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Query: UMLS:C0020538 (
hypertension
)
170,190
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Neurons that contain PNMT, the epinephrine-forming enzyme, have their cell bodies in brain stem regions in rat brain and send projections mainly into other brain stem areas, hypothalamus, and spinal cord. These neurons can be affected pharmacologically by various kinds of drugs. Epinephrine neuronal systems might play a part in some pharmacologic actions of
MAO
inhibitors and uptake inhibitors as well as alpha and beta agonists and antagonists. PNMT inhibitors currently represent the only means of modifying epinephrine neurons pharmacologically without also altering norepinephrine or dopamine neurons in brain. The continued study of drugs affecting epinephrine neurons should be useful in elucidating functions of these neurons. Drugs that affect epinephrine neurons may be of use in the treatment of
hypertension
, psychiatric disorders, neuroendocrine dysfunction, and possibly other diseases.
...
PMID:Pharmacology of brain epinephrine neurons. 680 16
The objective of the present investigation was to determine whether or not tyramine induces coma in experimental animals with impaired mitochondrial
monoamine oxidase
function, and whether the coma in these animals was a function of increased cerebrospinal fluid (CSF) pressure. Ten mongrel dogs were treated (orally) daily with the
monoamine oxidase
-inhibiting drug, phenelzine (4.5 mg/kg), over a period of 1 month. The present studies indicated that in phenelzine-treated animals with liver disease and behavioral side effects (n = 4), the i.v. administration of tyramine (1 mg/kg) caused substantial elevation in CSF pressure that exceeded 30 mm Hg (initial pressure 12.5 +/- 2.1). This was followed by substantial accumulation of tyramine, dopamine and norepinephrine concentrations in CSF of these animals. The animals became comatose soon afterward. The administration of tyramine to pretreated (n = 10) or phenelzine-treated animals without liver disease (n = 6) caused only the expected transient increase in blood pressure but with no significant effect on CSF pressure of these animals. These animals recovered fully from the experiment without any ill effect. These studies suggest that tyramine may have obvious implications in the development of intracranial
hypertension
in Reye's syndrome.
...
PMID:Similarity between tyramine-induced neurotoxicity and the coma of Reye's syndrome. 687 68
We present the case of a 28-year-old man being treated with Nardil for chronic depression who developed a hypertensive crisis and a severe occipital headache one hour after ingesting an over-the-counter appetite suppressant. The adverse reactions between
MAO
inhibitors and phenylpropanolamine and discussed, as are the dangers of using Demerol to treat the headache and Aldomet to treat the
hypertension
.
...
PMID:Hypertensive crisis resulting from an MAO inhibitor and an over-the-counter appetite suppressant. 711 95
Phenylephrine hydrochloride is a potent, effective, relatively safe drug with few ocular side effects. Side effects from topical instillation are uncommon but include severe systemic cardiovascular effects with elevated blood pressure and stroke. Ten percent phenylephrine should be used with caution in patients with known cardiac disease,
hypertension
, aneurysms, long-standing insulin-dependent diabetes, or advanced arteriosclerosis. A 2.5% concentration is generally indicated for ophthalmic examination as well as for use in infants and in the elderly. Phenylephrine should not be used in patients with narrow-angle glaucoma, and it is also contraindicated in patients taking
monoamine oxidase
inhibitors or tricyclic antidepressants.
...
PMID:3. Phenylephrine hydrochloride. 724 10
A case of tranylcypromine (Parnate) overdose is presented in which the main toxic effects were headache, obtundation,
hypertension
, and diffusely peaked T-waves on ECG. The latter effect, which occurred in the absence of hyperkalemia, has not been previously associated with
monoamine oxidase
inhibitors (MAOI). Recent case reports of tranylcypromine toxicity are briefly reviewed, confirming the potential for
hypertension
, hypotension, shock, hyperpyrexia, intracranial hemorrhage, agitation, hyperkinesis, coma and death in association with overdosage, or concomitant ingestion of sympathomimetic substances or other drugs. These ECG changes add to the worrisome list of potential toxicities in an era in which MAOI are finding increased clinical use.
...
PMID:Peaked "T" waves with tranylcypromine (parnate) overdose. 726 32
Blood pressure and circulating levels of norepinephrine (NE), epinephrine (Epi), and dopamine-beta-hydroxylase (DBH) were measured sequentially in sinoaortic-denervated (SAD) Wistar rats and in sham-operated (SO) rats. Systolic tail pressure, plasma NE and E, and plasma DBH all increased significantly within 2 days in SAD rats. In separate studies of rats with indwelling arterial catheters, arterial pressure and plasma NE and DBH were increased in SAD rats in home cages; restraint caused similar increases of pressure and catecholamines in both groups. Systolic pressure remained increased up to 4 mo and plasma DBH for 10 wk in SAD rats; plasma NE and E, however, declined by 3 wk and thereafter remained close to values of SO rats. Additionally, DBH was increased in heart, mesenteric blood vessels and adrenal glands of SAD rats up to 6 wk; tissue
monoamine oxidase
activity was also increased up to 4 mo. These findings suggest that activation of the sympathetic nervous system initiates and probably sustains
hypertension
in SAD rats up to 6 wk after operation; thereafter some other mechanism(s) sustains the
hypertension
.
...
