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)

Dopamine (DA), via DA-1 receptors, regulates Na+ transport in the kidneys. Dopamine is synthesized from L-DOPA in the proximal tubule and presumably secreted as an autocrine/paracrine substance to stimulate DA-1 receptors localized on proximal tubular cells. We have previously reported the presence of DA-1 receptors in renal cortical homogenates and on the isolated proximal tubule of the rat and rabbit, consistent with the dopamine autocrine/paracrine model. We have localized DA-1 receptors in the proximal straight tubule of the rabbit, and in the cortical collecting duct of the rabbit and rat, but not in the distal collecting tubule or the cortical thick ascending loop of Henle. The presence of functional DA-1 receptors has been substantiated by the coexistence of DA-1 agonist-stimulated adenylate cyclase activity in the same nephron segments in which DA-r receptors have been found. Increased concentrations of intrarenal dopamine induced by dopamine-beta-hydroxylase inhibition with SKF-102698 caused a down regulation of proximal tubular DA-1 receptors and almost complete ablation of DA-1 agonist stimulated adenylate cyclase activity. Thus, dopamine may play a role in the regulation of DA-1 receptors and their linkage with adenylate cyclase. Since alterations in the renal dopaminergic system have been measured in some forms of experimental hypertension, we studied DA-1 receptors and their coupling to adenylate cyclase in the spontaneously hypertensive rat (SHR).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A renal dopamine-1 receptor defect in two genetic models of hypertension. 197 47

This study was undertaken to determine whether midazolam alleviates sympathoadrenal response evoked by tracheal intubation in elderly patients with hypertension. Anesthesia was induced with midazolam in a sleep dose followed by vecuronium 0.1 mg.kg-1. Heart rate and blood pressure were recorded before, 1 and 3 minutes after induction with intubation. Free and total catecholamine (CA) in plasma were measured at each time. Dopamine, norepinephrine and epinephrine (EN) were determined using fluorescence derivatization with diphenylethylenediamine by HPLC. Although heart rate and diastolic pressure rose in some degree 1 min after intubation, free and total CA concentrations did not increase during study period. Free and total EN levels decreased significantly 3 min after intubation. The absence of elevation in plasma CA concentrations, especially in free CA, which is physiologically active, would contribute to produce circulatory stability on laryngoscopy and tracheal intubation. However, the mystery of why hyperdynamic state was produced without the increase in CA concentrations remains to be solved, even though it occurred for a short period of time.
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PMID:[Plasma catecholamine response to tracheal intubation after midazolam and vecuronium in elderly patients with hypertension]. 198 26

The influence of the degree of sympathetic nervous system activation on the cardiovascular effects of dopamine was studied during abdominal aortic surgery in 13 patients. The arterial plasma norepinephrine concentration (NE) was used as an index of sympathetic nervous system activity. During anesthesia with nitrous oxide and fentanyl, 7 patients (group 1) had a NE above 700 pg/mL and an increased mean arterial pressure (MAP) compared with the preanesthetic level (150 +/- 6 v 117 +/- 10 mm Hg; p less than 0.01, mean +/- SEM). The other 6 patients (group 2) had no significant change in MAP compared with the preanesthetic MAP (119 +/- 7 v 105 +/- 4 mm Hg). Dopamine, 4 micrograms/kg/min, decreased MAP in group 1 by 19% (150 +/- 6 to 121 +/- 8 mm Hg; P less than 0.05) because of a 32% +/- 9% decrease (P less than 0.05) in systemic vascular resistance. MAP was not altered by dopamine in group 2 (119 +/- 7 v 123 +/- 6 mm Hg; not significant). Following termination of dopamine, the anesthetic was supplemented with thoracic epidural anesthesia (TEA). This reduced MAP to 65 +/- 7 mm Hg (P less than 0.01) and 56 +/- 3 mm Hg (P less than 0.01), and NE to 441 +/- 76 (P less than 0.05) and 235 +/- 45 pg/mL (P less than 0.05) in groups 1 and 2, respectively. During TEA, dopamine increased MAP similarly in both groups, to 85 +/- 7 mm Hg (P less than 0.01) and 82 +/- 9 mm Hg (P less than 0.05), respectively. In conclusion, dopamine, at the same dosages, counteracted hypertension during general anesthesia and counteracted hypotension during general anesthesia combined with TEA.
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PMID:Dopamine counteracts hypertension during general anesthesia and hypotension during combined thoracic epidural anesthesia for abdominal aortic surgery. 213 84

