[Effect of glucocorticoids and other steroids on arginine vasopressin release from rat hypothalamic slices].

Rat hypothalamic slices sectioned with vibratome (containing paraventricular and supraoptic nuclei) were incubated in static microchamber and the Arginine vasopressin (AVP) released from the slices was measured by radioimmunoassay. The effect of glucocorticoids (GC) and other steroids on AVP release was investigated. The results were as follows: (1) AVP was steadily released at a rate of 9.06 +/- 1.23 pg/min for as long as 6 h (not including the 90 min for recovery of slices). (2) Corticosterone (B) inhibited AVP release within 20 min in a dose-dependent manner from 10(-7) to 10(-4) mol/L. (3) Cortisol, 17 beta-estradiol, or testosterone (10(-6) mol/L) also inhibited AVP release within 20 min, but dexamethasone, aldosterone, progesterone, RU486, or cholesterol had no significant effect. (4) RU486 (10(-5)-10(-3) mol/L) could partially block the rapid inhibitory effect of corticosterone. These results suggested that GC might exert in situ a regulatory negative feedback action on the AVP release from hypothalamus of rat through a non-genomic rather than a genomic mechanism.

[Alteration of plasma amino acid content in primary liver cancer patients].

Twenty-two plasma free amino acid contents from 22 primary liver cancer (PLC) patients were assayed by means of HPLC and compared with those from 16 normal subjects. The results showed that in PLC patients, plasma total amino acid (TAA), branched chain amino acid (BCAA), glycogenic amino acid, glutamine, histidine and arginine were lowered, while plasma aromatic amino acid (AAA) and methionine did not decrease significantly resulting in the BCAA/AAA ratio decline. Comparing 8/22 subclinical and 14/22 clinical liver cancers with healthy controls respectively, it was found that there was a decrease of plasma TAA, glutamine, arginine, histidine, BCAA and BCAA/AAA ratio, and an increase of tyrosine, in subclinical stage of PLC. It suggests that alteration of most amino acids occur in the early stage of PLC and become more obvious in the moderate and late stages. The changes of plasma amino acid contents in PLC were different from those in chronic liver diseases. The alteration of plasma amino acid contents in subclinical stage of PLC suggests that the disturbance of amino acid metabolism be resulted from malignancy. Correction of the amino acid metabolic disturbance in PLC patients may enhance the inhibition of tumor growth and improve the host metabolism and anti-cancer effect.