title: Concerted action of dopamine on renal and intestinal Na(+)-K(+)-ATPase in the rat remnant kidney.
abstract: The present study evaluated renal and intestinal adaptations in sodium handling in uninephrectomized (Unx) rats and the role of dopamine. Two weeks after uninephrectomy, the remnant kidney in Unx rats weighed 33 +/- 2% more than the corresponding kidney in sham-operated (Sham) animals. This was accompanied by increases in urinary levels of dopamine and major metabolites [3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid] and increases in maximal velocity values (169 vs. 115 nmol. mg protein(-1). 15 min(-1)) for renal aromatic L-amino acid decarboxylase, the enzyme responsible for the synthesis of renal dopamine. High salt (HS) intake increased (P < 0.05) the urinary excretion of dopamine and DOPAC in Unx and Sham rats. However, the urinary levels of L-3,4-dihydroxyphenylalanine, dopamine, and DOPAC in Sham rats during HS intake were lower than in Unx rats. Blockade of dopamine D(1) receptors (Sch-23390, 2 x 30 microg/kg) reduced the urinary excretion of sodium in Unx (31% decrease) more pronouncedly than in Sham (19% decrease) rats. However, inhibition of renal Na(+)-K(+)-ATPase activity by dopamine was of similar magnitude in Unx and Sham rats. In parallel, it was observed that uninephrectomy resulted in a significant reduction in jejunal sodium absorption and Na(+)-K(+)-ATPase activity in jejunal epithelial cells. In jejunal epithelial cells from Sham rats, dopamine (1 microM) failed to inhibit Na(+)-K(+)-ATPase activity, whereas in Unx rats it produced a significant reduction. It is concluded that uninephrectomy results in increased renal dopaminergic activity and dopamine-sensitive enhanced natriuresis. Furthermore, it is suggested that decreased jejunal absorption of sodium may take place in response to partial renal ablation, as an example of renal-intestinal cross talk.
authors.affiliation: Institute of Pharmacology and Therapeutics, Faculty of Medicine, 4200 Porto, Portugal.
authors.forename: M A
authors.initials: MA
authors.lastname: Vieira-Coelho
authors.forename: P
authors.initials: P
authors.lastname: Serrão
authors.forename: J T
authors.initials: JT
authors.lastname: Guimarães
authors.forename: M
authors.initials: M
authors.lastname: Pestana
authors.forename: P
authors.initials: P
authors.lastname: Soares-da-Silva
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D001142:Aromatic-L-Amino-Acid Decarboxylases / Q000378:metabolism; D002394:Catechol O-Methyltransferase / Q000378:metabolism; D004298:Dopamine / Q000031:analogs & derivatives / Q000502:physiology* / Q000652:urine; D004573:Electrolytes / Q000652:urine; D006719:Homovanillic Acid / Q000652:urine; D007422:Intestines / Q000201:enzymology*; D007583:Jejunum / Q000201:enzymology / Q000378:metabolism; D007668:Kidney / Q000201:enzymology*; D007980:Levodopa / Q000378:metabolism; D008297:Male; D008995:Monoamine Oxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012982:Sodium, Dietary / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D014883:Water-Electrolyte Imbalance / Q000378:metabolism; D005723:gamma-Glutamyltransferase / Q000378:metabolism
chemical_list: D004573:Electrolytes; D012982:Sodium, Dietary; D015102:3,4-Dihydroxyphenylacetic Acid; D007980:Levodopa; D008995:Monoamine Oxidase; D002394:Catechol O-Methyltransferase; D005723:gamma-Glutamyltransferase; D000469:Alkaline Phosphatase; D001142:Aromatic-L-Amino-Acid Decarboxylases; D000254:Sodium-Potassium-Exchanging ATPase; C001746:3-methoxytyramine; D004298:Dopamine; D006719:Homovanillic Acid