To investigate the brain stem monoamine mechanism in the development and maintenance of hypertension of spontaneously hypertensive rats (SHR), we determined monoamine contents and norepinephrine turnover in discrete brain stem nuclei which are known to relate with cardiovascular control. Specific areas and brain stem nuclei were dissected from serial frozen slices of 300 microns thickness according to the atlas of Palkovits and Jacobowitz. The dissected tissues were homogenized, centrifuged and the supernatants were injected into high performance liquid chromatography with electrochemical detection (HPLC-ECD). Norepinephrine (NE), dopamine (DA), serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) contents were determined. NE turnover was also determined 2 hour after alpha-methyl-p-tyrosine administration (250 mg/kg, i.p.). In 4-week old SHR, the only significant change observed was decreased NE contents in the nucleus tractus solitarii (NTS). Such decreases in NE contents of the NTS were also found in 8- and 16-week old SHR. However, there were no differences in NE turnover in the NTS between SHR and WKY. Increased NE contents were found in the A1, A5, and nucleus reticularis gigantocellularis (RG) in the later stages (8 and 16 weeks) in SHR. Furthermore, increased NE turnover was seen in the RG of SHR at 16-week old, indicating increased neuronal activity. Dopamine, 5-HT and 5-HIAA showed no consistent changes between SHR and WKY. Increased NE levels were observed in later stages after development of hypertension, suggesting the increased NE in adult SHR may represent a central adaptive change secondary to the established hypertension. Since increased NE levels were consistently found in or around the regions which are known as vasomotor centers, we assume that these increased NE might serve to maintain hypertension or to inhibit a further increase in blood pressure. In contrast, the NE contents were decreased with constant turnover in NTS of SHR aged 4, 8, and 16 weeks. Constant turnover in NE could not compensate for reduced NE in NTS and may lead to a functional reduction or reduced noradrenergic activity. This defect in intrinsic noradrenergic neurons in NTS may trigger the development of genetic hypertension in SHR. In conclusion, the present results demonstrate that NE levels of SHR in the NTS were consistently decreased compared with those of WKY in all age groups. In later stages, increased NE levels were observed in A1, A5 and RG of SHR. These results indicate that brain stem monoamine system, especially noradrenergic neurons, contributes to the development and maintenance of hypertension in SHR.
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PMID:[Monoamine contents and norepinephrine turnover in brain stem nuclei of young and adult spontaneously hypertensive and Wistar-Kyoto rats]. 227 99

The levels of dopamine and its metabolites in the adenohypophysis of the normo- and hypertensive rats were determined. Dopamine was present as the free and sulfate-conjugated form in the adenohypophysis of the spontaneously hypertensive rat (SHR), Wistar Kyoto (WKY) and Sprague-Dawley (SD) rats. The levels of both the free and conjugated dopamine in the adenohypophysis of the SHR were 5.49 +/- 2.91 (mean +/- SEM) and 4.27 +/- 3.31 pmoles/mg protein respectively. These values were not significantly different from those of the WKY and SD. 3,4-Dihydroxyphenylacetic acid (dopac), present as the free and sulfate-conjugated form, was found to be the only metabolite of dopamine in the adenohypophysis of the three animals. The levels of both free and conjugated dopac in the adenohypophysis of the SHR were 7.0 +/- 2.5 and 75.5 +/- 33.5 pmoles/mg protein respectively and these values were significantly different from those of the WKY (1.12 +/- 0.47 and 4.17 +/- 0.48 pmoles/mg protein) and SD (1.87 +/- 0.62 and 3.5 +/- 1.11 pmoles/mg). The results indicate that (a) there is no deficiency of free dopamine in the adenohypophysis of the SHR and hypertension in these animals is unlikely to be related to the catecholamine level in the endocrine gland, (b) the dopamine turnover in either the tuberoinfundibular tract or the adenohypophysis of the SHR is greatly enhanced.
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PMID:Levels of dopamine and 3,4-dihydroxyphenylacetic acid in the adenohypophysis of normo- and hypertensive rats. 235 38

Sodium loading reduces aldosterone responses to angiotensin II (AII) when compared to the sodium restricted state. Recent investigations suggest that dopamine inhibits the aldosterone secretion and may contribute to the alteration in aldosterone response to AII with sodium intake, since administration of the dopamine antagonist, metoclopramide, enhances the aldosterone responses to AII on a high but not a low salt diet. Nonmodulating hypertension is characterized, in part, by a decreased aldosterone response to AII, raising the possibility that an increased dopaminergic inhibition of aldosterone secretion underlies the adrenal defect in nonmodulating hypertension. To assess this possibility, 69 patients with hypertension were characterized in relationship to their modulation status on a low sodium intake. Dopamine levels were significantly higher (P less than .05) in nonmodulators. To assess the physiologic relevance of these findings, the aldosterone response to AII infusion was assessed before and during administration of the dopamine antagonist, metoclopramide, in 13 patients. The adrenal response to AII did not change after metoclopramide in either hypertensive subgroup. Thus, it is unlikely that the adrenal defect is due to the increase in dopamine levels observed in nonmodulators. In the next study, the impact of dietary sodium intake on urinary dopamine levels was compared in normotensive and hypertensive subjects characterized as modulators and nonmodulators. Both modulators and normotensive subjects demonstrated an increase in urinary dopamine excretion in response to a high sodium intake--a feature that was not observed in the nonmodulators. Thus, the sodium retaining tendency of nonmodulators may reflect, at least in part, a reduction in intrarenal dopamine production in response to a sodium load.
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PMID:Dopamine and nonmodulating hypertension. 238 75

