STRUCTURE OF HUMAN RENIN AND EXPRESSION OF THE RENIN GENE

The amino acid sequence of human renin was identified for the first time. This was determined from the nucleotide sequence of exons in the human renin gene identified in a genomic library by recombinant DNA techniques. Examination of amino acid residues involved in the enzymatic hydrolysis by human renin of the unique Leu10-Val11 bond of human angiotensinogen revealed features peculiar to this highly specialized aspartyl protease. The expression of the renin gene was examined with a hybridization probe for renin mRNA in sections and extracts of tissues. In the submandibular gland of mice renin mRNA, like renin, increased during development and in response to testosterone in females; sodium depletion increased renin mRNA in kidney.     

RENIN SECRETION AND RENAL VASCULAR RESISTANCE FOLLOWING PROLONGED ADMINISTRATION OF DESOXYCORTICOSTERONE (DOC) IN RATS DRINKING NORMAL SALINE

1. The effect of long-term administration of desoxycorticosterone (DOC)-saline on arterial blood pressure, renal vascular resistance and renin secretion rate was studied in the rat. 2. Renin secretion rate and peripheral plasma renin activity was markedly reduced in the DOC-saline treated rats. Renal vascular resistance was comparable to that found in a corresponding control group. Responsiveness to isoprenaline suggested that the β-adrenoceptor mediating renin release was grossly intact. 3. A significant rise in blood pressure occurred in only 50% of the treated animals: However, no differences in weight gain, renal vascular resistance or renin levels were apparent when compared with animals which remained normotensive. 4. These findings indicate that suppression of renin secretion during prolonged DOC-saline administration cannot be directly attributed to changes in arterial pressure, renal vascular resistance or β-adrenoceptor sensitivity.     

USE OF SYNTHETIC OLIGONUCLEOTIDE AND RECOMBINANT DNA PROBES TO STUDY RENIN GENE EXPRESSION

Using hybridization histochemistry renin gene expression has been localized in the juxtaglomerular apparatus (JGA) of the renal cortex in both mouse and sheep kidney. This technique also located renin gene expression in afferent arterioles and interlobular arteries distant from the glomerular tuft in lamb renal cortex. A short (30 mer) synthetic oligonucleotide probe, complementary to a region of the mouse submaxillary gland renin gene, specifically labelled mouse submaxillary gland and kidney. Hybridization histochemistry and Northern blot analysis using both the synthetic oligonucleotide (mouse) probe and a 700 base pair recombinant (sheep) probe showed differences in renin gene expression in the kidney in response to Na restriction in the mouse and Na depletion in the sheep.     

数种因子对人胎肺细胞分泌t─PA的影响

原代人胎肺细胞培养２０ｄ后，更换１％ＢＳ培养基，细胞生长停止，ｔ－ＰＡ分泌量低；在１％ＢＳ培养基中使Ｃａ２＋浓度增加到３．５ｍｍｏｌ／Ｌ，ＬＨ浓度增加到１％，细胞表现较高ｔ－ＰＡ分泌活性，与１％ＢＳ组差异显著。以此配方为基础培养基，再分别补充以下因子：５μｇ／ｍｌ转铁蛋白，５ｍｇ／ｍｌ白蛋白，２．５ｍｇ／ｍｌ葡萄糖，１ｍｇ／ｍｌ甘露糖，１μｇ／ｍｌ氢化可的松，２Ｕ／ｍｌ胰岛素，２ｍｍｏｌ／Ｌ谷氨酰胺，２０ｎｍｏｌ／Ｌ亚硒酸钠。除谷氨酰胺和甘露糖外，其他因子均显著提高肺细胞的ｔ－ＰＡ分泌活性（Ｐ＜０．０５）     

苦参碱对纤维蛋白纤维蛋白原降解产物诱导血管细胞损伤、增殖及腹腔巨噬细胞释放IL-1的影响

目的：研究苦参碱（Ｍａｔ）对纤维蛋白纤维蛋白原降解产物（ＦＦＤＰ）作用的影响。方法：大鼠主动脉内皮细胞损伤以乳酸脱氢酶释放测定;大鼠主动脉平滑肌细胞增殖采用结晶紫染色法测定;白细胞介素１活性采用小鼠胸腺细胞增殖法测定。结果：ＦＦＤＰ能促进大鼠主动脉内皮细胞释放乳酸脱氢酶,诱导大鼠主动脉平滑肌细胞增殖,并促使小鼠腹腔巨噬细胞分泌ＩＬ１增加。结论：Ｍａｔ可抑制ＦＦＤＰ的作用。对动脉粥样硬化的防治可能有一定意义。     

EFFECT OF TRANSFORMING GROWTH FACTOR-β1 ON PLATELET-DERIVED GROWTH FACTOR RECEPTOR BINDING AND GENE EXPRESSION IN VASCULAR SMOOTH MUSCLE CELLS FROM SHR AND WKY RATS

1. This study examined the effects of transforming growth factor-βl (TGF-β1) on platelet-derived growth factor-BB (PDGF-BB)-stimulated DNA synthesis, [¹²⁵I]-PDGF-BB receptor binding and PDGF-β receptor mRNA expression in vascular smooth muscle cells (VSMC) isolated from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 2. TGF-β1 inhibited by 40% DNA synthesis stimulated by PDGF-BB in VSMC from WKY rats but potentiated by 20% growth factor-stimulated DNA synthesis in VSMC from the SHR. 3. Since the difference in effect of TGF-β1 could not be attributed to differential regulation of [¹²⁵I]-PDGF-BB binding activity and PDGF-β receptor mRNA expression, it is suggested that alterations in intracellular signalling pathways may account for the differential effects of TGF-β1 on PDGF-BB-stimulated DNA synthesis in VSMC from SHR and WKY rats.