Increased sympathetic nervous system activity in rat spleen and heart following vitamin A depletion.
The effect of vitamin A depletion on the functional state of the sympathetic nervous system (SNS) was evaluated in rats. Urinary excretion of norepinephrine (NE) and epinephrine (E) significantly increased in the vitamin A-depleted rats. Vitamin A depletion caused a significant increase in NE turnover in heart and spleen, which was determined from the rate of fall in NE content in these tissues after blockade of NE biosynthesis. In rats rendered vitamin A depleted there was a loss in the number of beta-adrenergic receptors in the spleen with a concomitant decrease in the apparent KD for the receptors. These changes in beta-adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor. The effects of quinacrine on such changes indicate that phospholipids may be involved in modulating the changes in the number of receptors and their affinity to the ligand. This study suggests that the SNS in rat spleen and heart are stimulated following vitamin A depletion.
D000818:Animals; D004837:Epinephrine / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D011796:Quinacrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism; D013154:Spleen / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014802:Vitamin A Deficiency / Q000503:physiopathology*
D011943:Receptors, Adrenergic, beta; D011796:Quinacrine; D009638:Norepinephrine; D004837:Epinephrine