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

A dopaminergic mechanism has been proposed to suppress aldosterone secretion. To assess the possibility that a defect in the dopaminergic mechanism might enhance aldosterone secretion in hypertensive patients, we determined basal and adrenocorticotropic hormone (ACTH)-stimulated plasma aldosterone (PA), cortisol, renin activity, and potassium concentrations before and during dopamine receptor stimulation with dopamine infusion and bromocriptine administration and dopamine receptor blockade with metoclopramide. The patient study groups included: (a) seven patients with low-renin hypertension and abnormal aldosterone suppression with sodium loading and presumed bilateral zona glomerulosa hyperplasia (ZGHP); (b) two patients with aldosterone-producing adenoma; (c) five patients with low-renin hypertension but normal aldosterone suppression with sodium loading; and (d) six patients with normal-renin hypertension. Dopamine infusion in patients with ZGHP caused PA to fall (P less than 0.01) into the normal range, but did not block the enhanced (P less than 0.05) aldosterone response to ACTH that is characteristic of these patients. Dopamine infusion in patients with low-renin hypertension but normal aldosterone suppression also suppressed PA (P less than 0.01), whereas it had no effect upon PA in patients with normal-renin hypertension or aldosterone-producing adenoma and did not blunt the PA response to ACTH in either group. Bromocriptine administration had no effect upon basal or ACTH-stimulated PA. Dopamine infusion in patients with ZGHP also enhanced (P less than 0.05) diuresis and natriuresis in comparison with normal-renin patients. Metoclopramide administration increased (P less than 0.01) PA in all patients. Thus, a dopaminergic mechanism appears to be important in the regulation of aldosterone secretion in patients with ZGHP and in other low-renin hypertensives with normal aldosterone suppression with sodium loading. In contrast, this latter group does not exhibit an enhanced aldosterone response to ACTH. Both of these groups differ from normal-renin hypertensives, who have no PA suppression with dopamine infusion.
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PMID:Aldosterone suppression with dopamine infusion in low-renin hypertension. 630 9

Bromocriptine was used to test the hypothesis that the abnormality of the dopaminergic system described in haemodialysis patients may cause enhanced sympathetic activity and high blood pressure. Bromocriptine significantly reduced supine mean blood pressure and plasma noradrenaline. Moreover, although the increments in plasma noradrenaline during tilt tests were reduced by bromocriptine there was a significant improvement in the response of blood pressure. These results suggest that dopaminergic control of sympathetic activity may be impaired in haemodialysis patients and may be a cause of high blood pressure. Moreover, a restoration of a normal relationship between noradrenaline and adrenergic receptors would be consistent with the present results.
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PMID:Dopaminergic control of sympathetic activity and blood pressure in haemodialysis patients. 665 50

The effects of intravenous bromocriptine were studied on the systolic pressor responses elicited by stimulation of afferent nerves (vagus, saphenous and superior laryngeal nerves) in urethane anaesthetized dogs. Bromocriptine alone decreased these pressor responses. Pretreatment with sulpiride failed to modify the depressor action of bromocriptine on the pressor responses to vagal stimulation. In contrast, sulpiride prevented bromocriptine-induced decrease in the pressor responses elicited by saphenous or laryngeal activation. These data confirm the potential antihypertensive properties of bromocriptine and show that this effect is only partly due to an activation of prejunctional dopaminergic receptors. They suggest that the mechanism of the antihypertensive action of bromocriptine may vary according to the level of blood pressure, the kind of arterial hypertension and the species.
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PMID:Influence of bromocriptine on the pressor responses to afferent nervous stimulation. 673 75

Some investigators have reported that plasma prolactin levels are elevated in hypertensive men and that both their hyperprolactinemia and hypertension were controlled by bromocriptine, a dopamine agonist. They concluded that reduced central dopaminergic activity may be a factor in maintaining essential hypertension. We examined the serum prolactin and thyrotropin (TSH) responses to thyrotropin releasing hormone (TRH), metoclopramide (a dopamine antagonist) and bromocriptine in 10 normal and 10 hypertensive normoreninemic men. TRH caused significant increase of both prolactin and TSH and metoclopramide caused significant increase of prolactin in both normals and hypertensives. Bromocriptine suppressed prolactin and TSH significantly in both groups. There were no significant differences in prolactin and TSH levels between the normal and hypertensive groups before or during the tests. These results provide no support for the hypothesis that alterations in the activity of central dopaminergic neurons are involved in the maintenance of the elevated blood pressure of normoreninemic men with essential hypertension.
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PMID:Is normoreninemic essential hypertension caused by disordered central dopaminergic regulation? 677 64

