or 160 mg of propranolol; over 90% of patients in each group achieved control with lower doses, i.e. 50-75 mg of indoramin or 80-120 mg of propranolol. Although heart rate decreased from baseline values by approximately 9/min with both agents, the decreases were not significantly different between the treatment groups, and neither agent caused orthostatic hypotension. There were no statistically significant differences between the groups in the types or frequency of side-effects. Indoramin is well tolerated and is as effective as propranolol in black patients with essential hypertension who are not controlled by a thiazide diuretic alone.
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PMID:Double-blind study comparing indoramin and propranolol in the treatment of black patients with hypertension. 306 Oct 32

Diagnosis of pheochromocytoma has been made by the determination of urinary noradrenaline and adrenaline excretion for 24 hours. The assay procedure and the collection of urine for 24 hrs. are intricate. In the present study, we have ascertained the clinical significance of urinary normetanephrine (NM) and metanephrine (M), chemically stable metabolites of catecholamines, in single voided urine for a diagnosis of pheochromocytoma. Urine and plasma samples were collected from 361 normal subjects, 59 patients with essential hypertension, 22 patients with chronic renal failure and 22 patients with pheochromocytoma. Urinary NM and M concentrations were determined by radioimmunoassay with prior hydrolysis by acidification with 1N HCl. Plasma NM and M concentrations in normal subjects were 71.8 +/- 30.7 pg/ml and 41.5 +/- 8.61 pg/ml, respectively. Plasma NM was increased in 8 and plasma M was increased in 20 of 21 patients with pheochromocytoma, although many of these overlapped with those patients with chronic renal failure (NM, 285.9 +/- 175.1 pg/ml; M, 206.3 +/- 186.7 pg/ml) and essential hypertension (NM, 107.7 +/- 90.7 pg/ml; M, 46.7 +/- 20.2 pg/ml). Urinary NM and M concentrations did not show specific diurnal variation and there was significant correlations between the values in single voided urine and those in the 24 hour urine. Urinary NM and M concentrations in normal controls were 197.5 +/- 46.7 ng/mg Cr. and 125.3 +/- 37.1 ng/mg Cr., respectively. Urinary NM concentration was increased in 14 and urinary M concentration was increased in all of 17 patients with pheochromocytoma. In addition, urinary M concentration was higher in most of the 17 patients with pheochromocytoma than that in the patients with chronic renal failure and essential hypertension. However, the values in three patients with Sipple's syndrome with a small adrenal tumor or recurrent cases overlapped with those in other diseases. Relationships between urinary concentrations of NM and/or M and tumor size showed positive correlations. Urinary NM and M concentrations showed significant decreases after surgical removal of the tumors. These results suggest that NM and/or M concentrations in single voided urine could be a sensitive and specific diagnostic tool for pheochromocytoma.
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PMID:[Biochemical diagnosis of pheochromocytoma by determining normetanephrine and metanephrine concentrations in single voided urine]. 322 27

In a six-week multicenter, double-blind comparison study, moxonidine and clonidine HCl were tested in 122 and 30 outpatients, respectively, with mild to moderate hypertension (World Health Organization stage I and II; highest measured diastolic blood pressure, 90 to 115 mm Hg). Each agent reduced systolic and diastolic blood pressure to a similar significant extent: moxonidine, 25.4 and 12.4 mm Hg, respectively; clonidine, 25.3 and 10.0 mm Hg, respectively (P less than .001 vs baseline). The mean individually titrated dose of moxonidine and clonidine HCl was found to be 0.36 mg/d. Clonidine slightly reduced heart rate in patients assuming an upright position by 3 beats/min at the end of dose titration (P = .018), while moxonidine did not. Two patients receiving moxonidine and three patients taking clonidine HCl discontinued therapy because of side effects. However, patients administered clonidine experienced significantly more side effects (53%) compared with a 30% incidence of adverse effects associated with moxonidine (P = .031). The most frequent adverse effect of both agents was dryness of mouth, which was mentioned significantly more often with clonidine (47%) than with moxonidine (20%) (P = .005). Edemas were found in 0.8% and 17% of patients during six-week treatment with moxonidine and clonidine, respectively (P = .001). Accordingly, moxonidine was tolerated significantly better than clonidine (P less than .001) in this parallel comparison study. Moxonidine is as effective as clonidine in monotherapy of mild to moderate essential hypertension and, additionally, neither drug produces clinically important changes in biochemical parameters.
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PMID:Comparison of moxonidine and clonidine HCl in treating patients with hypertension. 331 4

