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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac hypertensive structural changes, catecholamine-related cardiomyopathy, and congestive heart failure (CHF) have been encountered in pheochromocytoma, as a result of prolonged exposure to high concentrations of endogenous catecholamines. A 34-year-old man presented with severe hypertension, cardiomegaly, and CHF, presumably as a result of continuous alpha-adrenergic intoxication with oxymetazoline hydrochloride, phenylephrine hydrochloride, and ephedrine hydrochloride, consumed in massive doses by an overuse of nasal decongestants and cough syrup (daily doses of 20, 100, and 300 mg, respectively). Coadministered chlorpromazine hydrochloride and trimeprazine tartrate may have also contributed to the clinical presentation through their anticholinergic and antihistaminic properties. The possibility of an overuse of these over-the-counter drugs should be considered in the differential diagnosis of hypertensive emergencies, especially with the simultaneous use of anticholinergic and antihistamine medications, beta-blocking agents, or monoamine oxidase inhibitors.
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PMID:Hypertensive crisis from chronic intoxication with nasal decongestant and cough medications. 172 79

Drug-induced orthostatic hypotension is an important clinical problem. When symptomatic, it is poorly tolerated by the patient, and can be a cause for discontinuing treatment. It may have more serious consequences if it leads to syncope, falls and injury, or to sustained loss of perfusion of vital organs resulting in heart attack or stroke. Orthostatic hypotension is easily detected by procedures available to all physicians, who should maintain a high index of suspicion when prescribing drugs commonly known to cause this condition, especially in the elderly. Since the medical conditions calling for the use of these drugs are extremely prevalent, the screening and monitoring of orthostatic hypotension should be instituted as a routine precaution in appropriate patients. Hypertension affects two-thirds of elderly patients. Orthostatic hypotension is an infrequent adverse effect of most of the drugs in current use in the treatment of hypertension; it is, however, more common with alpha 1-blockers (first dose), adrenergic blockers and centrally acting drugs. Sudden loss of blood volume, or excess diuresis, may precipitate orthostatic hypotension in any hypertensive patient. Drugs used for the treatment of psychiatric illnesses are all associated with a significant incidence of orthostatic hypotension: phenothiazines, tricyclic antidepressants and monoamine oxidase inhibitors. Cardiovascular drugs associated with hypotension include dopamine agonists, antianginals and antiarrhythmics.
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PMID:Drug-induced orthostatic hypotension. 179 21

Rate of serotonin and benzylamine deamination was increased in liver tissue of rats with spontaneous hypertension. The increase was due to elevation in Vmax value for monoamine oxidases of the A and B types as compared with the corresponding values of control animals. The Vmax value was increased in kidney of hypertensive animals for MAO of the B type (benzylamine as a substrate). At the same time, Km for MAO of the B type was increased in liver tissue, while Km for MAO of the A type was decreased in brain of hypertensive animals. Titration of the MAO active sites exhibited their increased concentration in the B type MAO in liver mitochondria of experimental animals. The data obtained suggest an important role of alterations in the MAO catalytic activity in pathogenesis of spontaneous hypertension.
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PMID:[Changes in kinetics of deaminated biogenic amines in spontaneous hypertension]. 185 44

Some distinctions were revealed in serotonin metabolism in brain areas in two strains of rats with hereditary arterial hypertension - SHR (spontaneously hypertensive rats) and HSIAH (hereditary stress induced arterial hypertension). These distinctions include regional and qualitative changes of the serotonin concentration, activity of type A monoamine oxidase and tryptophan hydroxylase.
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PMID:[Serotonin metabolism in the brain of rats with two forms of hereditary arterial hypertension]. 188 98

Effects of bromocriptine on hemodynamics and catecholamine exchange were evaluated in patients with borderline arterial hypertension with respect to their family history. The agent was shown to be able to bring down blood pressure and decrease plasma catecholamine levels. With this, platelet monoamine oxidase activity was increased in persons with a family history of hypertensive disease.
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PMID:[Effects of bromocriptine on catecholamine metabolism in subjects with borderline arterial hypertension]. 206 74

The authors describe two series of patients: 12 treated simultaneously with fluoxetine and a monoamine oxidase inhibitor and 6 patients started on treatment with an MAOI 10 days or more after stopping fluoxetine treatment. All patients had extremely refractory depression and were treated in open fashion before general knowledge was obtained of the side effects that may accompany the fluoxetine-MAOI combination. During the fluoxetine-MAOI trial, most patients continued to receive other psychotropic combinations that had been partially helpful. The use of fluoxetine and an MAOI, either together or in close succession, was accompanied by a very high incidence of adverse effects, especially the "serotonergic syndrome." This syndrome was characterized by mental status changes, such as hypomania and confusion, and physical symptoms, such as myoclonus, hypertension, tremor, and diarrhea. Because of the high incidence of side effects and the lack of definite efficacy, the concurrent use of fluoxetine and MAOIs should generally be avoided. The long half-lives of fluoxetine and norfluoxetine, as well as the prolonged metabolic effects of MAOIs, may also dispose patients to an interaction if one of the drugs is started soon after stopping the other.
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PMID:Adverse consequences of fluoxetine-MAOI combination therapy. 199 42

