Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the effect of dietary NaCl loading on renin gene expression in one-gene, two-gene and transgenic mouse strains. By Northern blotting, we found an approximate twofold reduction in renin messenger (m) RNA in the kidneys of high-NaCl-treated compared with low-NaCl-treated animals. Using an RNase-protection assay designed to discriminate between the different renin gene transcripts, we have shown that renin mRNAs derived from the Ren-1C gene of one-gene strains and the Ren-1D and Ren-2 genes of two-gene animals are all NaCl-responsive. Renin mRNA derived from a 19 kilobase Ren-1D transgene is also NaCl-responsive.
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PMID:Modulation of mouse renin gene expression by dietary sodium chloride intake in one-gene, two-gene and transgenic animals. 269 76

Tissue kallikrein gene expression in rat kidney was examined by in situ hybridization histochemistry. A rat tissue kallikrein cDNA probe, 534 bases in length and complementary to the 3' end of kallikrein mRNA was first used in Northern blot analysis to demonstrate the existence of tissue kallikrein mRNA in rat kidney. Then, kallikrein mRNA's localization in rat kidney sections was studied in situ hybridization histochemistry using the same probe. Positive signals were concentrated in the renal cortex at the vascular pole of the glomeruli and to a lesser degree, the distal tubular cells. Prehybridization with the unlabeled probe can abolish the positive signal; the same result can also be achieved by pretreatment of the tissue section with ribonuclease. By using the same technique, tissue kallikrein mRNA was also localized in granular convoluted tubule and striated duct cells of rat submandibular gland. The results suggest a new site of renal kallikrein synthesis at the vascular pole of the glomerulus. These findings, coupled with the previous studies that tissue kallikrein can participate in activation and releasing of renin, raise a potential physiological role of kallikrein in renin release or prorenin processing at juxtaglomerular cells.
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PMID:Renal kallikrein mRNA localization by in situ hybridization. 277 Jan 12

Expression of the renin gene in several rat organs is demonstrated by the detection of renin mRNA using a ribonuclease-protection technique. In two of these sites, the brain and the liver, renin mRNA levels are unaffected by changes in dietary salt which markedly affect renal renin mRNA levels. The findings provide the basis for an important ubiquitous local regulatory role for the renin-angiotensin system extending beyond the circulation.
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PMID:Expression of the renin gene in extra-renal tissues of the rat. 305 27

The promoter region of the renin gene in man, mouse and rat contains several putative transcription start sites, which in mouse have been shown to be tissue specific and differently regulated. To investigate which of these start sites are used during stimulation of renin gene transcription by the major physiological control factors, we determined the transcription start sites of rat renin in the kidney and adrenal glands by RNase protection using a cRNA probe spanning 387 bases upstream and 121 bases downstream from the canonical transcription initiation site. To stimulate renin gene expression, we used renal artery stenosis, angiotensin II antagonists, furosemide and isoprenaline infusions and low sodium diet. Our results suggest that only one TATA box is functional in rat kidney and adrenal.
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PMID:Rat renin gene transcription is initiated at a single start site. 755 59

This study aimed to investigate the inter-relation between the angiotensin II (ANG II) AT1 receptor and renin gene expression in rat kidneys. To this end, renin mRNA levels and mRNA levels for AT1a and AT1b were assayed by RNase protection in the kidneys of normal rats, in animals treated with the AT1 antagonist losartan and in rats bearing 0.2-mm left renal artery clips for 2 days. In normal rats, we found a negative correlation between renin mRNA levels and AT1a receptor mRNA levels. Losartan led to a fourfold increase in renin mRNA levels without changing AT1 receptor mRNA levels. Unilateral renal artery clipping increased renin mRNA levels fourfold in the clipped kidney and suppressed renin mRNA levels in the contralateral kidneys. AT1 receptor mRNA levels were not changed in the contralateral intact kidneys, but were significantly decreased by 15-25% in the clipped kidneys. Renin mRNA levels were inversely correlated to AT1a mRNA levels in the clipped, but not in the contralateral, kidneys. Our findings suggest that the systemic activity of the renin angiotensin system has no regulatory influence on renal AT1 receptor gene expression. Renin mRNA levels in normal and in clipped kidneys appear to be negatively determined by the level of AT1a receptor gene expression. Thus modulation of AT1a receptor gene expression could be a pathway for indirect modulation of renin gene expression by ANG II. This conclusion is in agreement with the observation that AT1 receptor antagonists are powerful stimulators of the renin system.
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PMID:Renin gene and angiotensin II AT1 receptor gene expression in the kidneys of normal and of two-kidney/one-clip rats. 767 36

This study was done to investigate the mechanisms that underly the changes of renal renin gene expression upon hypoperfusion of one kidney. To this end the left renal arteries of male Sprague-Dawley rats were clipped with 0.2 mm silver clips and renal renin mRNA levels were assayed by RNase protection during the first ten days after clipping. Unilateral reduction of renal blood flow led to transient maximal fivefold increases of renin mRNA levels in the clipped kidneys and to sustained suppression of renin gene expression to 20% of the control value in the contralateral intact kidneys. Inhibition of prostaglandin (PG) formation by meclofenamate or EDRF synthesis by L-NAME markedly attenuated the increase of renin mRNA levels in response to clipping, and a combination of PG/EDRF inhibition almost abolished the increase of renin mRNA levels. Inhibition of PG/EDRF formation did not change the suppression of renin mRNA levels in the contralateral intact kidneys. Neither did renal denervation nor inhibition of macula densa function by furosemide prevent the suppression of renin gene expression in response to unilateral renal artery clipping. Only converting enzyme inhibition by ramipril and blockade of Ang II-AT1 receptors by losartan attenuated the decrease of renin mRNA levels in the contralaterals to clipped kidneys. These findings suggest that intact PG and EDRF synthesis represent stimulatory signals for renin gene expression that are required for the elevation of renin mRNA levels upon unilateral renal hypoperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Control of renin gene expression in 2 kidney-1 clip rats. 770

