Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind controlled, randomized, parallel, multicenter 12-week study was conducted to compare the antihypertensive efficacy of lisinopril with that of metoprolol in treatment of moderate to severe hypertension. Initially, 118 patients were recruited on lisinopril and 61 on metoprolol; and for the purpose of efficacy analysis at week 8, 115 patients on lisinopril and 60 on metoprolol were included. The doses of lisinopril or metoprolol were 40-80 mg/day and 100-200 mg/day, respectively. At week 4, the pretreatment diastolic blood pressure of 111 mm Hg was decreased to 97 mm Hg (p less than 0.01) with lisinopril: metoprolol decreased the diastolic blood pressure from 110 to 99 mm Hg (p less than 0.01). Similar decreases were noted at week 8; however, the drop in blood pressure with lisinopril was not significantly different from that with metoprolol. Systolic blood pressure also demonstrated a decrease of about 18 mm Hg with lisinopril and 12 mm Hg with metoprolol (p less than 0.01). This larger decrease in systolic blood pressure with lisinopril was statistically significant at week 4 (p less than 0.05). These decreases in systolic blood pressures were maintained at week 8, again with statistical significance (p less than 0.01). Of the 118 lisinopril-treated patients, four were discontinued from lisinopril therapy because of headache, dizziness, rash, flushing, or lymphadenopathy. Four patients out of 61 (9.8%) were discontinued from metoprolol therapy because of fatigue, somnolence, asthenia, weight gain, flatulence, tremor, or bronchospasm. In conclusion, lisinopril 40-80 mg once daily is as effective as metoprolol 100-200 mg once daily in reducing diastolic blood pressure in patients with moderate to severe hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of antihypertensive efficacy of lisinopril compared to metoprolol in moderate to severe hypertension. 244 53

Throughout the developed world, populations are growing older. Blood pressure, especially systolic blood pressure, increases with aging, and this increase leads to increased risks of cardiovascular morbidity and mortality. Clinical trials demonstrate that treatment of hypertension in the elderly reduces overall cardiovascular mortality, cardiac mortality, nonfatal cardiovascular events, congestive heart failure, progression to severe hypertension, and strokes. Drug treatment has been well tolerated, but diuretic therapy has been known to increase plasma glucose, uric acid, and creatinine. Therapeutic trials of nonpharmacologic treatment may be indicated in those with mild elevation in blood pressure and no serious end organ disease. However, most people up to age 80 will require drug treatment. Many drugs are effective in the elderly, but, some like beta-blockers, may not be as effective as in younger patients. Controlled clinical trials demonstrate that nitrendipine, a calcium channel blocking drug, significantly reduced mean systolic and diastolic blood pressure in older hypertensive patients, (successfully controlling pressure in a high percentage) and was well tolerated. Drug effects persist for 12 h or more. The drug decreased the exercise-induced rise in the rate-pressure product. Although there is a temporary increase in heart rate, this returns to baseline after a short time. Side effects include headache, flushing, dizziness, edema, and palpitations. Therefore, nitrendipine offers a reasonable and useful alternative to many other drugs in the treatment of combined systolic and diastolic hypertension in the elderly.
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PMID:Epidemiologic aspects of elderly hypertensive patients and the results of treatment with nitrendipine. 248 68

The antihypertensive efficacy of a combination of calcium-channel blockers and angiotensin-converting-enzyme (ACE) inhibitors in severe primary hypertension is well known, but a synergistic action of this drug combination in mild to moderate primary hypertension is still not established. Therefore, the aim of the present study was to evaluate the efficacy and tolerability of monotherapy with nitrendipine (20 mg) or captopril (100 mg), and of their combination (nitrendipine 10 mg plus captopril 50 mg), in patients suffering from mild to moderate primary hypertension, according to a single-blind, randomized, placebo-controlled design. After the first 4-week monotherapy period, both nitrendipine and captopril induced a significant decrease in systolic and diastolic blood pressure (BP) (p less than 0.001). Furthermore, nitrendipine caused a significant increase in heart rate (HR), while no change in HR was observed in patients treated with captopril. Several side effects were observed, both in the nitrendipine-treated patients (facial flushing, headache, malleolar edema) and in the captopril-treated patients (initial hypotension, dizziness, gastrointestinal disorders). However, these side effects were mild and were well tolerated. In the second combined 4-week therapy period, systolic and diastolic BP of patients treated with 10 mg nitrendipine combined with 50 mg captopril continued to decrease to a degree significantly lower (p less than 0.001) than that observed at the end of the monotherapy period. Simultaneously, no change in HR values occurred when compared to basal values. Furthermore, the incidence and intensity of some side effects observed during the combined therapy period were lower than those of the monotherapy period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium-channel blockade (nitrendipine) in combination with ACE inhibition (captopril) in the treatment of mild to moderate hypertension. 248 3