Heart rate, systolic and diastolic blood pressure, and left ventricular pressure were continuously measured in volume overload experiments with SHR and WKY rats. The index for contractility dp/dtmax was determined. The initial data and the changes during overload are tabulated and compared between the strains. Overload led to a marked increase of the end-diastolic left ventricular pressure in WKY rats. The SHR overload model reacts less to the standard drug Dopamine than the normotensive strain. It combines chronic hypertension with acute volume overload and is suitable for circulation basic research and special screening experiments with prospective new cardiovascular drugs. It is bound to a high technical and preparative expenditure.
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PMID:Experiments with volume overload in SHR/Frid and WKY/Frid. 240 52

Several studies suggested that dopamine may be one of the inhibitory modulators of aldosterone secretion. Metoclopramide, a selective antagonist for dopamine D-2 receptors, increases both basal plasma aldosterone levels and the aldosterone response to angiotensin II (Ang II) in rats and humans kept on a high sodium intake, these effects being blocked by dopamine infusion. Dopamine, which has no significant effects on Ang II-induced aldosterone secretion in sodium-replete subjects, inhibits the hormonal response to Ang II infusion in sodium-depleted normal subjects, suggesting that the sodium balance state may be an important factor in the dopaminergic mechanisms controlling aldosterone secretion. The effect of dopamine on the hormone production is mediated by D-2 receptors in the adrenal cortex as shown by in vitro studies with isolated adrenal glomerulosa cells. Clinical studies have shown that dihydroergotoxine, a selective D-2 agonist, suppresses the aldosterone secretion induced by sodium depletion in hypertensive patients, an effect blocked by sulpiride. This mechanism could be of relevant therapeutic interest in its contribution to the natriuretic effects of dopaminergic agonists, which have clinical applications in the treatment of hypertension and congestive heart failure.
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PMID:Dopaminergic receptor mechanisms modulating the renin-angiotensin system and aldosterone secretion: an overview. 248 40

Direct effects of dopamine on renin release were examined using static incubations and perifusions of rat renal cortical slices. Dopamine (10(-5)M) significantly stimulated renin release compared with control. To determine which receptors are involved in dopamine-elicited renin release, studies were performed with specific dopamine-1 and dopamine-2 receptor agonists and antagonists, as well as with alpha- and beta-adrenergic antagonists. Fenoldopam, a dopamine-1 receptor agonist, dose dependently stimulated renin secretion both in static incubations and perifusions; whereas quinpirole (10(-7)-10(-5)M), a dopamine-2 receptor agonist, was ineffective. Phentolamine (10(-4)M), an alpha-adrenergic antagonist, did not alter dopamine- or fenoldopam-induced renin release. Similarly, propranolol, a beta-blocker, did not interfere with the renin stimulation of dopamine (10(-5)M) or fenoldopam (10(-6)M) incubations or perifusion experiments; whereas propranolol significantly blocked isoproterenol action. SCH 23390 (10(-5)M), a specific dopamine-1 antagonist, blocked dopamine- and fenoldopam-induced renin. In contrast, pimozide, a dopamine-2 receptor antagonist, was ineffective. These studies indicate that dopamine is a direct renin secretogogue, and its effects seem to be mediated by specific dopamine-1 receptor activation, as neither alpha- nor beta-adrenergic blockers nor dopamine-2 receptor antagonists altered dopamine actions. The results suggest that dopamine produced locally in the kidney may stimulate renin secretion directly by dopamine-1 receptor activation.
Hypertension 1989 May
PMID:Evidence that specific dopamine-1 receptor activation is involved in dopamine-induced renin release. 256 77

Up to now, no studies have been performed in normal humans to investigate the role of renal hemodynamic abnormalities in relation to acute-cyclosporin A (CsA) renal dysfunction and to verify whether the specific renal vasodilator, dopamine, can counteract these abnormalities. Eight normal subjects were examined both (A) after oral CsA (12 mg/kg body wt) and (B) after oral CsA + dopamine infusion (2 mg/kg body wt/min), under water diuresis. Both in protocols A and in B, four basal renal clearances were performed before CsA and every twenty minutes for four hours after CsA administration. In protocol A, after CsA, inulin (GFR) and PAH clearance (RPF) fell by up to 27% and to 41%, respectively, so that filtration fraction (FF) increased (P less than 0.01). A slight (not significant) hypertension occurred while renal resistances were markedly raised (P less than 0.001). Fractional urine and Na+ excretion as well as CH2O decreased, while UOsm increased (P less than 0.01). In protocol B, dopamine was infused from 120 to 180 minutes after CsA (that is, when the maximal adverse effects of CsA on renal hemodynamics had been observed in A). Dopamine infusion could reverse completely the effects of CsA on RPF, GFR, fractional urine output and CH2O; only UOsm remained higher than normal in conclusion with an increased fractional excretion of sodium (P less than 0.01). No changes were observed in plasma renin activity, aldosterone and in urinary epinephrine and norepinephrine excretion both in protocols.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute cyclosporine renal dysfunction reversed by dopamine infusion in healthy subjects. 260 Dec 57


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