We have recently found that vascular natriuretic peptide (NP)-A receptor mRNA is upregulated in genetically hypertensive (SHR-SP/Izm) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In the present study, we examined the effects of antihypertensive treatments on aortic NP-A receptor mRNA expression in these hypertensive rats using ribonuclease protection assay. Oral administration of an angiotensin converting enzyme inhibitor, derapril, but not a calcium channel blocker, manidipine, produced a significant decrease of the NP-A receptor mRNA level after 4 weeks, while both antihypertensive agents showed similar hypotensive effects. Plasma renin was high in SHR-SP/Izm and low in DOCA-salt rats. These results suggest that the vascular renin-angiotensin system rather than the blood pressure has an important role in the regulation of the vascular NP-A receptor.
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PMID:Angiotensin converting enzyme inhibitor but not calcium blocker down-regulates gene expression of vascular natriuretic peptide receptor in hypertensive rats. 781 Dec 41

Extrahepatic synthesis and localization of angiotensinogen (ATN) have been described in animals, thus establishing the tissue renin-angiotensin (RA) system. However, there had been no reports of tissue RA systems in human organs, including the heart. In earlier, we have reported the possibility of ATN synthesis in the human heart using ribonuclease protection assay system. ATN mRNA was detected not only in the liver, but also in both the atrial and ventricular heart tissues, suggesting that ATN is synthesized in the human heart. In this report, we looked for the distribution of ATN in diseased human heart. Northern blot hybridization of cDNA with total RNA extracted from human liver, brain, kidney, atrial and ventricular tissues revealed that ATN mRNA exists in cardiac ventricule. Immunohistochemical studies using a specific antibody to ATN revealed a stronger reaction in the endocardial layer of the human left ventricle, than in the epicardial layer, and intense immunoreactivity in the conduction system and right atrium. This distribution pattern was similar to that of human atrial natriuretic peptide (hANP), which functions a smooth muscle relaxant. Double immunostaining of ATN and hANP demonstrated that all myocytes in the right atrium had immunopositive reactions to ATN, hANP or both of ATN and hANP. Double immunoelectron staining enabled us to show more detailed localization of ATN and hANP; hANP only existed in the specific granules and ATN existed in the myofibril, but not in the granule. Furthermore, our experiments provide evidence of ATN in healthy human hearts and also reveal a widespread immunopositive reaction for ATN in the left ventricle of diseased hearts.
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PMID:Distribution of angiotensinogen in diseased human hearts. 807 4

To examine the regulation of angiotensin receptors in vascular smooth muscle cells, we studied the effects of antihypertensive drugs on angiotensin type 1A (AT1A) receptor gene expression in aortic smooth muscle cells (ASMCs) from spontaneously hypertensive rats (SHRs) using both ribonuclease protection assay and reverse-transcription polymerase chain reaction. An increase in AT1A receptor gene expression in ASMCs of SHRs was induced by treatment with an angiotensin converting enzyme inhibitor (enalapril) for 2 weeks and 4 weeks, but not by other types of antihypertensive drugs such as alpha-blocker (doxazosin), alpha, beta-blocker (arotinolol), Ca antagonist (nicardipine) or vascular smooth muscle relaxant (hydralazine). Since all antihypertensive drugs lowered the blood pressure of the rats almost equally, our results suggest that AT1A receptor gene expression in ASMCs of SHRs may be regulated by the vascular renin-angiotensin system.
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PMID:Angiotensin-converting enzyme inhibitor increases angiotensin type 1A receptor gene expression in aortic smooth muscle cells of spontaneously hypertensive rats. 815 34

The catalytic reaction of renin, an aspartyl proteinase, with angiotensinogen is the rate-limiting step fo the renin-angiotensin system involved in the maintenance of blood pressure and electrolyte balance in mammals. We have characterized species-specific expression of the hepatic renin gene by RNase protection experiment, primer extension analysis, and promoter assay using an in vitro DNA transfection. RNase protection experiments revealed that the renin gene is expressed in rat liver, but neither in mouse nor in human. Primer extension analysis identified the putative promoter region of the rat renin gene, which contains TATAAAA sequence, a canonical regulatory DNA element. In order to test whether the upstream region of the renin gene with respect to the putative transcription initiation site is a functional promoter, we have examined the ability of the 5'-flanking sequences of the rat renin gene as well as the human and mouse genes to activate expression of a reporter gene containing the bacterial chloramphenicol acetyltransferase (CAT)-coding sequences, by transient transfection assays. In transfected HepG2 cells, a hepatoma cell line, only the rat renin promoter was capable of driving the CAT gene expression. These results suggested that the rat-specific renin gene expression in the liver could be primarily determined by its promoter specificity.
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PMID:Species-specific expression of the hepatic renin gene. 820 34


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