UMLS:C0016382 - FACTA Search

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

We studied the effects of nifedipine on blood pressure and on clinical and analytical parameters in hypertensive patients. Seven male and eight female subjects (mean age of 46.27 +/- 5.38 years, range of 41-56 years) with essential arterial hypertension were given nifedipine (20 mg b.i.d.) for 3 months. Before and after treatment, history, blood pressure, and biochemical values were recorded [blood: Na, K, Ca, creatinine, uric acid, triglycerides, cholesterol, HDL cholesterol, antidiuretic hormone (ADH), and aldosterone; urine: Na, K, Ca, creatinine, ADH, aldosterone, and percentage fraction of Na, K, and Ca excreted]. After 3 months of treatment, we found (a) significant decreases in systolic (147 +/- 18 vs. 166 +/- 16 mm Hg, p less than 0.001) and diastolic blood pressure (90 +/- 8 vs. 107 +/- 8 mm Hg, p less than 0.0007), triglycerides (107 +/- 47 vs. 120 +/- 49 mg/dl, p less than 0.0007), and cholesterol (236 +/- 4 vs. 257 +/- 44 mg/dl, p less than 0.00075) in blood, and in K excretion (50 +/- 19 vs. 46 +/- 19 mEq/g of creatinine, p less than 0.0007) and excreted fraction of K (49 +/- 6% vs. 8 +/- 5%, p less than 0.0012) in urine; (b) significant increases in HDL cholesterol (65 +/- 13 vs. 58 +/- 13 mg/dl, p less than 0.001) in blood, and in Na (115 +/- 73 vs. 109 +/- 69 mEq/g of creatinine, p less than 0.0007) in urine; and (c) no significant change in the remaining biochemical parameters, or in heart rate. Secondary effects included flushing (34%), headache (20%), ankle swelling (17%), dizziness (13%), palpitations (4%), and pruritus (4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic and antihypertensive effects of nifedipine in hypertensive patients. 137 8

Co-dergocrine mesylate (Cod), which inhibits norepinephrine secretion by stimulating presynaptic dopamine receptors, and has no known metabolic side effect, has an additive antihypertensive effect to that of Nifedipine (Nif). Plasma norepinephrine, epinephrine, renin activity and aldosterone have been measured after acute administration of Nif and Cod alone and in combination to 18 patients with a diastolic blood pressure greater than 105 mmHg in a cross-over, randomized, double-blind study. Every patient received 4 mg Cod then 20 mg Nif, placebo then 20 mg Nif and 4 mg Cod then placebo. The second treatment was always given 1 h after the first medication. Blood pressure was measured before and every 15 min during the study period. Blood for measurement of catecholamines, aldosterone and renin activity was collected before medication, 1 h after the first dose and 90 min after the second treatment. Blood pressure was significantly lower (P less than 0.05) where Cod preceded Nif. Cod caused a significant decrease in plasma norepinephrine from 293 to 202 pg.ml-1 and in epinephrine from 67 to 55 pg.ml-1. The Nif-induced increase in norepinephrine from a pre-treatment value of 293 pg.ml-1 with preceding Cod to 331 pg.ml-1 was much less than the increase with placebo as premedication, from 284 to 440 pg.ml-1. Nif caused an increase in renin activity but no increase in aldosterone. Nif-related side effects, such as flushing and headache, occurred in 6 patients of whom 5 had no received Cod as premedication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Co-dergocrine mesylate inhibits the increase in plasma catecholamines caused by nifedipine in essential hypertension. 207 34

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

An automated high-performance liquid chromatographic assay for the determination of an aldosterone antagonist (I) is described using column switching for direct injection of urine samples. After dilution with buffered internal standard solution, the sample was injected onto a clean-up column (17 X 4.6 mm I.D.), dry-packed with C18 reversed-phase material (particle size 30 micron). Polar urine components were removed by flushing the clean-up column with water. Retained substances, including I and the internal standard, were desorbed by backflush elution onto a 5-micron ODS-silica analytical column (125 X 4 mm I.D.), separated with water-methanol-tetrahydrofuran, and detected at 295 nm. After backflushing the analytical column and re-equilibrating the clean-up column, the system was ready for the next injection. The limit of quantification was ca. 100 ng/ml, using a 100-microliter specimen of diluted urine. The mean inter-assay precision of the method up to 25.6 micrograms/ml was 2%. Practicability and accuracy of the new method were demonstrated by the application to excretion studies performed with human volunteers.
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PMID:Determination of an aldosterone antagonist in urine by high-performance liquid chromatography using automated column switching. 373 79

