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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we compared the effects of nitrendipine (20-40 mg daily) and enalapril (20-40 mg daily) in 44 patients with mild to moderate essential hypertension. After a 4-week placebo period, the patients entered a double-blind, crossover study of 16 weeks, divided by a second 4-week placebo period. Sitting and standing blood pressures (standard mercurymeter) were measured every 2 weeks. Ten patients dropped out, so 34 patients were evaluable. Two patients dropped out because of surgery, one patient was withdrawn because of accelerating hypertension, and seven patients discontinued because of side effects (two on placebo, four on enalapril, and one on nitrendipine). Sitting blood pressures decreased from 172 +/- 3/107 +/- 1 to 159 +/- 3/94 +/- 1 mm Hg on nitrendipine (p less than 0.001) and to 157 +/- 4/96 +/- 2 mm Hg on enalapril (p less than 0.001). The heart rate did not change. Both compounds had no significant effect on serum lipids and on renal function. With regard to side effects, flushing occurred in 10 patients on nitrendipine and in 3 on enalapril (p less than 0.05); cough was noted in 3 patients on enalapril. When using a diastolic pressure less than 95 mm Hg as a response, 72% responded on nitrendipine and 64% on enalapril (n.s.). In conclusion, nitrendipine and enalapril, given as monotherapy, were equally effective antihypertensive agents in this group of patients with uncomplicated, moderate, essential hypertension. The use of either of the tested agents seems to be more limited by its specific side effects than the lack of antihypertensive efficacy.
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PMID:A comparative study of the effects of nitrendipine and enalapril in essential hypertension. 172 60

Improved measurement of plasma concentrations of nitrendipine demonstrates a plasma half-life of 17 to 21 h allowing once daily dosing for antihypertensive treatment. To determine the effectiveness and tolerability of nitrendipine given once versus twice daily, 78 patients with mild to moderate essential hypertension were randomized in a double-blind fashion to 12 weeks of treatment with either nitrendipine 20 mg once daily (n = 39) or nitrendipine 10 mg bid (n = 39). Blood pressures measured at the end of the dosing interval were similar on 20 mg once daily and 10 mg bid. Adverse events considered to be drug related (flushing and headaches) occurred mostly at the beginning of active treatment and more frequently on the once daily dosing, resulting in a greater number of patients being withdrawn from the once daily treatment group. Thus, nitrendipine 20 mg once daily lowered blood pressure as effectively as 10 mg bid but was associated with a higher incidence of adverse events. These could be minimized by starting at nitrendipine 10 mg once daily and increasing to 20 mg once daily after two to four weeks.
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PMID:Effectiveness and tolerability of once versus twice daily nitrendipine in the treatment of mild to moderate hypertension. The Canadian Nitrendipine Study Group. 204 84

Sudden hypertensive surges are often observed in patients with primary hypertension. Even though the possibility of a pheochromocytoma almost automatically comes to mind, this diagnosis is confirmed only in a few patients (less than 1%). The case of a 55 yr old patient with very high posture-or emotion-induced hypertensive paroxysms, often associated with chest pain and flushing is described. All laboratory tests were normal except for plasma catecholamines, which were high especially during stress tests (Tab. II). The existence of a pheochromocytoma was excluded on the basis of repeatedly normal urinary catecholamine levels after hypertensive crises and a negative CT abdominal scan and I131 MIBG adrenal scintigraphy. An alteration of the baroreceptor reflex was ruled out, as the blood pressure response to autonomic function tests was normal. The cause of the orthostatic hypertensive crises could not be attributed to hypovolemia, as plasma volume proved normal. Measurement of circulating catecholamines showed elevated free plasma epinephrine with low conjugated epinephrine indicating a defective conjugation of this amine. This finding suggests an injured inactivation of epinephrine and might be involved in the pathogenesis of the hypertensive crises observed. Continuous intra-arterial blood pressure monitoring demonstrated the existence of mild hypertension with a normal 24-hour blood pressure pattern. However, the tracings were interspersed with numerous blood pressure peaks. Average 24 hour blood pressure was normalized by the therapy, but the hypertensive crises were not controlled by any of the drugs used. The absence of target organ damage despite the spectacular rises in blood pressure suggests that the cardiovascular system is well able to withstand hypertensive episodes if they are short lived.
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PMID:["Essential" hypertension with extreme pressure variability. Description of a case and considerations]. 207 89