The analysis of data obtained for 101 bronchial asthma (BA) sufferers with hypertension and 30 normotensive patients demonstrated the dependence of arterial hypertension in BA patients on a significant increase in the systemic peripheral resistance, pulmonary circulation pressure, diastolic dysfunction, reduced cardiac output, pulse brain filling as well as on elevated serotonin level and monoamine oxidase hyperactivity. The findings provided additional information on the causes and triggering mechanisms of arterial hypertension in BA patients, are helpful in design of antihypertensive treatment and the disease prevention.
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PMID:[Myocardial status, hemodynamics and pressor humoral substances in patients with bronchial asthma and arterial hypertension]. 262 58

This monograph comprises a review of the cardiovascular effects of the various types of antidepressant drugs in clinical use. The frequency, severity and clinical importance of these effects are placed in perspective. Most antidepressants can cause changes in blood pressure. Both the tricyclic type (TCA) and the monoamine oxidase inhibitors (MAOIs) can produce postural hypotension which may be dose-limiting. In addition, the MAOIs may be associated with severe hypertension when amine-containing foods or medicines are ingested. It is unlikely that therapeutic doses of any available antidepressant drug could impair cardiac contractility. Typical TCAs can cause abnormalities of cardiac conduction and arrhythmias, but this affects less than 5% of patients, mostly to a clinically insignificant extent. Newer compounds such as lofepramine, mianserin, trazodone and viloxazine seem safer in this respect. Reports of an association between therapeutic use of TCAs and sudden death are far from convincing. Overdosage with the MAOIs, lithium and carbamazepine is dangerous but not common; overdose with a TCA is a major source of morbidity and mortality. Lofepramine, mianserin and trazodone are relatively safe in overdose. The use of various antidepressants in patients with hypertension, cardiac failure, angina pectoris, myocardial infarction, or cardiac arrhythmias is discussed and guidelines suggested for the selection and use of antidepressant medication.
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PMID:The cardiovascular effects of antidepressants. 269 Jan 61

The cheese reaction following use of the irreversible monoamine oxidase inhibitors (MAOIs) began to be reported in the UK with increasing frequency from about 1961. By 1965, the underlying mechanism (tyramine-provoked hypertension) had been essentially elucidated. Thereafter, this potentially severe side-effect could have been largely avoided by the use of fairly simple dietary precautions. Unfortunately, suspicion and fear burgeoned, and both the seriousness and the frequency of risk were dramatically inflated. This was a major factor in the subsequent general disuse of the irreversible MAOIs. Second-generation MAOIs which are selective for monoamine oxidase-A and B are now being synthesised and may eliminate the eventuality of hypertension without special dietary precautions.
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PMID:Tyramine and irreversible monoamine oxidase inhibitors in clinical practice. 269 26

Catechol and indole metabolism in rostral ventrolateral medulla (RVLM or C1) was studied in response to changes in blood pressure across different rat strains. Sprague-Dawley, Wistar Kyoto normotensive and spontaneously hypertensive rats were anesthetized with urethane and had a 250 mu carbon paste in vivo electrochemical electrode implanted in RVLM area. Two electrochemical peaks were detected in this region. The first was at 0.12 V and the second at 0.28 V. To identify the electrochemical peaks, inhibitors of monoamine metabolism were administrated. alpha-Methylparatyrosine (tyrosine hydroxylase inhibitor), fusaric acid (dopamine-beta-hydroxylase inhibitor), pargyline (monoamine oxidase inhibitor) and LY 134046 (phenylethanolamine-N-methyltransferase inhibitor) showed that the first peak measured in the RVLM is likely to have multiple components including epinephrine, norepinephrine and 3,4-dihydroxyphenylacetic acid. The second peak most likely represents 5-hydroxyindole acetic acid. Phenylephrine or nitroprusside was infused to increase or decrease the blood pressure. Phenylephrine-induced hypertension reduced the catechol peak and increased the indole peak. By contrast, nitroprusside-induced hypotension produced reciprocal results. Hypotension led to an increase in the catechol peak and a reduction in the indole peak. The same pattern was observed in all three rat strains. We conclude that catechol and serotonin metabolism in RVLM changes in close relation to changes in blood pressure.
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PMID:Catechol and indole metabolism in rostral ventrolateral medulla change synchronously with changing blood pressure. 272 47


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