title: Salt intake and intestinal dopaminergic activity in adult and old Fischer 344 rats.
abstract: We have earlier shown that the renal dopaminergic system failed to respond to high salt (HS) intake in old (24-month-old) Fisher 344 rats (Hypertension 1999;34:666-672). In the present study, intestinal Na+,K+-ATPase activity and intestinal dopaminergic tonus were evaluated in adult and old Fischer 344 rats during normal salt (NS) and HS intake. Basal intestinal Na+,K+-ATPase activity (nmol Pi/mg protein/min) in adult rats (142+/-6) was higher than in old Fischer 344 rats (105+/-7). HS intake reduced intestinal Na+,K+-ATPase activity by 20% (P<0.05) in adult, but not in old rats. Dopamine (1 microM) failed to inhibit intestinal Na+,K+-ATPase activity in both adult and old Fischer 344 rats (NS and HS diets). In adult animals, co-incubation of pertussis toxin with dopamine (1 microM) produced a significant inhibitory effect in the intestinal Na+,K+-ATPase activity. L-DOPA and dopamine tissue levels in the intestinal mucosa of adult rats were higher (45+/-9 and 38+/-4 pmol/g) than those in old rats (27+/-9 and 14+/-1 pmol/g). HS diet did not change L-DOPA and DA levels in both adult and old rats. DA/L-DOPA tissue ratios, an indirect measure of dopamine synthesis, were higher in old (1.1+/-0.2) than in adult rats (0.6+/-0.1). Aromatic L-amino acid decarboxylase (AADC) activity in the intestinal mucosa of old rats was higher than in adult rats. HS diet increased the AADC activity in adult rats, but not in old rats. It is concluded that intestinal dopaminergic tonus in old Fisher 344 rats is higher than in adult rats and is accompanied by lower basal intestinal Na+,K+-ATPase activity. In old rats, HS diet failed to alter the intestinal dopaminergic tonus or Na+,K+-ATPase activity, whereas in adult rats increases in AADC activity were accompanied by decreases in Na+,K+-ATPase activity. The association between salt intake, increased dopamine formation and inhibition of Na+,K+-ATPase at the intestinal level was not as straightforward as that described in renal tissues.
authors.affiliation: Institute of Pharmacology and Therapeutics, Faculty of Medicine, Porto, Portugal.
authors.forename: M A
authors.initials: MA
authors.lastname: Vieira-Coelho
authors.forename: P
authors.initials: P
authors.lastname: Serrão
authors.forename: T
authors.initials: T
authors.lastname: Hussain
authors.forename: M F
authors.initials: MF
authors.lastname: Lokhandwala
authors.forename: P
authors.initials: P
authors.lastname: Soares-da-Silva
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D001142:Aromatic-L-Amino-Acid Decarboxylases / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D007583:Jejunum / Q000201:enzymology / Q000378:metabolism*; D007980:Levodopa / Q000378:metabolism; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D012965:Sodium Chloride / Q000008:administration & dosage*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D012965:Sodium Chloride; D007980:Levodopa; D001142:Aromatic-L-Amino-Acid Decarboxylases; D000254:Sodium-Potassium-Exchanging ATPase; D004298:Dopamine