Although calcium antagonists may impair insulin release in vitro, clinical studies have produced conflicting results. Felodipine is a highly selective dihydropyridine calcium antagonist effective in the treatment of hypertension. The efficacy of felodipine was assessed in a double-blind randomized placebo cross-over study of 21 Type 2 diabetic patients with primary hypertension, 13 men and 8 women, with an age of 61 (range 46-73) years. Thirteen were controlled on oral hypoglycaemic therapy and 8 on diet alone. Mean (SD) blood pressure (mmHg) was 176(20)/102(8) after a 2-4 week placebo run-in period, 169(21)/101(8) during the subsequent placebo period compared with 151(15)/88(9) after 4 weeks felodipine therapy (p less than 0.001). Nineteen patients required 5 mg twice daily and 2 patients 10 mg twice daily to achieve a target diastolic pressure of 95 mmHg. Side-effects seen with felodipine included ankle oedema, facial flushing, headache, and dizziness. During oral glucose tolerance tests performed after the felodipine and placebo phases, mean (SD) fasting blood glucose was 9.5(3.1) and 9.0(3.0) mmol l-1, respectively (NS), and the 90 min (peak) blood glucose was 19.1(4.8) and 18.1(4.8) mmol l-1, respectively (NS). Glycosylated haemoglobin and fructosamine concentrations likewise showed no significant changes.
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PMID:A trial of the calcium antagonist felodipine in hypertensive type 2 diabetic patients. 253 42

Amonafide (benzisoquinolinedione, NSC 308847) is a new synthetic imide antineoplastic agent with DNA intercalative properties that has been evaluated in a phase I clinical trial. The drug was administered as a single intravenous (IV) infusion over 30 to 120 minutes repeated every 28 days. Ninety-five courses of therapy at doses ranging from 18 to 1,104 mg/m2 were administered to 38 patients with refractory solid tumors. Granulocytopenia was dose limiting. Leukopenia was seen in 13 of 31 courses at doses of 690 mg/m2 or greater. Life-threatening granulocytopenia (less than or equal to 250 microliters) was noted in 1/6 patients treated at 800 mg/m2, 1/8 patients treated at 918 mg/m2, and 2/5 patients treated at 1,104 mg/m2. No definite relationship between myelotoxicity and prior treatment status was noted. Rate-of-infusion dependent, nonhematologic toxicities included diaphoresis, flushing, dizziness, and tinnitus, all of which were ameliorated by increasing the duration of drug infusion to 120 minutes. In addition, nausea and vomiting (grades 1 and 2) were seen in 29/56 courses at doses greater than or equal to 519 mg/m2, but were easily controlled by phenothiazine antiemetics. Amonafide plasma and urine concentrations were determined by high-pressure liquid chromatography (HPLC). Plasma concentrations declined biexponetially with a terminal harmonic mean terminal half-life (t 1/2) of 5.5 h. The mean apparent volume of distribution at steady-state and total body clearance were 532 L/m2 and 84 L/h/m2, respectively. Less than 5% of the total dose of amonafide was excreted unchanged in the urine. Antitumor activity has been noted in one patient with non-small-cell lung cancer (one complete response exceeding 29 months duration) and in one patient with prostatic cancer (complete pain relief and improvement in bone scan for 9 months). The recommended dose for phase II trials with this schedule of amonafide is 918 mg/m2 with dose escalation to amonafide is 918 mg/m2 with dose escalation to myelotoxicity.
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PMID:Phase I clinical investigation of amonafide. 254 5

A total of 126 patients from general practice with chronic stable angina pectoris entered the treatment phase of this open, randomized, crossover comparison of 20 mg isosorbide-5-mononitrate, and 20 mg nifedipine. Both treatments were given orally, three times daily, for 4 weeks and sublingual administration of glyceryl trinitrate was allowed throughout. Over the whole treatment period, there was no statistically significant difference between treatments for anginal attacks. However, significantly fewer glyceryl trinitrate tablets were required by patients receiving prophylaxis with nifedipine, although this difference was too small to be of clinical significance. No statistical difference existed between treatments in respect of scores for 'overall intensity of pain', 'physical exercise ability' and 'general well-being'. Of those patients who expressed a preference, the majority preferred the second treatment with no statistically significant difference between isosorbide-5-mononitrate and nifedipine. Both treatments showed similar levels of adverse events, the major difference (not significant) being for flushing of the skin which occurred in five patients given nifedipine compared with one patient given isosorbide-5-mononitrate. It is concluded that, in clinical terms, the two treatments were similar. Headache and dizziness/giddiness were the most frequently recorded adverse events.
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PMID:A multicentre open comparison of isosorbide-5-mononitrate and nifedipine given prophylactically to general practice patients with chronic stable angina pectoris. 265 33

