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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of angiotensinogen messenger RNA (mRNA) was assessed in total RNA extracted from hepatoma, glioma, neuroblastoma, and glioma-neuroblastoma hybrid cell lines. Total RNA from 1 X 10(7) cells was extracted, transferred to a membrane, and hybridized with a 32P-labeled, full-length (1650-base pair) rat angiotensinogen complementary DNA (cDNA). Angiotensinogen RNA sequences could be definitively detected only in hepatoma cells. Steroids were used in an attempt to increase the angiotensinogen mRNA level. Dexamethasone (2 X 10(-6) M) or 17 beta-estradiol (1 X 10(-7) M) was added to the cultures 18 to 24 hours prior to harvest. Dexamethasone treatment of the hepatoma cells resulted in a large increase in angiotensinogen mRNA, whereas estradiol had no effect. Steroids failed to induce detectable levels of angiotensinogen mRNA in total RNA from the other cell lines. That the RNA was intact was ensured by hybridizing duplicate Northern blots to a 32P-labeled actin cDNA. Actin mRNA sequences were detected in all cell lines. Blot hybridization of poly(A)+RNA resulted in the visualization of a weak angiotensinogen mRNA signal for a glioma cell line and a glioma-neuroblastoma hybrid line. However, the ability to detect angiotensinogen mRNA in a cell may depend on the phenotype expressed, which can be governed by culture conditions.
Hypertension 1987 Jun
PMID:Presence of angiotensinogen messenger RNA in various cultured cell lines. 359 87

Angiotensinogen (renin substrate) and its messenger RNA are known to accumulate in the rat brain. We have cloned rat preangiotensinogen cDNAs and used them as probes to measure the accumulation of preangiotensinogen messenger RNA sequences in eight regions of rat brain, as well as in liver and kidney. The brain regions examined were the cerebral cortex, hippocampus, striatum, cerebellum, diencephalon (including basal forebrain structures), midbrain, brainstem, and pituitary. On a tissue weight basis, the accumulation of preangiotensinogen RNA sequences was greatest in the liver, midbrain, and brainstem. The relative concentrations of messenger RNA were ranked as follows: liver, brainstem, midbrain greater than cerebellum, diencephalon greater than hippocampus greater than cortex, striatum, kidney greater than pituitary. Relative RNA concentrations from liver to kidney varied over a 16-fold range. Liver and brain preangiotensinogen RNA sequences were indistinguishable in size as measured by gel electrophoresis; however, the kidney sequences appeared some 100 nucleotides larger. Our data agree with previous measurements of angiotensinogen in the rat brain as assayed by renin-catalyzed angiotensin I release.
Hypertension 1986 Jun
PMID:Localization of preangiotensinogen messenger RNA sequences in the rat brain. 371 May 60

The renal renin-angiotensin system plays an important role in the control of renal hemodynamics and in the etiology of some types of hypertension. Angiotensinogen is the prohormone for angiotensins I and II. In the present communication, we report for the first time the presence of mRNA coding for angiotensinogen in the kidney. Indeed, the intrarenal location appears to be predominantly in the renal medulla. Additionally, an investigation of the effect of uninephrectomy on the intrarenal angiotensinogen mRNA suggests that regulation of mRNA levels in the kidney does occur.
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PMID:Intrarenal localization of angiotensinogen mRNA by RNA-DNA dot-blot hybridization. 394 13

Angiotensin II-sensitive neurons in the brain of spontaneously hypertensive rats (SHR-sp) and of Wistar Kyoto rats (WKY) treated with the angiotensin-converting enzyme inhibitor Captopril were investigated for possible differences at receptor sites. Furthermore, the concentrations of angiotensinogen and renin were measured in different brain regions of these animals by biochemical assay. The higher receptor sensitivity of septal neurons to angiotensin II which existed in SHR-sp as compared to WKY was diminished by Captopril. Angiotensinogen concentrations were lower in the anterior hypothalamus but not in the septum of SHR-sp as compared to WKY. Captopril increased the level in both strains. Renin concentrations did not differ in SHR-sp and WKY. Chronic treatment with Captopril induced an increase of about 20% in septum and hypothalamic regions of SHR-sp and WKY rats. Whether these changes are causally linked to the hypertension in SHR-sp remains to be investigated.
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PMID:Angiotensin-converting enzyme blockade by Captopril changes angiotensin II receptors and angiotensinogen concentrations in the brain of SHR-sp and WKY rats. 629 70

