Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of benign cerebral angiopathy in a 37 year-old woman in the postpartum period occurring after bromocriptine therapy to suppress lactation. She presented with severe headache, hyperthermia and bradycardia. She had partial seizure. Angiography excluded cortical vein thrombosis but revealed multiple narrowing of intracerebral arteries. Bromocriptine was stopped. The patient totally recovered. A second angiography performed 3 months later was normal. Postpartum cerebral angiopathy is considered as rare but the prevalence is probably underestimated. Neurological features of this affection are multiple. Diagnosis is made by angiography performed in emergency and which showed narrowing of intracerebral arteries which are reversible. Prognosis is good. Reversible vasoconstriction may be due to acute arterial hypertension, sometimes triggered by ergot derivatives.
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PMID:[Benign angiopathy of the puerperium: a clinicoradiological case associated with ingestion of bromocriptine]. 897 78

-Dopamine and angiotensin II (Ang II) receptors have been reported to exhibit an interaction in renal proximal tubules. The present study was designed to investigate the regulation by a D2-like dopamine receptor of Ang II-mediated stimulation of Na,K-ATPase activity in the renal proximal tubules. Ang II (10(-13) to 10(-9) mol/L) stimulated Na,K-ATPase activity in the proximal tubules that was completely abolished when the tubules were pretreated with the D2-like receptor agonist bromocriptine (1 micromol/L) for 30 minutes. The effect of bromocriptine on Ang II response was prevented by domperidone (1 micromol/L), a D2-like dopamine receptor antagonist. Similarly, the inhibition of forskolin (1 micromol/L)-induced cAMP accumulation caused by Ang II (10 pmol/L) was also abolished in bromocriptine-pretreated tubules. Basal and forskolin-stimulated cAMP was not significantly different in bromocriptine-treated tubules compared with the control. [3H]-Ang II binding sites (angiotensin type 1 [AT1] receptors) were reduced by approximately 65% in bromocriptine-treated proximal tubules, a result that was further substantiated by Western blot analysis revealing a 50% decrease in AT1 receptors in bromocriptine-treated tubules compared with the control. Western blot analysis of G proteins revealed a 2-fold increase in Gsalpha and a 20% decrease in Gialpha1 and Gialpha2 in the bromocriptine-treated proximal tubules. Bromocriptine (1 micromol/L) alone stimulated Na,K-ATPase activity during the first 30 minutes of incubation, and thereafter the stimulation fell to the basal level. Similarly, bromocriptine-mediated inhibition of cAMP lasted only up to 20 minutes. The data suggest that preactivation of D2-like dopamine receptors abolishes Ang II-mediated stimulation of Na,K-ATPase activity and inhibition of cAMP accumulation. This phenomenon may be a consequence of a decrease in AT1 receptors and alterations in G protein levels in the proximal tubules. We propose that such a regulation of Ang II response by bromocriptine is the result of heterologous desensitization of the D2-like receptor system.
Hypertension 1998 Dec
PMID:Bromocriptine regulates angiotensin II response on sodium pump in proximal tubules. 985 73

Pituitary adenomas are the most common pituitary disorder affecting pregnancy, and prolactinomas are the most common of the hormone-secreting pituitary adenomas. Hyperprolactinemia must be corrected to allow ovulation and fertility. Bromocriptine has been shown to be safe for use during early gestation. There is less than a 2% risk of microprolactinoma enlargement during pregnancy but a greater than 15% risk of symptomatic enlargement of a macroprolactinoma. Treatment options for patients with macroadenomas include stopping bromocriptine when pregnancy is diagnosed and reinstituting with tumor enlargement, continuous bromocriptine throughout pregnancy, and prepregnancy tumor debulking by surgery. The diagnosis of acromegaly may be difficult to make during pregnancy and relies, in part, on the persistence of the normal pulsatile secretion of growth hormone and loss of this secretory characteristic with a tumor. The growth hormone oversecretion may exacerbate tendencies to gestational diabetes, fluid retention, and hypertension. Treatment for acromegaly and other tumors generally may be deferred until after delivery. There are rare reports of enlargement of clinically nonfunctioning and growth hormone secreting tumors during pregnancy, and surveillance is needed. Tumors may need to be differentiated from lymphocytic hypophysitis. Patients with chronic hypopituitarism usually will need treatment with gonadotropins or pulsatile GnRH to become pregnant and may need increased steroid coverage during labor and delivery. Hypopituitarism developing during pregnancy is usually caused by lymphocytic hypophysitis and usually also will require steroid replacement therapy. Hypopituitarism arising postpartum may be caused by either lymphocytic hypophysitis or Sheehan's syndrome, and the latter may present as an acute or chronic syndrome. Borderline diabetes insipidus may manifest during pregnancy because of increased vasopressin degradation caused by markedly increased levels of placental vasopressinase. Treatment with desmopressin usually is satisfactory. Patients presenting with either anterior or posterior pituitary insufficiency in the peripartum period should always be evaluated for function of the other portion of the pituitary.
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PMID:Pituitary diseases in pregnancy. 988 Jan 16