1. The antihypertensive efficacy of a long acting formulation of the calcium channel blocking drug, nicardipine, was assessed using clinic and ambulatory (Remler M2,000) blood pressure measurements. 2. Eleven patients with essential hypertension (mean +/- s.e. mean; 173 +/- 6.6/103 +/- 1.9 mmHg) completed a randomised double-blind, placebo-controlled, cross-over study. The dose of nicardipine used was 60 mg twice daily for 4 weeks. 3. Mean ambulatory blood pressure was reduced from 164 +/- 5.3/97 +/- 2.9 to 151 +/- 5.2/88 +/- 2.4 mmHg (P less than 0.01); this effect was shown to be sustained for 8 h after the morning dose. Mean ambulatory heart rate was not significantly affected by treatment. 4. Clinic lying systolic blood pressure was reduced on treatment from 169 +/- 7.1 to 157 +/- 5.9 mmHg (P less than 0.2) and diastolic blood pressure from 99 +/- 3.6 to 89 +/- 3.9 mmHg (P less than 0.05). 5. One patient was withdrawn because of dizziness and flushing while on nicardipine; vasodilatory side effects such as headache, palpitations and flushing on nicardipine were noted by three patients. 6. We conclude that the long acting formulation of nicardipine studied in a dose of 60 mg twice daily is effective as monotherapy and is relatively well tolerated in mild hypertension. 7. This study highlights the importance of ambulatory blood pressure measurement in detecting significant changes in blood pressure, thereby permitting the study of small numbers of patients.
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PMID:The effect of slow-release nicardipine on ambulatory and clinic blood pressure in mild hypertension. 267 16

Most side-effects of calcium channel blockers are related to their pharmacological properties. This is best illustrated by the most common cardiovascular side-effects, which reflect the differences between the drugs of such a heterogeneous group. Side-effects related to excessive vasodilating activity (headache, dizziness, flushing, peripheral edema, and palpitations) are most likely with drugs such as nifedipine and other dihydropyridines, which are most active on vascular smooth muscle. Those related to depressed cardiac contraction and conduction are more likely with verapamil, whereas diltiazem is intermediate between the other two drugs. In the event of the occurrence of these adverse reactions, factors such as pharmacokinetics, galenic form, and the administration mode play a role. The pathological status of the patient also comes into play. Other less common reactions such as neuropsychic, gastrointestinal and endocrine effects and gingival hyperplasia appear as a consequence of the numerous sites of action of these molecules. Hepatic, haematological and cutaneous reactions appear to be relevant to immunological mechanisms. Therefore, most of the adverse effects of calcium channel blockers originate in the common mechanism of action of these drugs.
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PMID:[Side-effects of calcium inhibitors]. 267 81

51 hypertensive outpatients, whose diastolic blood pressure exceeded 100 mmHg after a 2-week period on atenolol alone (100 mg once daily) participated in this long-term study. They received, in addition to atenolol, the vasodilator cadralazine (ISF 2469; 10 to 30 mg once daily) for a standard period of 24 weeks, according to an open design. Cadralazine caused a progressive and important decrease in both systolic and diastolic blood pressure, from 173/111 mmHg (end of atenolol alone) to 154/99 mmHg (12th week, p less than 0.01/p less than 0.01; mean dose, 24.5 mg/day). At this time a diuretic was added as a third-step drug in 15/51 initial patients (29%), and final blood pressure in all patients was 150/96 mmHg (p less than 0.01/p less than 0.01), with positive results in 88% of the cases. During cadralazine treatment, heart rate was always significantly lower than before atenolol alone; the most common side effects, many of which were already present during treatment with atenolol alone, included headache, asthenia, dizziness, palpitation and flushing, and tended to disappear spontaneously as therapy progressed. Routine laboratory tests did not show important changes; sodium excretion was not reduced. In conclusion, the therapeutic efficacy of cadralazine, its low or absent salt and water retention effects, its good tolerability, and the high compliance obtained with once daily administration allowed the use of this vasodilator as a second-step drug for long-term treatment of hypertension.
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PMID:Cadralazine, a new vasodilator, in addition to a beta-blocker for long-term treatment of hypertension. 285 65

The so-called Oriental flushing reaction associated with ingestion of small amounts of alcohol was antagonized by combined antihistamine administration. In stage one of the study, the flushing reaction to low doses of alcohol was produced in Orientals. Most subjects experienced a cutaneous flush, increase in skin temperature, decrease in blood pressure, increase in pulse rate and subjective symptoms such as dizziness, sleepiness, anxiety, headache, generalized weakness and nausea. One half of the group of subjects was then given diphenhydramine, 50 mg (H1 receptor antagonist) and cimetidine, 300 mg (H2 receptor antagonist) and the second half received placebo tablets before the administration of alcohol. The clearest difference between the antihistamine group and placebo group was in the skin flushing reaction. The antihistamine group showed a statistically significant reduction in the skin flush. The antihistamines also neutralized the systolic hypotension induced by the administration of alcohol.
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PMID:Combined antihistamine antagonism of the flushing reaction to alcohol. 289 99


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