The brain renin-angiotensin system (RAS) has been suggested as contributing to the pathogenesis of spontaneous hypertension in rats. Brain angiotensinogen- and angiotensin II (AII)-sensitive neurons were therefore investigated in stroke-prone spontaneously hypertensive rats (SHR-sp) and in Wistar-Kyoto (WKY) rats with and without treatment by captopril (CAP). Angiotensinogen was decreased in the anterior hypothalamus but increased in the cortex, the hippocampus, and cerebellum of SHR-sp. There were no differences between SHR-sp and WKY rats concerning the angiotensinogen content of posterior hypothalamus, brain stem, and septum. The sensitivity of the septal neurons to microiontophoretically applied AII was elevated, however, in SHR-sp as compared to WKY rats with regard to threshold and maximal response for AII-evoked neuronal discharges. The excitation characteristics did not change with the age of animals in both WKY rats and SHR-sp. The treatment of SHR-sp with CAP (50 mg/kg/day per os) starting in weanlings kept animals normotensive and reduced the high sensitivity of septal neurons to AII. Simultaneously angiotensinogen content was increased in the anterior hypothalamus and suppressed in the hippocampus. The same treatment of WKY rats reduced blood pressure somewhat and increased the angiotensinogen content in the anterior hypothalamus without affecting the neuronal sensitivity to AII. Thus, malfunction of the brain RAS may participate in the hypertension of SHR-sp, since converting enzyme blockade with CAP inhibited the blood pressure rise, augmented the angiotensinogen content of the anterior hypothalamus, and decreased the sensitivity of AII receptors in the brains of these rats.
Hypertension
PMID:Influence of captopril treatment on angiotensin II receptors and angiotensinogen in the brain of spontaneously hypertensive rats. 631 52

Angiotensinogen was measured in the brain and cerebrospinal fluid (CSF) of spontaneously hypertensive rat (SHR) and the normotensive Wistar-Kyoto strain at 4, 7 and 16 weeks of age. Levels of angiotensinogen were elevated in a number of areas of SHR, primarily in the 4 and 7 week old animals. CSF levels did not correlate with the brain levels. These results suggest that the regulation of the brain angiotensin system maybe altered during the development of hypertension.
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PMID:Changes in brain angiotensinogen during development of hypertension. 635 56

Angiotensinogen is the most important component of the renin-angiotensin system present in the cerebrospinal fluid (CSF) of the rat. Its physiological significance as well as its origin have not been clearly elucidated. In this experiment we have examined plasma renin activity (PRA) and plasma and CSF angiotensinogen concentration under the following experimental conditions in male rats of the Wistar strain: 1) adrenalectomy (Adx) 4 days prior to sample collection; controls were sham Adx animals; 2) nephrectomy (Nx) 48 hours before blood and CSF collection; controls were sham Nx rats; 3) DOC-salt treatment (Cortexon depot, 50 mg/kg.s.c. twice a week) plus saline to drink was given during 4 weeks; controls were intact rats; 4) DOC-salt plus captopril: captopril (100 mg/kg/day) in the drinking fluid was added to the treatment of experimental and control animals of Group 3; 5) two-kidney, two clip hypertension: silver clips placed in both renal arteries 8 weeks before samples collection; control: sham-operated rats; 6) water deprivation: rats deprived of water for 5 days; controls: intact rats; 7) peripheral sympathectomy: 6-hydroxydopamine (6-HODA) injected s.c. from birth until 16 weeks of age, adrenodemedullectomy and adrenal denervation performed at 8 weeks; controls were vehicle-injected animals. Determination of angiotensinogen concentration in plasma and CSF was accomplished by incubation of the samples with excess hog renin. The angiotensin I released as well as PRA were evaluated using an specific radioimmunoassay technique. PRA was significantly increased by Adx, captopril treatment, and water deprivation, and was almost suppressed by Nx, DOC-salt, and DOC-salt plus captopril treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Angiotensinogen concentration in the cerebrospinal fluid in different experimental conditions in the rat. 636 Aug 80