The antihypertensive effect of a new vasodilator with betablocking properties (SK & F 92657) was investigated in 10 patients with mild to moderate essential hypertension. After a mean treatment period of 26,5 weeks (6,5-49 weeks) blood pressure was significantly reduced, from 168 +/- 22/106 +/- 6 mmHg to 144 +/- 19/94 +/- 12 mmHg (p less than 0.05 and 0.025). The mean dose was 410 mg (100-700 mg). Heart rate decreased slightly from 77 +/- 12 to 70 +/- 8 beats/min. Plasma renin activity and plasma aldosterone showed only minor changes. Nausea, heavy dreams, facial and hand flushing and mild depression were reported as side effects. In most patients the symptoms disappeared without reduction in the dose. In one patient anaemia developed after 7 weeks and treatment with prizidilol was stopped. A slight but statistically significant decrease in haemoglobin concentration of 1.1 +/- 0.6 g/dl was observed in 5 of the 10 patients (p less than 0.02). Thus, a mean dose of prizidilol of 410 +/- 242 mg/day had a mean blood pressure lowering effect of 24/12 mmHg. In 7 of the 10 patients (70%) diastolic blood pressure could be reduced to 95 mmHg or less. However, the observed haematological side-effects should be carefully monitored in further studies and may limit the clinical use of prizidilol.
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PMID:Prizidilol (SK & F 92657), a new vasodilator with beta-blocking properties in the treatment of essential hypertension. 612 80

The acute hemodynamic effects of intravenous prostacyclin (PGI2), in doses of 22 +/- 11 ng/kg per min were studied in nine patients with severe congestive heart failure refractory to digitalis and diuretic drugs. After prostacyclin infusion, mean (+/- standard deviation) pulmonary capillary wedge pressure decreased from 21.0 +/- 7.9 to 15.0 +/- 6.6 mm Hg (p less than 0.001), mean arterial pressure from 98.9 +/- 12.8 to 76.2 +/- 7.0 mm Hg (p less than 0.001), systemic vascular resistance from 2,574 +/- 384 to 1,368 +/- 283 dynes s cm-5 (p less than 0.001), pulmonary vascular resistance from 1,008 +/- 451 to 443 +/- 135 dynes s cm-5 (p less than 0.001) and pulmonary arteriolar resistance from 330 +/- 111 to 189 +/- 73 dynes s cm-5 (p less than 0.001). Heart rate increased from 78 +/- 21 to 82 +/- 24 beats/min (p = not significant [NS]), cardiac index from 2.0 +/- 0.37 to 3.2 +/- 0.59 liters/min per m2 (p less than 0.001) and stroke index from 27.6 +/- 8.69 to 42.0 +/- 0.62 cc/m2 (p less than 0.001). With prostacyclin, moreover, coldness of the limbs and face disappeared, and patients felt warmth and mild flushing of the face. After prostacyclin, plasma norepinephrine levels, renin activity and aldosterone concentrations rose from 824 +/- 375 to 880 +/- 468 pg/ml (NS), 0.68 +/- 1.36 to 0.95 +/- 1.21 ng/ml per h (NS), and 6.64 +/- 2.50 to 6.38 +/- 2.88 ng/dl (NS), respectively, while plasma epinephrine increased from 140 +/- 80 to 250 +/- 154 pg/ml (p less than 0.025).
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PMID:Prostacyclin therapy in patients with congestive heart failure. 704 86

Unexplained episodic hypertension, hypotension, or orthostatic intolerance, tachycardia, anxiety, and flushing in 21 patients were investigated for the possibility of hypovolemia by blood volume and individual plasma catecholamines (including autocrine paracrine-born dopamine), determinations baseline, in response to upright posture and catecholamines only during the episodic blood pressure swings. Blood volume was determined by Cr51 fixed to patients' hemoglobin, free norepinephrine, epinephrine, and dopamine with dopamine sulfate following sulfatase hydrolysis, radioenzymatically. The recumbent mean 27.4+/-3% (SE) blood volume decrease from predicted values accentuating to 33.5+/-4% upright was associated with normal baseline plasma free norepinephrine, epinephrine, dopamine, dopamine sulfate, plasma renin activity, and aldosterone with normal mean postural responses from all patients except a hyperresponsive compared to controls (p < 0.04), plasma renin activity increase from 0.657+/-0.1 to 4.47+/-1.8 ng/mL/hr. During the hypertensive, hypotensive, or tachycardic episodes the moderate increase of free norepinephrine and epinephrine (p < 0.04) (but not free dopamine) contrasted with an increase of dopamine sulfate from 2.5+/-0.9 to clearly pathological values of 16.8+/-8.3 ng/mL (p < 0.0003 on % increase of individual values). We conclude that the normal (but to the degree of hypovolemia inappropriately low orthostatism- and episodes-associated sympathetic arousal) is outpaced by considerable episodic dopamine sulfate surges, reflecting extraneuronal dopamine discharge. Whether this increase contributes to the increased natriuresis directly or by inhibiting aldosterone response to renin-angiotensin, perpetuating hypovolemia, remains to be established.
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PMID:Idiopathic hypovolemia: a self-perpetuating autonomic dysfunction? 986 52

