PubMed · 13199338
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B E MILES, A PATON, H E DE WARDENER. 1954-10-16. Maximum urine concentration.. https://doi.org/10.1136/bmj.2.4893.901
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Recent evidence supports the viewpoint that vasopressin, a neurohypophyseal peptide, should be also considered as a neuroendocrine modulator of immune and inflammatory responses. In this work we investigated the role of vasopressin in the regulation of prostaglandin E(2) synthesis by human dermal fibroblasts. Recombinant human interleukin-1 beta increased prostaglandin E(2) synthesis in fibroblasts about sixfold. The prostaglandin E(2) response to interleukin-1 beta was attenuated by lower concentrations of vasopressin (10(-10)-10(-9) M). By contrast, higher concentrations (10(-8)-10(-7) M) of vasopressin effected significant enhancement of the interleukin-1 beta-induced prostaglandin E(2) synthesis. In a similar way, vasopressin (10(-8)-10(-7) M), in the absence of interleukin-1, significantly increased prostaglandin E(2) production. An inhibitory effect of lower concentrations of vasopressin was also observed on basal production of prostaglandin E(2). The effects of vasopressin on basal and interleukin-1 beta-induced prostaglandin E(2) synthesis were antagonized by selective vasopressin receptor antagonists. The findings presented here disclose a novel modulatory role of vasopressin on prostaglandin E(2) synthesis in human dermal fibroblasts and suggest a possible role of vasopressin in the regulation of inflammation.
Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is caused by postnatal arginine vasopressin (AVP) deficiency resulting from mutations in the AVP gene encoding the AVP pre-prohormone. To advance the understanding of adFNDI further, we have searched for mutations in the AVP gene in 15 unrelated kindreds in which diabetes insipidus appeared to be segregating. In nine kindreds, seven different previously described mutations were identified. In each of the other six kindreds, unique novel mutations were identified. Two of these (225A>G and 227G>A) change a nucleotide in the translation initiation codon of the signal peptide, whereas the other four (1797T>C, 1884G>A, 1907T>G, and 2112C>G) predict amino-acid substitutions in the neurophysin II moiety of the AVP prohormone, namely V67A (NP36), G96D (NP65), C104G (NP73), and C116W (NP85). Among these, the mutation predicting the V67A (NP36) substitution is remarkable. It affects a region of the neurophysin II not affected by any other mutations, produces only a minor change, and its inheritance suggests an incomplete penetrance. Our findings both confirm and further extend the mutation pattern that has emerged in adFNDI, suggesting that the mutations affect amino-acid residues known or reasonably presumed to be important for the proper folding and/or dimerization of the neurophysin II moiety of the AVP prohormone.
Corin is a recently discovered pro-atrial natriuretic peptide (ANP) convertase that is abundantly expressed in the heart. ANP is a cardiac hormone but can be secreted ectopically by certain cancers including small cell lung cancer (SCLC). In this study, we examined the role of corin in ANP production by SCLC cells. Reverse transcription-PCR detected corin mRNA expression in all nine SCLC cell lines examined and ANP mRNA expression in seven of the nine cell lines. In contrast, arginine vasopressin mRNA was detected in only five of the nine SCLC cell lines studied. Corin-expressing SCLC cells were capable of converting recombinant human pro-ANP to biologically active ANP, as determined by Western analysis and a cyclic GMP assay. Transfection of small interfering RNA duplexes directed against the corin gene completely blocked the processing of pro-ANP in the SCLC cells. Our results show that corin functions as a pro-ANP convertase in SCLC cells. We also suggest that the expression of corin may contribute to the pathogenesis of the syndrome of inappropriate secretion of antidiuretic hormone associated with certain cancers.