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

The purpose of the study was to compare the renal effects of low doses of exogenous dopamine to assess the responsiveness of renal dopaminergic receptors in normotensive and hypertensive subjects. Eight hypertensive patients and seven normotensive volunteer subjects were studied. Inulin and para-aminohippuric (PAH) clearances, natriuresis, and fractional excretion of sodium increased significantly after intravenous dosing with dopamine (2 micrograms/min/kg) in both groups. These increases were significantly higher in hypertensive than in normotensive subjects: 31.8% +/- 3.7% vs. 16.2% +/- 1.2% for inulin clearance (P less than 0.01), 83.3% +/- 10.5% vs. 41.1% +/- 3.4% for PAH clearance (P less than 0.01), and 331% +/- 38% vs. 216% +/- 26% for natriuresis (P less than 0.01). These findings suggest hyperresponsiveness to dopamine during hypertension. This enhanced response to exogenous dopamine can be considered as a further argument favoring the existence of a deficit in dopaminergic activity during hypertension. Dopamine also induced a significant reduction in blood pressure and increased heart rate in hypertensive subjects but no significant change in blood pressure and heart rate occurred in normotensive subjects.
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PMID:Enhanced dopamine renal responsiveness in patients with hypertension. 378 Jan 22

Right ventricular (RV) function and pulmonary hemodynamics were studied in burned patients during dopamine infusion. The dopamine dose varied between 0 to 9.0 +/- 0.7, (mean +/- Se) micrograms/kg/min. No significant improvement in RV hemodynamics was observed as measured by RV end-diastolic volume index and RV ejection fraction. However, with infusion of dopamine, significant elevation in mean pulmonary artery pressures were noted, particularly in patients with pulmonary artery hypertension. Dopamine, in the doses administered, does not improve RV or systemic hemodynamics; in some burned patients, dopamine may have deleterious effects on the pulmonary circulation.
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PMID:Right ventricular function and pulmonary hemodynamics during dopamine infusion in burned patients. 394 49

Calcium channel blockers are used in the treatment of angina pectoris, cardiac arrhythmia, and hypertension. Sporadic reports of hypotensive reactions to verapamil have indicated that these reactions are not reversed readily by catecholamine administration. This study was conducted to test the hypothesis that verapamil pretreatment does not alter the ability of dopamine in conventional doses to augment cardiac output. Twelve mongrel dogs, weighing 19 to 25 kg, were anesthetized with pentobarbital and placed on a respirator. Heart rate, cardiac output, and the right atrial, pulmonary artery, pulmonary capillary wedge, and central aortic pressures were measured directly. Dopamine, 10 micrograms/kg/min, increased cardiac index by 52.4 mL/kg/min over baseline. The dopamine was stopped and the animals were allowed to return to baseline. Dopamine, 10 micrograms/kg/min, was administered again after pretreatment with 0.15 mg/kg verapamil, and it increased cardiac index by 47.9 mL/kg/min over the second baseline control. The results were not statistically different using the Student t test for paired data (P greater than .05). It is concluded that verapamil does not affect dopamine's ability to augment cardiac output in the dosages tested.
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PMID:The influence of verapamil on dopamine's ability to augment cardiac output. 403 74

The chronotropic effects of dopamine were studied in the conscious dog with chronic A-V block. Dopamine at 12.5-200 micrograms/kg and 12.5-50 micrograms/kg/min lowered atrial rate independently of dose. After blockade of muscarine receptors or alpha-adrenoceptors, it raised atrial rate. After blockade of dopamine receptors, dopamine still lowered atrial rate, and did so dose-relatedly after blockade of beta-adrenoceptors. It raised ventricular rate, and at high doses also induced ventricular rhythm disorders. Blockade of muscarine receptors enhanced the ventricular cardioaccelerator effect of dopamine (P less than 0.025) at 100 micrograms/kg, while blockade of alpha-adrenoceptors reduced it (P less than 0.05). Blockade of dopamine receptors did not modify this effect, but blockade of beta-adrenoceptors reversed it. Dopamine at 25-200 micrograms/kg raised mean blood pressure. This effect was enhanced by blockade of muscarine receptors, reversed by blockade of alpha-adrenoceptors, and was unaffected by blockade of beta-adrenoceptors or dopamine receptors. These results show that the atrial cardiomoderator effect of dopamine is a vagal reflex response to its hypertensive action, and that it is limited by its direct beta-adrenergic stimulating action. They also show that the ventricular cardioaccelerator effect of dopamine is attenuated by a reflex vagal depressor effect consequent to the induced hypertension. No evidence was found for the existence of positive chronotropic dopamine receptors in either atria or ventricles.
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PMID:Dopamine in the conscious dog with chronic heart-block. Mechanisms of chronotropic cardiac effects. 614 63

The endogenous catecholamine dopamine lowers blood pressure by acting on two receptor subtypes: dopamine 1 and dopamine 2. Dopamine 1 receptors subserve vasodilation, especially in the renal, coronary, mesenteric, and cerebral vascular beds. Dopamine 2 receptors have been located at the endings of postganglionic sympathetic nerves and, when activated, inhibit norepinephrine release. Inhibition of emesis and inhibition of prolactin release also appear to be dopamine 2-mediated phenomena. The receptor subtypes have been classified by differences in chemical structure of agonists and by specific antagonists. Dopamine also acts on beta 1 receptors to stimulate the heart and alpha 1 and alpha 2 receptors to cause vasoconstriction. Alpha adrenergic activity and lack of oral availability limit the use of dopamine in the treatment of hypertension. However, studies with the selective dopamine 1 agonist, fenoldopam, and dopamine 2 agonists such as LY 141865 and bromocriptine, indicate that agonists of both receptor subtypes can lower blood pressure in experimental animals and in hypertensive patients. Initial use of dopamine agonists in the treatment of hypertension and its possible involvement in the etiology and maintenance of hypertension are discussed.
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PMID:Dopamine receptors and hypertension. Physiologic and pharmacologic implications. 614 92

