Calapai G, Parente L, Nava F, Facciolà G, Marciano M C, Caputi A P
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
Life Sci. 1997;60(7):457-64. doi: 10.1016/s0024-3205(96)00675-3.
Interleukin-1 beta (IL-1 beta) causes inhibition of drinking behaviour. Moreover it induces formation of prostaglandins (PGs) and nitric oxide (NO). Both PGs and NO are able to inhibit drinking stimulated by water deprivation or by intracerebroventricular (i.c.v.) administration of angiotensin II. In this study, we studied in the preoptic area (POA) the possible role of PGs and NO in the antidipsogenic action induced by IL-1 beta. IL-1 beta was injected in the lateral cerebral ventricle (i.c.v.) (2.5, 10, 20, and 40 ng/rat) or into POA (0.625, 1.25, 2.5, and 10 ng/rat). L-arginine (12.5, 25, 50, and 100 ng/rat), the precursor of NO, or NG-nitro-L-arginine methyl ester (L-NAME) (25, 50, and 100 ng/rat), an inhibitor of nitric oxide synthase (NOS), were injected only into POA. Drinking behaviour was induced by water deprivation (24 h). IL-1 beta injected either i.c.v. or into POA caused dose dependent inhibition of drinking. In the POA a treatment with acetylsalicylic acid (ASA) (33, 66, and 135 micrograms/rat), but not with L-NAME, antagonized the inhibition of drinking behaviour induced by the highest doses of IL-1 beta in the POA. In the POA, a treatment with ASA or L-NAME antagonized the inhibition of drinking behaviour caused by injection of the highest doses of L-arginine. Our data suggest that the central inhibition of drinking behaviour of IL-1 beta is mediated through the formation of PGs, but not NO, in the POA.
白细胞介素 -1β（IL -1β）可抑制饮水行为。此外，它还能诱导前列腺素（PGs）和一氧化氮（NO）的形成。PGs和NO都能够抑制因缺水或脑室内（i.c.v.）注射血管紧张素II所刺激的饮水。在本研究中，我们在视前区（POA）研究了PGs和NO在IL -1β诱导的抗饮水作用中可能发挥的作用。将IL -1β注射到侧脑室（i.c.v.）（2.5、10、20和40 ng/大鼠）或注射到POA（0.625、1.25、2.5和10 ng/大鼠）。仅将NO的前体L -精氨酸（12.5、25、50和100 ng/大鼠）或一氧化氮合酶（NOS）抑制剂NG -硝基 -L -精氨酸甲酯（L - NAME）（25、50和100 ng/大鼠）注射到POA。通过缺水（24小时）诱导饮水行为。无论是经i.c.v.还是注射到POA中的IL -1β均引起剂量依赖性的饮水抑制。在POA中，用乙酰水杨酸（ASA）（33、66和135微克/大鼠）而非L - NAME进行处理，可拮抗POA中最高剂量IL -1β诱导的饮水行为抑制。在POA中，用ASA或L - NAME进行处理可拮抗注射最高剂量L -精氨酸所引起的饮水行为抑制。我们的数据表明，IL -1β对饮水行为的中枢抑制是通过POA中PGs的形成介导的，而非NO。