A single oral intake of 10 mg of Bromocriptine can modify both plasma renin activity (PRA) and arterial blood pressure (BP). The changes in both variables depend on the integrity of the central dopaminergic systems. The parkinsonians whose extrapyramidal symptoms are markedly improved by L-Dopa in association with a decarboxylase inhibitor (IDC) and the untreated parkinsonians are the only patients whose PRA and BP are lowered 1 h after Bromocriptine ingestion. The results obtained in the L-dopa-induced dyskinetic parkinsonians are similar to those obtained in the group of L-Dopa-resistant patients. This points to the paradoxical hypothesis of dopaminergic hyposensitivity in the dyskinetic patients. In spite of the absence of correlation between PRA and BP, it is possible that lowering of BP by Bromocriptine is linked to the parallel decrease of PRA. An increase of the BP may be obtained in the dyskinetic and L-Dopa-resistant groups. These data point to a possible involvement of central dopaminergic systems in some aspects of hypertension.
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PMID:The use of bromocriptine for testing central dopaminergic reactivity. 677 8

The effects of bromocriptine administered by peripheral or central routes were studied in neurogenic hypertensive dogs. The acute hypertension was elicited by deafferentation (sino-aortic denervation). Intravenous (0,15 to 0,30 mg/kg) bromocriptine induced an important decrease in blood pressure of the debuffered dog (Fig. I). Bromocriptine reduced the arrhythmia induced by deafferentiation, but not the tachycardia of the debuffered dog (Table I). Bromocriptine was active by intracisternal route, at a dose (0,15 mg/kg) effective by intravenous route (Fig. 2). This antihypertensive effect of bromocriptine was also observed in debuffered dogs with binding of both vertebral and carotid arteries (i.e. when an effect of the drug on central structures was ruled out) (Fig. 3), and was suppressed by pretreatment with haloperidol, a dopaminergic antagonist (Fig. 4). These results imply that the mechanism underlying the hypotensive effect of bromocriptine is dopamine receptor stimulation; we consider that an effect on central nervous structures does not play a significant role in the hypotensive effect of this drug following acute intravenous administration in the dog.
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PMID:[Hypotensive action of a dopaminergic agonist, bromocriptine, in the dog]. 679 32

Treatment of 2-month-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) normotensive controls with the dopamine agonist, bromocriptine, for 7 days significantly affected hormonal responses to immobilization stress in both groups. However, basal blood pressures and pressor responses to immobilization stress were significantly reduced only in SHR. Basal levels of catecholamines were similar in the two groups of rats, but catecholamine responses to immobilization stress following saline (vehicle) treatment were marked greater in SHR; following bromocriptine treatment for 7 days, catecholamine responses were similar in the two groups. Basal serum prolactin levels and prolactin responses to immobilization were greater in SHR after saline treatment; after bromocriptine, they were similar in the two groups. Basal plasma renin activity (PRA)and PRA responses to immobilization were significantly less in SHR following saline treatment; after bromocriptine treatment these responses were paradoxically greater in SHR without being significantly changed in WKY. Basal levels of plasma aldosterone and corticosterone following saline were significantly greater, but responses to immobilization less, in SHR. Bromocriptine treatment decreased aldosterone and corticosterone responses to stress in WKY but paradoxically increased these responses in SHR. These results suggest that increased pressor responses to stress are dependent on heightened sympathetic nerve activity, perhaps secondary to decreased central dopaminergic activity. Increased basal prolactin levels and stress-mediated prolactin responses may be related to decreased central dopaminergic activity. Paradoxical PRA, plasma aldosterone, and corticosterone responses to stress following bromocriptine suggest altered dopaminergic modulation of these hormones in the SHR.
Hypertension
PMID:Effects of bromocriptine on responses to stress in spontaneously hypertensive rats. 702 8

