INTERACTION BETWEEN EPIDERMAL GROWTH FACTOR AND ARGININE VASOPRESSIN IN RENAL MEDULLARY MEMBRANES

1. Epidermal growth factor is a potent mitogen that causes natriuresis, diuresis and inhibition of arginine vasopressin-induced water reabsorption. 2. The aim of this study was to determine any interaction between epidermal growth factor and the V1 (vascular) and/or V2 (antidiuretic) arginine vasopressin receptor subtypes. 3. Radioligand binding displacement assays demonstrated that although arginine vasopressin related peptides displaced both radioligands from renal medullary membranes at low concentrations epidermal growth factor displaced neither. 4. Arginine vasopressin V2 receptor second messenger cyclic adenosine monophosphate (CAMP) production was inhibited by epidermal growth factor (IC₅₀ 2 ± 10^?7 mol/L) as was sodium fluoride cAMP production but only at much higher concentrations. 5. Therefore the diuretic effect of epidermal growth factor is not via direct antagonism of arginine vasopressin receptors but seems mediated via inhibition of the V2 second messenger system.     

The Recognition of Hypothalamo-Neurohypophysial Functions by Developing T Cells

Neuropeptide signals and specific neuropeptide receptors have been described in the thymus supporting the concept of a close dialogue between the neuroendocrine and the immune systems at the level of early T-cell differentiation. In this paper, we review recent data about neurohypophysial (NHP)-related peptides detected in the thymus from different species. We suggest that we are dealing in fact with other member(s) of the NHP hormone family, which seems to exert its activity locally through a novel model of cell-to-cell signaling, that of cryptocrine communication. This model involves exchange of signals between thymic epithelial cells and developing thymocytes. The NHP-related peptides have been shown to trigger thymocyte proliferation and could induce immune tolerance of this highly conserved neuroendocrine family.     

偏头痛和慢性紧张型头痛血浆精氨酸加压素、催产素及环核着酸含量测定

用放射免疫分析法测定了２８例偏头痛、１０例慢性紧张型头痛患者和１６例健康对照组血浆精氨酸加压素（ＡＶＰ）、催产素（ＯＴ）、环磷酸腺苷（ｃＡＭＰ）及环磷酸鸟苷（ｃＧＭＰ）含量。结果表明，偏头痛发作期ＡＶＰ含量下降、ｃＡＭＰ含量升高，偏头痛间歇期ｃＧＭＰ含量下降，血浆ＯＴ含量在发作期和间歇期均明显下降。慢性紧张型头痛患者血浆ＡＶＰ、ＯＴ、ｃＡＭＰ和ｃＧＭＰ与对照组比较均无显著性差异。结果提示，血浆ＡＶＰ和ＯＴ水平降低以及环核苷酸的代谢异常与偏头痛发病机制有关。     

中枢和外周脑钠素(BNP)调节醛固酮分泌的不同作用

将BNP和AT-Ⅱ、ACTH AVP单独或BNP与这3种肽分别合并在大鼠icv或iv注入后观察血Ald浓度的变化。实验结果表明:①iv给予AVP(5μg/3ml·h~(-1))、ACTH(5μg/3ml·h~(-1))和AT-Ⅱ(5 v.g/3 ml·h(-1)),1h后均能增加血Ald的浓度。iv给予BNP(5μg/3ml·h(-1))能明显抑制AVP和ACTH的刺激作用,而不影响AT-Ⅱ的刺激作用。②icv给予BNP(2 Vg/10 pl NS)能降低血Aid浓度。icv给予AVP(2μg/10μl NS)能增加血Aid浓度,但ACTH(2μg/10μl NS)和AT-Ⅱ(2μg/10μl NS)无此种作用。但如脑室同时给予BNP(2μg/10μlNS)却可明显刺激Aid分泌。③icv注入BNP对外周注入的3种多肽的刺激作用无任何影响。从上述的实验结果可看出:脑内BNP可“反常”地增加AT-Ⅱ、ACTH和AVP对Ald分泌的刺激作用,与外周抑制AVP,ACTH的刺激作用不同。而脑内BNP不影响这3种多肽的外周刺激作用。结论是脑内BNP以其独特的方式调节Ald的分泌,控制水盐代谢。     

左旋硝基精氨酸诱导高血压大鼠心肌肥大

一氧化氮合酶（ＮＯＳ）抑制剂Ｎ－左旋硝基精氨酸（Ｎ－ＬＮＡ）诱导持续性高血压大鼠１２只，随机分成２组测右颈动脉压，ＮＯ代谢物亚硝酸盐（ＮＯ２）浓度，心肌组织胶原蛋白含量及丝裂活化蛋白激酶（ＭＡＰＫ）活性，观察左心室心肌病理变化，发现与高血压比较，自然归组大鼠动脉血完全逆转（Ｐ〈０．０１）；ＮＯ２水平及ＭＡＰＫ活性轻度逆转，但均未达到正常对照组水平（Ｐ〈０．０１），胶原蛋白含量，心脏及左心室相对重量     