The concentrations and alpha-methyl-p-tyrosine (alpha-MPT) induced disappearance of catecholamines, adrenaline, noradrenaline and dopamine, were measured in selected areas of the brainstem and hypothalamus of spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The catecholamine levels were measured by a sensitive radioenzymatic assay method combined with microdissection of the rat brain. The adrenaline concentration was higher in the area A1 of young SHR, but not in adult SHR, than in age-matched control rats. Noradrenaline concentrations and the alpha-MPT induced noradrenaline disappearance were less in the rostral part of the nucleus tractus solitarii (NTS) and the nucleus hypothalamic anterior of young SHR, and in the rostral part of the NTS of adult SHR. On the other hand in DOCA-salt hypertensive rats, the concentrations of adrenaline and noradrenaline were the same as in control rats in the examined areas. The alpha-MPT induced noradrenaline disappearance was less in the rostral part of the NTS of DOCA-salt hypertensive rats. Dopamine concentrations and the alpha-MPT induced dopamine disappearance were the same in the examined areas of SHR and DOCA-salt hypertensive rats. The results suggest that SHR have a change in adrenergic neural activity in the brainstem and a decrease in noradrenergic neural activity in the brainstem and hypothalamus while DOCA-salt hypertensive rats have a decrease in noradrenergic neural activity in the brainstem. Such changes in brain catecholaminergic neurons may have played an important role in the development of hypertension in these rats.
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PMID:Brain catecholamines in spontaneously hypertensive and DOCA-salt hypertensive rats. 614 70

Until recently, the key pharmacologic tools necessary for major advances in understanding and studying cardiovascular and renal dopamine receptors have been lacking. This communication describes new advances in the pharmacology of dopamine receptors as studied with a series of newly synthetized benzazepines. Fenoldopam (SK&F 82526) is a selective (DA1) dopamine-receptor agonist. Initial studies with fenoldopam on splenic arterial ring segments of the rabbit have suggested that the endothelium as well as vascular smooth muscle may possess hemodynamically important dopamine receptors, and that cyclic adenosine monophosphate can be a second messenger mediating dopaminomimetic vasodilatation. Significant advances in DA1-selective antagonists have also recently been made. SK&F 83566 is a potent antagonist of both dopamine and fenoldopam in the vasculature. Dopamine-receptor selective agonists and antagonists represent an emerging strategy for the treatment of several cardiovascular diseases, including hypertension and edema. Moreover, these compounds are important tools for the characterization and study of dopamine receptors.
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PMID:Cardiovascular dopamine receptors: recent advances in agonists and antagonists of the DA1-receptor. 621 Apr 23

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

Studies have shown that dopamine inhibits angiotensin II (AII)-induced aldosterone secretion in bovine adrenal cells in vitro, but does not alter aldosterone responses to AII in sodium-replete normal humans. We investigated six normal men with plasma cortisol concentrations less than 2 micrograms/dl during oral administration of dexamethasone 0.5 mg every 6 hours for 2 days and in balance at 10 mEq sodium/day intake (UNa V 22 +/- 5 mEq/24 hr). The subjects received either dopamine 4 micrograms/kg/min or vehicle intravenously (i.v.) for 270 minutes on 2 consecutive days. After 120 minutes of dopamine infusion, AII was given in cumulative doses of 0.5, 1, 2, 4, and 6 pmol/kg/min i.v., each dose for 30 minutes. Control plasma aldosterone concentrations before vehicle or dopamine were 12 +/- 2 (mean +/- 1 SE) and 15 +/- 3 ng/dl, respectively. Aldosterone responses to AII were greater with vehicle than dopamine at AII doses of 4 and 6 pmol/kg/min (p less than 0.02). The slope of the AII-aldosterone dose-response curve was steeper with vehicle (0.36) than with dopamine (0.13), p less than 0.0001. Plasma renin activity and serum potassium concentrations were similar with vehicle and dopamine. Dopamine inhibits AII-induced aldosterone secretion during sodium deficiency in humans.
Hypertension
PMID:Dopamine modulates sodium-dependent aldosterone responses to angiotensin II in humans. 637 91

The second known case of a malignant catecholamine-secreting (DA)-secreting carotid body paraganglioma is presented. Dopamine synthesis and secretion can be increased in malignant tumors derived from neural crest cells. Whether this is true, in addition, for extra-adrenal paragangliomas is not yet clear. Malignant paragangliomas of the carotid body and larynx, although rare, frequently have been accompanied by increased catecholamine secretion. Malignant catecholamine-secreting carotid body paragangliomas are best treated by composite resection (internal carotid artery and neck dissection), with special attention being given to measures preventing severe hypertension and arrhythmias in the perioperative period.
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PMID:Malignant catecholamine-secreting carotid body paraganglioma. 641 Mar 37


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