1. The aim of the study was to compare the efficacy and the tolerability of treatment with atenolol (50-100 mg once daily), nitrendipine (20-40 mg once daily) and their combination (atenolol 50 mg + nitrendipine 20 mg) once daily in patients with mild to moderate essential hypertension. 2. The study was a randomised, double-blind, placebo controlled parallel groups design: blood pressures were measured at 'trough' effect (i.e. 24 h after dosing) to assess the adequacy of once-daily treatment. 3. Mean blood pressures (mm Hg) recorded on four occasions over 12 weeks of treatment were significantly lower both with atenolol (155/97 sitting: 155/104 standing) and with the combination of atenolol plus nitrendipine (153/96 sitting: 152/104 standing) than with placebo (169/108 sitting: 169/114 standing). Nitrendipine alone had no significant effect on blood pressure 24 h after dosing (165/104 sitting: 165/110 standing). 4. Withdrawals due to adverse effects were more common during treatment with nitrendipine: 7/32 of the patients experienced adverse effects attributable to intense systemic vasodilatation (e.g., flushing, erythema, headache). 2/37 patients taking atenolol were withdrawn: one because he developed a psoriatic rash and the other because of impaired peripheral circulation. Of the 35 patients taking combination treatment, two were withdrawn: one developed headaches and dyspnoea, and the other asthma. 5. The results suggest that once daily dosing with nitrendipine does not control blood pressure throughout the 24 h period in the majority of patients, and is associated with a considerable burden of adverse effects. Combination treatment was better tolerated but appeared to offer no advantages over atenolol alone in terms either of blood pressure control or adverse effects.
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PMID:Comparison of once daily atenolol, nitrendipine and their combination in mild to moderate essential hypertension. 218 68

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c)AMP is known to act as a second messenger for platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP, for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side effects, primarily nausea, emesis, flushing, diphoresis and restlessness. In hypertensive patients blood pressure responses are complex and are influenced to some extent by secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and also has an indirect effect by activating the sympathetic nervous system. Thus it is useless as an antihypertensive agent even apart from its debilitating side effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize larger amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension, endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be defective. Some drugs (cicletanine, thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to abolish their antihypertensive effects. Whether stimulation of PGI2 synthesis affects the antihypertensive efficacy of these drugs is not yet known.
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PMID:Prostacyclin in hypertension. 225 88

We assessed the efficacy of long-acting nifedipine as monotherapy in 52 patients with mild to moderate essential hypertension in a randomized, controlled crossover study. Good blood pressure control was achieved in 34 of 40 patients (85%) receiving nifedipine (mean daily dose, 52 mg in 2 divided doses) compared with 23 of 40 patients (58%) receiving metoprolol (mean daily dose, 155 mg in 2 divided doses). After treatment for 4 weeks, the mean blood pressures with nifedipine (149.7 +/- 16.6/88.7 +/- 11.1 mm of mercury) and metoprolol administration (163.9 +/- 23.3/94.2 +/- 10.2 mm of mercury) were significantly lower than with placebo (176.7 +/- 17.3/100.9 +/- 7.1 mm of mercury) (P less than .05). The mean systolic pressure during nifedipine treatment was 14.2 mm of mercury lower (95% confidence interval [CI], 3.9 to 24.5 mm of mercury) and mean diastolic pressure 5.5 mm of mercury (95% CI, 0.3 to 10.7 mm of mercury) lower than with metoprolol therapy. Both drugs were reasonably well tolerated, and intolerance requiring withdrawal was encountered in 3 of 45 (7%) patients receiving nifedipine, compared with 1 of 45 (2%) of those taking metoprolol and placebo, respectively. Adverse effects of nifedipine, most of which were transient, included palpitations, headache, facial flushing, and ankle edema. Long-acting nifedipine is a promising agent when given alone for mild to moderate hypertension and can be safely administered in clinical practice.
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PMID:Long-acting nifedipine versus metoprolol as monotherapy for essential hypertension. A randomized, controlled crossover study. 240 30

From a hemodynamic point of view, the calcium antagonists represent an interesting way of treating hypertension, because they reduce total peripheral resistance without compromising cardiac output. Blood flow is also maintained during muscular exercise. Verapamil and diltiazem induce slight reduction in heart rate, but this is compensated by increase in stroke volume. Verapamil and diltiazem also prolong atrioventricular conduction time, in contrast to the dihydropyridines. Most clinical data are available for verapamil, diltiazem, and nifedipine. In patients with mild-to-moderate hypertension, these compounds seem as effective as diuretics and beta-blockers. They do not induce disturbances in glucose metabolism, serum uric acid, or serum potassium, and unwanted disturbances in blood lipids have not been described. The dihydropyridines may safely be combined with beta-blockers, but the combination of either verapamil or diltiazem with a beta-blocker should be avoided (because of the high risk of bradycardia). The calcium antagonists seem particularly useful in patients with the combination of hypertension and angina pectoris or peripheral vascular diseases or chronic obstructive lung diseases or diabetes. They are also effective in hypertensive crises. They may also be tried as a first line drug in patients with mild and moderate essential hypertension, particularly when diuretics or beta-blockers are contraindicated. Temporary side effects due to vasodilatation (headache, flushing, and palpitations) are seen frequently, particularly on the dihydropyridines. Edema is the most frequent serious side effect of the dihydropyridines, and constipation is most common with verapamil. At this point, few long-term data are available and it is not known whether the calcium antagonists will give better or worse results, with respect to morbidity and mortality, than the beta-blockers, diuretics, or other more recent antihypertensive agents.
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PMID:Clinical use of calcium antagonists in hypertension: update 1986. 245 35