Bromocriptine, a dopamine agonist, is known to lower cardiovascular mortality in L-dopa-treated patients with Parkinson's disease, probably by reducing the cardiac sympathetic activity. We aimed at unmasking the central effects of bromocriptine on the heart by power spectrum analysis. Ten healthy subjects (aged 31+/-2 years) in supine and sitting positions were evaluated after the administration of bromocriptine (2.5 mg) alone and after pharmacological peripheral D(2)-like blockade by domperidone (20 mg). We calculated (autoregressive method) the following: the low-frequency (LF) component (an index of cardiac sympathetic tone), the high-frequency (HF) component (an index of cardiac vagal tone), and the LF/HF ratio (an index of cardiac sympathovagal balance). With subjects in the supine position, bromocriptine alone induced a significant increase in the LF component and the LF/HF ratio, together with a reduction in norepinephrine plasma levels and blood pressure values. These conflicting effects can be explained as the combined result of direct and indirect (reflex-mediated) actions of bromocriptine in vivo. No changes in cardiac autonomic drive were observed with subjects in the sitting position. After domperidone pretreatment, bromocriptine induced a reduction in the LF component and in the LF/HF ratio. The sitting position caused an increase in heart rate and in the LF/HF ratio. We demonstrated both peripheral and central effects of bromocriptine. In particular, pretreatment with a peripheral antagonist (domperidone) allowed us to unmask the central effect of bromocriptine on cardiac sympathetic drive.
Hypertension 2001 Jul
PMID:Centrally mediated effects of bromocriptine on cardiac sympathovagal balance. 1184 7

A plethora of data from experimental animals provide strong support for the concept that reduced dopaminergic neuronal activity and enhanced noradrenergic tone in specific hypothalamic nuclei are involved in the pathogenesis of the metabolic syndrome. The available information on these neurotransmitter systems in insulin-resistant humans with obesity is in keeping with the postulate that analogous mechanisms may underlie their adverse metabolic profile. Treatment with bromocriptine, which has dopaminergic (D2 receptor agonist) and sympatholytic (alpha2-adrenoceptor agonistic and an alpha1-adrenoceptor antagonistic) actions, can reverse the metabolic anomalies in a variety of obese mammalian species. Combined D1/D2 receptor activation appears to exert even more powerful effects on fuel metabolism in various animal models of the metabolic syndrome. The currently available data on the metabolic effects of bromocriptine in humans with obesity and type 2 diabetes mellitus point in the same direction. Bromocriptine favorably affects glucose metabolism and various other components of the metabolic syndrome simultaneously to ameliorate the risk of damage to eyes, neural tissue, kidneys and the cardiovascular system in patients with type 2 diabetes mellitus. Moreover, a substantial number of studies indicate that bromocriptine lowers blood pressure in animals and humans with hypertension via its sympatholytic capacities. However, the effects of bromocriptine alone are relatively modest, the metabolic mechanism of action in humans remains uncertain, and the long-term efficacy and safety profiles of this compound are unknown. It seems important to seek for ways to boost the action of bromocriptine, by combining dopaminergic D2 and D1 receptor activation, for example. Notably, there is no antidiabetic drug that acts through central (dopaminergic) mechanisms. This novel approach may, therefore, result in synergistic actions with other available agents to favorably impact the risk of tissue damage in patients with type 2 diabetes mellitus.
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PMID:Modulation of monoaminergic neural circuits: potential for the treatment of type 2 diabetes mellitus. 1576 23