11 acromegalics were treated with bromocriptine for 2--18 months. Their hormonal response was assessed by an acute suppression test with bromocriptine (AST), an oral glucose tolerance test (GTT), and by measuring growth hormone (GH) concentrations during a day of hospital life. The GTTs and the 24-hour profiles were performed before and after bromocriptine. During the AST all patients showed a decrease of GH concentrations ranging from 33 to 86% of the basal. Following bromocriptine, the mean GH concentration was lowered in 7 out of 11 patients during the GTT, and in 8 out of 11 during the profile, but it was within the normal range in 4 patients only during the GTT, and in 1 during the profile. Bromocriptine normalises radioimmunoassayble GH levels in a percentage of patients (12%) which is less than those following conventional treatment of acromegaly, surgery (80%) and pituitary irradiation (70%). Clinically, however, bromocriptine was more effective than judged by the changes of GH levels. Subjective and objective symptoms of acromegaly, such as articular pain, excessive sweating, hypertension, amenorrhoea, urinary hydroxyproline excretion and heel pad thickness decreased in our patients after bromocriptine. A specific action of bromocriptine on the degradation rate of 'little' GH may result in a selective reduction of the bioactive monomeric component of GH and may explain the discrepancy between the clinical and the biochemical response to bromocriptine. This discrepancy might also be explained by a specific action of bromocriptine on the somatomedin levels.
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PMID:Reappraisal of bromocriptine treatment for acromegaly. 739 Apr 5

Bromocriptine, a dopamine agonist with central nervous system actions, may reduce sympathetic nervous system activity. We tested this hypothesis by measuring arterial blood pressure, central venous pressure, heart rate, muscle sympathetic nerve activity, and forearm blood flow before and after unloading the arterial baroreceptors with sodium nitroprusside (0.5 to 1.5 mcg/kg per minute IV), before and after unloading the cardiopulmonary baroreceptors with incremental lower body negative pressure (0 to -15 mm Hg), and before and after immersion of the hand in ice-cold water for 2 minutes (cold pressor test). After obtaining basal responses to provocative maneuvers, we gave 20 healthy subjects either 5 mg oral bromocriptine (n = 10) or placebo (n = 10) in a randomized, double-blind fashion. Bromocriptine did not affect resting mean arterial pressure, heart rate, or forearm blood flow. Bromocriptine decreased resting central venous pressure by 1.2 mm Hg (P < .05) and tended to increase total integrated muscle sympathetic nerve activity (from 151 +/- 44 to 212 +/- 82 U/min, P = NS). The reflex increases in muscle sympathetic nerve activity to nitroprusside infusion and lower body negative pressure were unchanged by bromocriptine; however, vascular responsiveness to both maneuvers was impaired after bromocriptine administration compared with control. Without bromocriptine, the reflex increase in muscle sympathetic nerve activity after nitroprusside-induced hypotension maintained forearm blood flow at a constant level, whereas with bromocriptine the forearm blood flow increased from 1.9 +/- 0.3 to 2.8 +/- 0.6 mL/min per 100 mL (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 May
PMID:Effects of bromocriptine on cardiovascular regulation in healthy humans. 773 19

Seven cases of empty sella syndrome were reported, among them 2 cases were primary empty sella syndrome, 5 cases were secondary empty sella syndrome. 5 cases were operated with the obliteration by transsphenoidal approach, 2 cases were operated by transfrontal approach. 6 cases were cured, the symptoms in one case was not improved due to the primary hydrocephalus. This syndrome is associated with defect of sellar diaphragm, benign intracranial hypertension, long-term administration of Bromocriptine, surgery and radiotherapy of pituitary gland. Main clinical features are headache, damage of vision and visual fields, hypopituitarism. Obliteration of empty sella by transsphenoidal approach is a simple and effective method.
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PMID:[Obliteration of empty sella for therapy of empty sella syndrome by transsphenoidal and transfrontal approach]. 803 3


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