PMID:Indices of sympathetic activity in the sinoaortic-denervated hypertensive rat. 737 23
A case is presented of a woman who, for six years, had been treated for depression with 45 mg daily of the
monoamine oxidase
inhibitor (MAOI), phenelzine, and who continued taking the drug throughout her pregnancy and labour. Well-documented and potentially fatal interactions between MAOIs and opioids, notably meperidine, meant that her labour analgesia needed careful planning. Opioid- and epinephrine-free epidural bupivacaine analgesia was instituted early with small increments of bupivacaine 0.25% to produce a T10 block, after which an infusion of 8 ml.hr-1 bupivacaine 0.125% was used to maintain analgesia. After 14 hr labour, the epidural was extended uneventfully to allow Caesarean section to be performed for failure to progress. Pressor agents were avoided as indirect-acting drugs can produce severe
hypertension
. The child appeared normal and the mother had an uncomplicated postoperative course. Epidural analgesia contributed to the safe conduct of labour and Caesarean delivery.
...
PMID:Anaesthetic management of labour and delivery in a woman taking long-term MAOI. 755
1. The clinical utility of plasma metadrenalines for examination of sympatho-adrenal function and catecholamine metabolism was assessed from plasma measurements of these metabolites in a number of clinical conditions (
hypertension
, cardiac failure, bilateral adrenalectomy and X-chromosomal deletions of the gene for
monoamine oxidase
), and before and during activation of sympathetic outflow or infusions of noradrenaline and adrenaline. 2. Plasma concentrations of normetadrenaline were less than 25% of those of noradrenaline, concentrations of metadrenaline and adrenaline were similar and those of sulphate-conjugated metadrenalines were 20- to 30-fold higher than free metadrenalines. Hypertensive patients had elevated plasma concentrations of adrenaline, noradrenaline and conjugated but not free metadrenalines. Cardiac failure patients had 2- to 4-fold increases in plasma noradrenaline and free and conjugated normetadrenaline. Adrenalectomy resulted in undetectable plasma concentrations of adrenaline, 91-97% decreases in free and conjugated metadrenaline and a 40% decrease in normetadrenaline relative to noradrenaline. Patients with X-chromosomal deletions of the gene for
monoamine oxidase
had 6- and 16-fold increases in plasma free and conjugated normetadrenaline and 2- and 4-fold increases in free and conjugated metadrenaline. 3. Infusion of catecholamines increased plasma concentrations of free metadrenalines by less than 6% of increases in precursor amines, indicating that most plasma normetadrenaline (84%) and metadrenaline (90%) is derived from metabolism of catecholamines before their entry into the circulation. Considerable O-methylation of catecholamines within the adrenals explains why sympatho-adrenal activation resulted in smaller proportional increases in plasma metadrenalines than catecholamines. 4. Plasma metadrenalines provide supplementary information about sympatho-adrenal activity to that provided by catecholamines, but are more useful for examination of the extraneuronal inactivation of catecholamines, particularly detection of neurochemical phenotypes in genetic disorders of catecholamine metabolism. Significant formation of metadrenalines within chromaffin tissue explains why measurements of plasma metadrenalines provide an extraordinarily sensitive method for diagnosis of phaeochromocytoma.
...
PMID:Plasma metadrenalines: do they provide useful information about sympatho-adrenal function and catecholamine metabolism? 761 12
A patient presented with paroxysmal
hypertension
and typical clinical features of phaeochromocytoma, but with a normal adrenal computed tomographic scan and much higher plasma noradrenaline than adrenaline concentrations. Urinary vanillylmandelic acid concentrations were only moderately elevated. This syndrome probably arose as a consequence of an interaction between the
monoamine oxidase
inhibitor selegiline, the sympathomimetic agent ephedrine, and a tricyclic antidepressant. The mechanism of the interaction is thought to be related to increased sympathetic release of noradrenaline by ephedrine, inhibition of catabolism by selegiline, and inhibition of reuptake of noradrenaline by the tricyclic. Although newer selective
monoamine oxidase
inhibitors are considered to be safer than earlier non-selective inhibitors, they can also contribute to drug interactions mimicking phaeochromocytoma.
...
PMID:Pseudo-phaeochromocytoma after multiple drug interactions involving the selective monoamine oxidase inhibitor selegiline. 758 30
There is a new, potentially fatal disorder that is infrequently reported. The apparent rareness may be because of a lack of recognition of the syndrome or its predisposing factors. Fluoxetine (Prozac, Dista Products Co, Division of Eli Lilly Co, Indianapolis, IN), sertraline (Zoloft, Roerig Division, Pfizer Inc, New York, NY), and paroxetine (Paxil, SmithKline Beecham Pharmaceuticals, Philadelphia, PA) belong to a new class of antidepressant medication: the serotonin reuptake-inhibitors (SRIs). The relative safety profile of the SRIs has led to their widespread use. However, a syndrome of excessive serotonergic activity, the "serotonin syndrome" (SS), has recently been recognized. It is characterized by changes in mental status,
hypertension
, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor. A high index of suspicion is required to make the diagnosis in these acutely ill patients. The most common agents implicated in SS are the
monoamine oxidase
inhibitors in combination with L-tryptophan or fluoxetine. A case of a patient with significant peripheral vascular disease who developed SS while taking paroxetine and an over-the-counter cold medicine is reported. There have been no prior reports of this interaction. Discontinuation of the offending agents, sedation, and supportive care are the mainstays of treatment. The interactions of serotonin with platelets and vascular endothelium are also discussed.
...
PMID:The serotonin syndrome associated with paroxetine, an over-the-counter cold remedy, and vascular disease. 766 67
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