The metabolic syndrome comprises a cluster of metabolic anomalies including insulin resistance, abdominal obesity, dyslipidemia, and hypertension. Previous studies suggest that impaired dopamine D2 receptor (D2R) signaling is involved in its pathogenesis. We studied the acute effects of bromocriptine (a D2R agonist) on energy metabolism in obese women; body weight and caloric intake remained constant. Eighteen healthy, obese women (BMI 33.2 +/- 0.6 kg/m(2), mean age 37.5 +/- 1.7, range 22-51 yr) were studied twice in the follicular phase of their menstrual cycle in a prospective, single-blind, crossover design. Subjects received both placebo (P; always first occasion) and bromocriptine (B; always second occasion) on separate occasions for 8 days. At each occasion blood glucose and insulin were assessed every 10 min for 24 h, and circadian plasma free fatty acid (FFA) and triglyceride (TG) levels were measured hourly. Fuel oxidation was determined by indirect calorimetry. Body weight and composition were not affected by the drug. Mean 24-h blood glucose (P < 0.01) and insulin (P < 0.01) were significantly reduced by bromocriptine, whereas mean 24 h FFA levels were increased (P < 0.01), suggesting that lipolysis was stimulated. Bromocriptine increased oxygen consumption (P = 0.03) and resting energy expenditure (by 50 kcal/day, P = 0.03). Systolic blood pressure was significantly reduced by bromocriptine. Thus these results imply that short-term bromocriptine treatment ameliorates various components of the metabolic syndrome while it shifts energy balance away from lipogenesis in obese humans.
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PMID:Activation of dopamine D2 receptors simultaneously ameliorates various metabolic features of obese women. 1680 51

Episodes of paroxysmal sympathetic hyperactivity, sometimes referred to as autonomic storms, are not uncommon in patients with severe traumatic brain injury. Their distinctive characteristics include fever, tachycardia, hypertension, tachypnea, hyperhidrosis, and dystonic posturing. The episodes may be induced by stimulation or may occur spontaneously. Their pathophysiology has not been fully elucidated, but the manifestations clearly indicate activation or disinhibition of sympathoexcitatory areas. These spells are often confused with seizures, leading to unnecessary treatment with antiepileptic drugs. General principles in the management of paroxysmal sympathetic hyperactivity include adequate hydration, exclusion of mimicking conditions (infection, pulmonary embolism, hydrocephalus, epilepsy), effective analgesia, and avoidance of triggers, when identified. The most useful pharmacologic agents are morphine sulfate and nonselective beta-blockers (eg, propranolol). Intrathecal baclofen may be effective in refractory cases. Bromocriptine and clonidine are helpful in some patients, but their efficacy is less consistent. Early recognition and adequate treatment of paroxysmal sympathetic hyperactivity is important to avoid prolongation of the patient's stay in the intensive care unit and to enable recovering patients to participate without restrictions in rehabilitation therapy.
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PMID:Treatment of paroxysmal sympathetic hyperactivity. 1833 37