Evidence for an intracellular pathway for angiotensin synthesis in the central nervous system (CNS) was examined using immunohistochemistry to compare the distribution of angiotensin I (AI), AII, angiotensinogen, and renin in the hypothalamic paraventricular nuclei (PVN) and supraoptic nuclei (SON), median eminence (ME), and pituitary gland in intact and nephrectomized rats. In intact rats injected intracerebroventricularly (i.c.v.) with colchicine, AII neurons were found in the parvocellular PVN, and terminals were seen in the external lamina of the ME. In the pituitary gland, AII was localized within cells of the anterior and intermediate lobes, whereas the posterior pituitary was unstained. In contrast, 24 to 48 hours following nephrectomy, AII-labeled neurons were observed in the magnocellular PVN and SON, even without the aid of i.c.v. colchicine. Likewise, axons within the internal layer of the ME were now labeled, but the pituitary was completely devoid of staining except for the intermediate lobe. AI-labeled neurons were observed only in the parvocellular PVN. Angiotensinogen was localized in the mediobasal hypothalamus, but the PVN and SON were not labeled. Immunoreactive renin was localized within the magnocellular PVN, SON, and posterior lobe of the pituitary in nephrectomized and intact animals. Because of the close overlap of AI and AII staining, these results suggest that AI and AII could represent a precursor product relationship in the CNS. In contrast, in the intact animals, renin and angiotensinogen do not appear to be associated with AII. However, a possible relationship between AII and renin may exist in the magnocellular PVN and SON, since labeled neurons were seen in these nuclei following nephrectomy.
Hypertension
PMID:Distribution of immunoreactive angiotensin II, angiotensin I, angiotensinogen and renin in the central nervous system of intact and nephrectomized rats. 637 93

Angiotensinogen and the product of its hydrolysis by renin, des-angiotensin I-angiotensinogen, were quantitated in human plasma and in cerebrospinal fluid (CSF) by a direct RIA. This assay was developed using polyclonal antibodies raised against pure human angiotensinogen. The antibodies recognized only primate angiotensinogen and des-angiotensin I-angiotensinogen. Results obtained with the direct RIA were compared with those of the indirect assay which measures angiotensinogen through angiotensin I liberated by an excess of renin. Both assays gave almost identical results in normal subjects whereas in three different conditions characterized by a high renin level (severe hypertension plus low sodium diet, converting enzyme inhibition, and adrenal insufficiency) higher results were obtained by the direct assay. This difference between the results of both methods was attributed to des-angiotensin I-angiotensinogen accumulation which is detected only in the direct assay. CSF angiotensinogen had similar immunochemical properties to plasma angiotensinogen and could also be measured by the direct RIA. Isoelectric focusing of plasma angiotensinogen and des-angiotensin I-angiotensinogen revealed a similar microheterogeneity. Microheterogeneity was also a characteristic of CSF angiotensinogen, but its isoelectric point was more basic than plasma angiotensinogen.
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PMID:Characterization of plasma and cerebrospinal fluid human angiotensinogen and des-angiotensin I-angiotensinogen by direct radioimmunoassay. 674 61

One approach to establish the existence and functionality of a brain angiotensin system is to demonstrate selective alterations in that system following perturbation of peripheral cardiovascular functions. The present study utilized this approach to quantify regional angiotensinogen levels in the rat brain following bilateral nephrectomy, a perturbation that severely disrupts salt and water homeostasis. Angiotensinogen, the precursor of any centrally-derived angiotensin, was analyzed since it should provide a marker for a putative angiotensin peptidergic system. Net brain angiotensinogen was determined by correcting total tissue concentrations of angiotensinogen with accurate values of contaminating plasma angiotensinogen. The latter was determined by quantifying regional plasma space utilizing tritiated inulin as a marker of cerebral vascular space. It was found that there were no detectable alterations in regional net brain angiotensinogen in the first 24 hours following nephrectomy despite over a twofold increase in plasma angiotensinogen and the absence of significant plasma renin. By 32 hours postnephrectomy, certain areas of the rat hypothalamus and midbrain exhibited significant elevations in net angiotensinogen content. These areas coincided with regions traversed by neural pathways shown to mediate angiotensin-induced drinking or blood pressure elevations. The results lend further support to the concept of an independent brain angiotensin system.
Hypertension
PMID:Regional changes in rat brain angiotensinogen following bilateral nephrectomy. 714 8


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