For the quantitative determination of dihydralazine (1) a derivative with acetylacetone in biological material was formed at pH = 4.9, extracted with n-hexane, and measured gaschromatographically with N-P-FID. Acid labile 1 was hydrolyzed with HCl (1 mol/l) for 24 h. The detection limit was 25 nmol/l plasma. Kinetic studies were performed in 16 patients with essential hypertension under steady-state conditions after the oral application of 50 mg 1. The acetylator phenotype was determined with sulfamethazine. Complete dihydralazine plasma level-time courses were found in only 5 cases. The concentrations were below the detection limit in 4 patients for the whole period. Only single values could be registered in the remaining patients. Maximal plasma levels of the free (58-314 nmol/l) and acid labile 1 (147-367 nmol/l) were reached 20-40 min after the application. The elimination half life was 23-47 min for the free 1, 55-92 min for the acid labile 1. Less than 0.5% of the applied drug were excreted into the 24 h urine in its free form, about 0.4% as acid labile derivatives. No correlation could be found between the acetylator phenotype of the patients and the kinetic behaviour of the drug. Preliminary studies concerning the biliary excretion of 1 after i. m. application in two patients with T-drain showed an accumulation of the free compound with bile/plasma ratios up to 7.4.
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PMID:[Quantitative determination and kinetics of dihydralazine in hypertension patients]. 409 28

Single oral doses of 1.5, 3.0, 4.5 and 6.0 mg/kg prizidilol HCl, an antihypertensive with vasodilator and beta-adrenoceptor blocking actions, were given to 12 patients with primary hypertension on separate days. Systolic and diastolic blood pressure (BP) decreased after 4.5 and 6.0 mg/kg and systolic BP also after 3.0 mg/kg. The antihypertensive effect was evident in 1 to 2 hr with maximum effect in 4 to 5 hr (supine systolic BP 20 and diastolic 13 mm Hg after 6.0 mg/kg); the effect was sustained for more than 8 hr. An initial slight reduction in heart rate (HR) after 1 to 2 hr was followed by a slight rise after 6 to 8 hr. There were higher plasma drug levels and greater antihypertensive effects after the 6.0-mg/kg dose in slow acetylators (n = 5) than in rapid acetylators (n = 7). Due to its hydrazine moiety, prizidilol, like hydralazine, seems to be a substrate for the polymorphic N-acetyltransferase enzyme system.
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PMID:Prizidilol, an antihypertensive with precapillary vasodilator and beta-adrenoceptor blocking actions, in primary hypertension. 611 9

Diltiazem HCl was administered p.o. at a fixed daily dose level of 180 mg to patients with essential hypertension, and the hypotensive effect of the drug was investigated. The following results were obtained: diltiazem HCl given alone exhibited a hypotensive effect on systolic pressure in 88.9% of the patients and on diastolic pressure in 66.7% of the patients. The concurrent use of diltiazem HCl with trichlormethiazide exerted a hypotensive effect on patients who were nonresponsive to diltiazem HCl alone. As regards side effects, one patient complained of gastric fullness and one of dizziness. However, the symptoms were so mild that further continuation of diltiazem HCl therapy was possible. From the results obtained, it is concluded that diltiazem HCl can effectively be used clinically as a hypotensive drug.
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PMID:Clinical study on the hypotensive effect of diltiazem hydrochloride. 721 50


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