During pregnancy, the maternal, placental and fetal physiological characteristics constantly evolve and thereby constantly alter drug bioavailability in the mother and feto-placental unit. Gastric emptying time is increased and bowel movements are reduced. Distribution in the maternal body is mainly influenced by body mass variations, water content and fat stores. Metabolic capacity of the liver appears unchanged but renal clearance of drugs is gradually increased. The placental transfer of most drugs mainly consists of passive diffusion between the maternal and fetal circulations, along their respective concentration gradients. Only the free, unbound and non-ionized fraction of the drug readily crosses the membranes. Four anti-hypertensive drugs have been granted a license for the treatment of PE since the year 2000: these are Clonidine (Catapressan), Nicardipine (Loxen+), Labetalol (Trandate), Dihydralazine (Nepressol). Dihydralazine, Labetalol and Nicardipine are not contraindicated in the breast feeding mother. The administration of a long acting Benzodiazepine during pregnancy can lead to new born intoxication of variable severity and duration. These symptoms may precede a withdrawal syndrome (hyper-excitability, tremor, gastro-intestinal upset, such as diarrhea or vomiting). Breast feeding by mothers using benzodiazepines (Nitrazepam and Midazolam) is not recommended. In France, the use of low molecular weight heparins is not recommended during pregnancy whereas in the United States, they are recommended as a prophylactic measure. Their high molecular weight prevents their diffusion across the placental membrane and therefore prevents any fetal or neonatal risk. Bromocriptine is used as an inhibitor of lactation. During the post-partum period, serious accidents have been described: these consist of systemic hypertension, fits, infarcts (cardiac and neurological). It is contraindicated in case of systemic hypertension.
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PMID:[Drugs during preeclampsia. Fetal risks and pharmacology]. 2034 63

Paroxysmal sympathetic storming (PSS) is a rare disorder characterized by acute onset of nonstimulated tachycardia, hypertension, tachypnea, hyperthermia, external posturing, and diaphoresis. It is most frequently associated with severe traumatic brain injuries and has been reported in intracranial tumors, hydrocephalous, severe hypoxic brain injury, and intracerebral hemorrhage. Although excessive release of catecholamine and therefore increased sympathetic activities have been reported in subarachnoid hemorrhage (SAH), there is no descriptive report of PSS primarily caused by spontaneous SAH up to date. Here, we report a case of prolonged PSS in a patient with spontaneous subarachnoid hemorrhage and consequent vasospasm. The sympathetic storming started shortly after patient was rewarmed from hypothermia protocol and symptoms responded to Labetalol, but intermittent recurrence did not resolve until 3 weeks later with treatment involving Midazolam, Fentanyl, Dexmedetomidine, Propofol, Bromocriptine, and minimizing frequency of neurological and vital checks. In conclusion, prolonged sympathetic storming can also be caused by spontaneous SAH. In this case, vasospasm might be a precipitating factor. Paralytics and hypothermia could mask the manifestations of PSS. The treatment of the refractory case will need both timely adjustment of medications and minimization of exogenous stressors or stimuli.
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PMID:Prolonged paroxysmal sympathetic storming associated with spontaneous subarachnoid hemorrhage. 2347 63

A 43-year-old woman with an 8-year history of diabetes, hypertension, and dyslipidemia presented with amenorrhea and convulsion. Her MRI scan revealed a 3.5-cm T2-hyperintense pituitary macroadenoma with suprasellar extension to the frontal lobe and bilateral cavernous sinus invasion. Her serum levels of GH and insulin-like growth factor-I (IGF-I) were elevated to 9.08 ng/mL (normal range: <2.1 ng/mL) and 1,000 ng/mL (normal range: 90-233 ng/mL, SD score +10.6), respectively. Bromocriptine insufficiently suppressed her GH levels, while octreotide paradoxically increased her GH levels. Together with her characteristic features, she was diagnosed with acromegaly caused by an invasive GH-producing pituitary macroadenoma. As performing a one-stage operation would have been extremely difficult, she was first treated with pasireotide long-acting release (40 mg monthly) for 5 months followed by a successful transsphenoidal surgery. One month after the first injection, biochemical control was achieved (IGF-I, 220 ng/mL; GH, 1.26 ng/mL), and tumor shrinkage of approximately 50% was observed. The resected tumor was histologically diagnosed as a sparsely granulated somatotroph adenoma, with higher expression of somatostatin receptor subtype 5 (SSTR5) than that of SSTR2A. The germline aryl hydrocarbon receptor interacting protein (AIP) mutation was negative, and several tumor cells were weakly immunoreactive for AIP. Despite the presence of a residual tumor postoperatively, biochemical control was achieved 6 months after the final injection of pasireotide. In conclusion, this case suggests that pasireotide may be an option for preoperative first-line therapy in invasive and octreotide-resistant sparsely granulated somatotroph adenomas.
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PMID:Impact of preoperative pasireotide therapy on invasive octreotide-resistant acromegaly. 3007 25


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