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Biomedical subjects

D F Schoors

Publications and source records attributed to D F Schoors.

25 records · Page 2Linked to original sources
PubMed1990

Further studies on the mechanism of the natriuretic response to low-dose dopamine in man: effect on lithium clearance and nephrogenic cAMP formation.

The effect of intravenous infusion of low-dose dopamine on electrolyte excretion, lithium clearance, nephrogenous cAMP formation and renal haemodynamics was investigated in healthy volunteers. Dopamine significantly increased the urine flow rate by 70.6% and urinary sodium excretion by 72%, but did not change creatinine clearance, PRA or plasma levels of AVP, ANP and cAMP. Renal plasma flow significantly increased by 48.6%; the glomerular filtration rate was not changed. Lithium per se increased basal PRA, but had no effect on the increments of urine flow rate, sodium excretion and renal blood flow induced by dopamine. Dopamine significantly increased the fractional excretion of lithium (representing fractional excretion of sodium at the proximal level). The increase in urinary sodium excretion during dopamine infusion, significantly correlated with the increase in fractional excretion of lithium (r = 0.94; P less than 0.01) and the increase in nephrogenous cAMP formation (r = 0.96; P less than 0.01). No correlation was found between the increase in urinary sodium excretion and the increase in renal blood flow. In conclusion, this study confirms that low-dose dopamine increases renal blood flow and urinary sodium excretion in healthy volunteers. This natriuretic response appears to be due to interaction with proximal tubular dopamine receptors, which are positively coupled to adenylate cyclase.

Adult↗
PubMed1990

A case of hyperdopaminuria due to increased renal dopamine production.

Increasing evidence suggests that dopamine is synthesized within the kidney and that this intrarenally formed dopamine plays a role in sodium handling. We report on a case, in which a patient had markedly elevated urinary dopamine levels, due to increased renal dopamine synthesis, while receiving chronic corticosteroid therapy. Blockade of the renal dopamine synthesis, by carbidopa, markedly reduced urinary dopamine output and urinary sodium excretion. These findings provide further evidence for the hypothesis that intrarenal dopamine plays a role in sodium handling and may be of pathophysiological importance in counteracting the sodium-retaining effects of chronic corticosteroid therapy.

Adrenal Cortex Hormones↗
PubMed1989

Effects of fenoldopam on alpha-methyl-p-tyrosine-stimulated prolactin secretion in conscious rats.

Pituitary dopamine D-2 receptors participate in the regulation of prolactin (PRL) release. No dopamine D-1 receptors have so far been identified in the pituitary gland. The present study was designed to assess the effects of fenoldopam, a selective dopamine D-1 receptor agonist, on alpha-methyl-p-tyrosine-stimulated PRL release. Fenoldopam dose dependently reduced the alpha-methyl-p-tyrosine-stimulated PRL secretion. This inhibitory effect of fenoldopam was abolished after pretreatment with SCH 23390, a specific dopamine D-1 receptor antagonist, suggesting the involvement of a dopamine D-1 receptor in PRL secretion.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Hypotensive and regional hemodynamic effects of the dopamine receptor agonist SK & F 85174 in the anesthetized rat.

The effects of the D1/D2 dopamine receptor agonist SK & F 85174, an N-allyl derivative of fenoldopam, on blood pressure and regional hemodynamics were studied in anesthetized normotensive rats. SK & F 85174 reduced blood pressure and enhanced blood flow in the renal, superior mesenteric and the hindquarters vascular beds. Calculated vascular resistances were reduced. The nonselective dopamine receptor antagonist RS-sulpiride abolished, while SCH 23390 (D1 antagonist), domperidone (D2 antagonist) and hexamethonium (ganglion blocker) each partly blocked the hypotensive effect. SCH 23390 antagonized the vasodilator effect more in the renal and superior mesenteric vascular beds, whereas domperidone antagonized the response more in the hindquarters vascular bed. RS-sulpiride antagonized vasodilatation in the three vascular beds. Hexamethonium abolished vasodilatation in the hindquarters vascular bed only. These results indicate that the hypotensive effect of SK & F 85174 is due to stimulation of both postsynaptic D1 and neuronal D2 receptors. The vasodilator effect in the renal and superior mesenteric vascular beds is mediated by D1 receptor stimulation, the vasodilator response in the hindquarters vascular bed is due to neuronal D2 receptor stimulation.

Animals↗