健康人加压素释放和渴感的渗透压阈值

报道１２名受试者在静滴５％ＮａＣｌ２ｈ（每分钟０．０６ｍｌ／ｋｇ）的过程中血钠、血渗、血浆精氨酸加压素（ＡＶＰ）浓度和渴感等级的变化。结果显示，血浆ＡＶＰ浓度及渴感等级分别与血渗呈线性相关，回归方程分别为：血浆ＡＶＰ浓度（ｐＡＶＰ）－０．２４［血浆渗透压（ｐＯｓｍ）－２７４］（ｒ＝０．７２，Ｐ＜０．００１）；渴感等级（Ｔｈ）＝０．２３（ｐＯｓｍ－２７９）（ｒ＝０．６２，Ｐ＜０．００１）．两者灵敏度及阈值均较国外文献报道的结果低，认为加压素释放及渴感的渗透压阈值可能与遗传因素及生活习俗有关，ＡＶＰ分泌及渴感的渗透压调节可能存在种族差异。     

NIFEDIPINE BLOCKS ACTH AND CORTISOL RELEASE IN MAN

1. The present study investigated the effect of prior administration of nifedipine on AVP-induced ACTH release in seven normal volunteers. Three protocols were used: 20 mg oral nifedipine; 0.14 pressor units intramuscular (i.m.) per kg bodyweight aqueous AVP; oral nifedipine plus i.m. AVP 90 min later. Plasma ACTH and cortisol were measured at intervals for 2.5 h during each test. 2. The mean peak plasma ACTH and cortisol levels and the mean peak changes from basal in these levels were significantly lower in the nifedipine/AVP test than in the AVP alone test. The integrated area under the cortisol time curve was significantly lower for the nifedipine/AVP test than that for the AVP test alone. Nifedipine alone caused no changes in ACTH or cortisol. 3. Acute administration of oral nifedipine caused an inhibition of AVP-stimulated ACTH and cortisol release in normal humans. This effect may be due to blockade of plasma membrane calcium channels normally activated during AVP stimulation of pituitary corticotrophs.     

Raised intracranial pressure,the syndrome of inappropriate antidiuretic hormone secretion,and arginine vasopressin in tuberculous meningitis

Intracranial pressure (ICP) monitored shortly after admission over a period of 1 h in 31 children with tuberculous meningitis (TBM) was significantly higher (median 22.5 mm Hg, range 8.4–50.9 mmHg) in 19 children with laboratory evidence of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) than in 12 children without such evidence (median 16.2 mmHg, range 5.8–42.5 mmHg; P = 0.027). Neither plasma nor cerebrospinal fluid arginine vasopressin (AVP) was related to ICP (r = 0.33 and 0.13 respectively). Mean arterial pressure (MAP) was measured in 23 children and a moderate correlation was found with plasma AVP (r = 0.62; P = 0.0019). In TBM, plasma AVP may be secreted as a response to raised ICP in an effort to raise MAP and maintain cerebral perfusion pressure. In this setting excess fluid may be inappropriately retained, leading to hyponatremia and hypo-osmolemia.     

Effects of arginine, S-adenosylmethionine and polyamines on nerve regeneration

Introduction - Axon growth and axon regeneration are complex processes requiring an adequate supply of certain metabolic precursors and nutrients. Material and methods - This article reviews the studies examining some of the processes of protein modification fundamental to both nerve regeneration and to the continuous and adequate supply of specific factors such as arginine, S-adenosylmethionine and polyamines. Results - The process of arginylation notably increases following nerve injury and during subsequent regeneration of the nerve, with the most likelyfunction of arginine-modification of nerve proteins being the degradation of proteins damaged through injury. It appears that defective methyl group metabolism may be one of the leading causes of demyelination, as suggested by the observation of reduced cerebrospinal fluid concentrations of s-adenosylmethionine (SAMe) and 5-methyltetrahydrofolate, the key metabolites in methylation processes, in patients with a reduction in myelination of corticospinal tracts. Polyamine synthesis, which depends strongly on the availability of both SAMe and arginine, markedly increases in neurons soon after an injury. This "polyamine-response" has been found to be essential for the survival ofthe parent neurons after injury to their axons. Polyamines probably exert their effects through involvement in DNA, RNA and protein synthesis, or through post-translational modifications that areindicated as the most relevant events of the "axon reaction." Conclusions - Nerve regeneration requires the presence of arginine, s-adenosylmethionine, and polyamines. Further studies are needed to explore the mechanisms involved in these processes.