INTESTINAL DOPAMINERGIC ACTIVITY IN OBESE AND LEAN ZUCKER RATS: RESPONSE TO HIGH SALT INTAKE

Abstract

The present study examined intestinal dopaminergic activity and its response to high salt (HS, 1% NaCl over a period of 24 hours) intake in obese (OZR) and lean Zucker rats (LZR). The basal Na⁺,K⁺-ATPase activity (nmol Pi/mg protein/min) in the jejunum of OZR was higher than in LZR on normal salt (NS) (OZR-NS=111.3±6.0 vs. LZR-NS=88.0±8.3). With the increase in salt intake, the basal Na⁺,K⁺-ATPase activity significantly increased in both animals (OZR-HS=145.9±11.8; LZR-HS=108.8±6.7). SKF 38393 (10 nM), a specific D₁-like dopamine receptor agonist, inhibited the jejunal Na⁺,K⁺-ATPase activity in OZR on HS intake, but failed to inhibit enzyme activity in OZR on NS intake and LZR on NS and HS intakes. The aromatic L-amino acid decarboxylase (AADC) activity in OZR was lower than in LZR on NS intake. The HS intake increased AADC activity in OZR, but not in LZR. During the NS intake the jejunal monoamine oxidase (MAO) activity in OZR was similar to that in LZR. The HS intake significantly decreased MAO activity in both OZR and LZR. The jejunal COMT activity in OZR was higher than in LZR on NS intake. The HS intake reduced COMT activity in OZR but not LZR. It is concluded that inhibition of jejunal Na⁺,K⁺-ATPase activity through D₁ dopamine receptors is dependent on salt intake in OZR, whereas in LZR, the enzyme failed to respond to the activation of D₁ dopamine receptors irrespective of their salt intake.

• Sodium
• Dopamine
• Intestine
• Na⁺, K⁺-ATPase