Goldstein D J, Marante Perez D J, Gunst J P, Halperin J A
Pharmacol Biochem Behav. 1979 Jun;10(6):895-8. doi: 10.1016/0091-3057(79)90064-9.
Intraperitoneally injected PGE1 (100 micrograms/Kg) inhibits specifically the drinking induced by both IP and IV 2 M NaCl (6 ml/Kg) and compound 48/80 (100 micrograms/Kg, IP). Probenecid (150 mg/Kg, IP) which is not a dipsogen, has no effect on the PGE1 induced inhibition of acute cell dehydration thirst. It is concluded the PGE1 acts upon the peripheral mast cells, inhibiting their secretion and thus affecting the water intake associated with the activation of these cells either by hypertonicity or specific stimulants of amine release. These results raise the possibility that endogenous prostaglandins might be involved in the modulation of some of the signals which convey to the brain information on the tonicity of the body fluids.
腹腔注射前列腺素E1（100微克/千克）可特异性抑制腹腔注射和静脉注射2M氯化钠（6毫升/千克）以及化合物48/80（100微克/千克，腹腔注射）所诱导的饮水行为。丙磺舒（150毫克/千克，腹腔注射）不是一种致渴剂，对前列腺素E1诱导的急性细胞脱水性口渴抑制作用没有影响。得出的结论是，前列腺素E1作用于外周肥大细胞，抑制其分泌，从而影响与这些细胞因高渗或胺释放的特异性刺激而激活相关的水摄入。这些结果增加了内源性前列腺素可能参与调节向大脑传递有关体液张力信息的某些信号的可能性。