Although the biological effects of adrenomedullin (AM) and PAMP have been reported extensively in animal studies and from in-vitro experiments, relatively little information is available on responses to the hormone administered to man. This review summarizes data from the few studies carried out in man. In healthy volunteers, i.v. infusion of AM reduces arterial pressure, probably at a lower rate of administration than is required to elicit other responses. AM stimulates heart rate, cardiac output, plasma levels of cAMP, prolactin, norepinephrine and renin whilst inhibiting any concomitant response in plasma aldosterone. Little or no increase in urine volume or sodium excretion has been observed. Patients with essential hypertension differ only in showing a greater fall in arterial pressure and in the development of facial flushing and headache. In patients with heart failure or chronic renal failure, i.v. AM has similar effects to those seen in normal subjects but also induces a diuresis and natriuresis, depending on the dose administered. Infusion of AM into the brachial artery results in a dose-related increase in forearm and skin blood flow, more prominent and more dependent on endogenous nitric oxide in healthy volunteers than in patients with cardiac failure. When infused into a dorsal hand vein, AM partially reversed the venoconstrictor action of norepinephrine. Although much more information is required to clarify the role of AM under physiological and pathophysiological circumstances, it is clear that it has prominent hemodynamic and neurohormonal effects, though generally lesser urinary effects when administered short-term in doses sufficient to raise its levels in plasma to those seen in a number of clinical disorders. The only study of PAMP in man showed that its skeletal muscle vasodilator potency, when infused into the brachial artery of healthy volunteers, was less than one hundredth that of AM, and it was without effect on skin blood flow.
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PMID:Bioactivity of adrenomedullin and proadrenomedullin N-terminal 20 peptide in man. 1175 60

Elevated blood pressure is a risk factor for a variety of cardiovascular disorders, including coronary heart disease, peripheral vascular disease, cardiac failure and cerebrovascular disease. The prevailing view is that an elevated systolic rather than diastolic blood pressure is the major contributor in mortality and morbidity attributed to cardiovascular disorders. Isolated high systolic blood pressure, especially in the elderly, is a major risk factor and should undoubtedly be a target for drug treatment. In the general population, systolic and diastolic blood pressure are highly correlated, and thus it is difficult to dissociate the effects of these two components of the blood pressure and specifically ascribe cardiovascular risk factors to just elevated systolic blood pressure. Therefore, the goal in therapy of an individual with hypertension must be to reduce elevated systolic and diastolic blood pressure in order to reduce mortality and morbidity. ACE and neutral peptidase inhibitors are a new class of drugs that may be beneficial in the treatment of patients with hypertension and heart failure. They may also be useful in the treatment of diabetic patients with hypertension and/or heart failure. Drugs of this class are dual inhibitors of ACE and neutral endopeptidase, and are capable of affecting vascular tone and fluid balance. They are capable of producing vasodilatation by virtue of inhibiting the production of angiotensin II, degradation of natriuretic peptides and bradykinin. They also appear to promote natriuresis and diuresis by amplifying the actions of natriuretic peptidase and reducing aldosterone effects. In addition, they should also attenuate trophogenic actions of the renin angiotensin system and the sympathetic nervous system. Omapatrilat is one drug that appears to be at the advanced stages of clinical development. This drug has been shown to be quite effective in the treatment of hypertension. Evidence also seems to indicate that treatment with omapatrilat results in a higher tendency towards preventing death and worsening heart failure when compared with treatment with a pure ACE inhibitor in patients with advanced heart failure. Overall safety with omapatrilat appears to be good, but like other ACE inhibitors the incidence of cough is higher when compared with placebo. Other common adverse effects noted are headaches, facial flushing/warm sensation, dizziness, nausea and dyspnoea. Of greater concern is the occurrence of angio-oedema, the true incidence of which remains to be fully established as part of the published medical literature.
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PMID:Dual ACE and neutral endopeptidase inhibitors: novel therapy for patients with cardiovascular disorders. 1501 94

Secondary hypertension is a type of hypertension with an underlying, potentially correctable cause. A secondary etiology may be suggested by symptoms (e.g., flushing and sweating suggestive of pheochromocytoma), examina- tion findings (e.g., a renal bruit suggestive of renal artery stenosis), or laboratory abnormalities (e.g., hypokalemia suggestive of aldosteronism). Secondary hypertension also should be considered in patients with resistant hyper- tension, and early or late onset of hypertension. The prevalence of secondary hypertension and the most common etiologies vary by age group. Approximately 5 to 10 percent of adults with hypertension have a secondary cause. In young adults, particu- larly women, renal artery stenosis caused by fibromuscular dyspla- sia is one of the most common secondary etiologies. Fibromuscular dysplasia can be detected by abdominal magnetic resonance imag- ing or computed tomography. These same imaging modalities can be used to detect atherosclerotic renal artery stenosis, a major cause of secondary hypertension in older adults. In middle-aged adults, aldosteronism is the most common secondary cause of hyperten- sion, and the recommended initial diagnostic test is an aldosterone/ renin ratio. Up to 85 percent of children with hypertension have an identifiable cause, most often renal parenchymal disease. Therefore, all children with confirmed hypertension should have an evaluation for an underlying etiology that includes renal ultrasonography.
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PMID:Diagnosis of secondary hypertension: an age-based approach. 2116 67

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