Felodipine was compared with prazosin in patients with essential hypertension whose blood pressure was not controlled by a beta-blocking drug. One hundred patients with a supine diastolic blood pressure greater than or equal to mm Hg after 4 weeks or more on a beta-blocking drug and placebo were randomly assigned to felodipine or prazosin tablets. The drugs were titrated at 2-week intervals if diastolic BP was greater than or equal to 90 mm Hg. Titration steps of felodipine were 5, 10, 20 mg b.i.d. and of prazosin were 1, 2, 4 mg b.i.d. The fall in blood pressure with felodipine 32/21 mm Hg was greater than the fall with prazosin 16/12 mm Hg (p less than 0.001); 36 patients achieved a diastolic blood pressure of less than 90 mm Hg with felodipine, which was a significantly greater number than the 20 patients who obtained such a level with prazosin (p less than 0.01). Both drugs were well tolerated, but more patients complained of vascular type side effects (flushing, peripheral edema) with felodipine than with prazosin. There was significant weight gain with prazosin but not with felodipine. Felodipine was shown to be a well-tolerated, effective antihypertensive agent when used with a beta-blocking drug and to be suitable for people with hypertension who fail to be controlled with a beta-blocking drug.
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PMID:Felodipine compared to prazosin as additional therapy to a beta-blocking drug. 245 50

Lisinopril, a long-acting angiotensin converting enzyme inhibitor, and the calcium channel blocker nifedipine in its retard formulation, were compared as monotherapy in a group of 45 patients with essential hypertension. Lisinopril in single daily doses (range 20-80 mg, median dose 40 mg) and nifedipine retard in twice daily doses (total daily dose range 40-80 mg, median dose 60 mg) were equally effective in controlling hypertension. The lisinopril group (n = 30), at baseline supine blood pressure 178/109 +/- 23/9 mm Hg (mean +/- 1 SD), after 12 weeks' therapy measured 148/88 +/- 27/14 mm Hg; the nifedipine group (n = 15), at baseline 185/110 +/- 23/11 mm Hg, after 12 weeks' therapy measured 151/89 +/- 14/10 mm Hg. The number of patients who experienced clinical adverse effects was significantly greater in the nifedipine group: 8 of 15 (53%) compared to 4 of 30 (13%) in the lisinopril group. The commonest adverse effects of patients on nifedipine were swollen ankles, flushing, and headache. Two patients on nifedipine were withdrawn from the study because of their adverse experiences. Of the patients on lisinopril there were single reports of flushing, ankle swelling, tiredness, and chest pain. No patient withdrew from lisinopril because of an adverse experience. No adverse laboratory experiences were recorded in either group. In conclusion, lisinopril and nifedipine retard were equally effective in controlling essential hypertension. Lisinopril was, however, better tolerated during this study.
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PMID:Comparative efficacy of lisinopril and nifedipine retard in essential hypertension: a double-blind, placebo-controlled trial. 245 54

The purpose of the present article is to review a number of studies dealing with the efficacy of calcium antagonists, in particular verapamil, in the treatment of essential hypertension. Several well-controlled studies have shown that verapamil causes a significant decrease in both systolic and diastolic pressure. Blood pressure decrease, which is of the same magnitude as with propranolol, is related to pretreatment values and, according to some authors, to age, but the latter statement is being refuted by others. Using a slow-release preparation, it can be shown that the 24-h blood pressure profile with once-daily administration is quite similar to the profile seen with three-times-daily administration of the regular formulation of verapamil. It has also been documented that the blood pressure decrease persists during 1-year continued administration. Optimal effect is seen at 240-320 mg/day. The most frequent side effects are constipation, flushing, and conduction disturbances. It is often proposed that the addition of a diuretic to verapamil does not increase the antihypertensive effect, but recent studies provide evidence to the contrary. Finally, ambulatory pressure recordings have shown that nifedipine does not decrease blood pressure variability. In general, calcium antagonists seem to be effective antihypertensive drugs but their place in the daily antihypertensive treatment has still to be defined.
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PMID:Calcium antagonists in the treatment of essential hypertension: review of international studies. 247 94


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