Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regional distribution of angiotensinogen, the prohormone of angiotensin I, was examined in rat brain. Quantification of brain angiotensinogen concentration was difficult because of the presence of an endogenous angiotensin I degrading (i.e. angiotensinase) activity which was active at the pH of the renin-angiotensinogen incubation. This degrading activity was unequally distributed throughout the brain, and its presence in homogenates invalidated measured levels of angiotensinogen. Only following removal of the angiotensinase activity by ammonium sulfate precipitation of the prohormone could the distribution of the prohormone be determined. Angiotensinogen was widely distributed throughout 31 brain regions; however there was an approximate 12-fold variation in concentration. Highest levels of the prohormone were found in the dorsal and ventral periventricular hypothalamus, area postrema, organum vasculosum lamina terminalis, periventricular thalamus, dorsal raphe and lateral reticular formation. Significantly lower amounts were found in the parietal cortex, cerebellum, septum and pituitaries. While the majority of regions examined exhibited similar concentrations of angiotensinogen, the demonstration of regions containing either significnatly low or high amounts of prohormone is consistent with a topographical distribution of angiotensinogen in rat brain.
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PMID:Regional distribution of angiotensinogen in rat brain. 21 73

1. Angiotensinogen (renin substrate) was purified from plasma of nephrectomized rats by a four step procedure using ammonium sulfate fractionation, chromatography on Blue Sepharose CL-6B and SP-Sephadex C-50, and gel filtration on Sephadex G-150. 2. The final preparation had a specific concentration of 9.3 microgram angiotensin I/mg (mean of six separate runs). The best preparation so far obtained contains 14.6 microgram angiotensin I/mg protein, which represents a purity of 62%. 3. By sodium dodecyl sulfate disc electrophoresis an apparent molecular weight of 56,400, and by isoelectric focusing an isoelectric point of 4.85 has been determined. These properties of rat angiotensinogen are similar to those reported for human angiotensinogen.
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PMID:Purification and characterization of rat angiotensinogen. 53 50

Angiotensinogen (a substrate of renin) was isolated from pig and sheep blood plasma. Content of angiotensinogen was estimated in the preparations obtained by an indirect biological method, which was based on estimation of an increase in blood pressure in rats, caused by angiotensin, liberated from angiotensinogen during incubation with renin. The preparation, obtained by ammonium sulphate fractionation of pig blood plasma, contained 0.4% of angiotensinogen. Angiotensinogen was also isolated from sheep blood plasma using ammonium sulphate fractionation, DEAE-Sephadex chromatography and gel filtration through Sephadex G-100; this preparation contained 10-13% of angiotensinogen.
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PMID:[Isolation and purification of angiotensinogen from swine and sheep plasma]. 73 81

Hemorrhage and hemorrhagic hypotension have been shown to be potent stimulators of renin release. However, the relationship between angiotensinogen consumption and angiotensinogen production has yet to be completely defined during this type of circulatory stress. Peripheral renin activity increased progressively as the blood pressure was decreased stepwise by hemorrhage to 50 mmHg and remained elevated throughout the shock phase of the experiment. Angiotensinogen did not change from control (809 ng/ml) throughout hemorrhabic hypotension and shock. During hemorrhagic hypotension, with the infusion of the angiotensin antagonist, [1-sarcosine, 8-alanine]angiotensin II, angiotensinogen concentration fell progressively from 693 to 208 ng/ml at 50 mmHg. Intravenous angiotensin II infused continuously after the mean blood pressure reached 50 mmHg significantly elevated plasma angiotensinogen concentration. In conclusion, during hemorrhagic hypotension and shock, the kidney and the liver appeared capable of maintaining elevated plasma renin activity and adequate plasma renin substrate, angiotensinogen, respectively. The mechanism responsible for the maintenance of plasma angiotensinogen is suggested to involve a positive-feedback effect of angiotensin II on the liver.
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PMID:Renin response and angiotensinogen control during graded hemorrhage and shock in the dog. 98 15

The aim of the present investigation was to (a) determine if renin-substrate (angiotensinogen) is present in cerebrospinal fluid; (b) investigate the effects of intracerebroventricular administration of renin on drinking and blood pressure; and (c) determine if such effects are mediated via the formation of angiotensin II. Angiotensinogen concentration in cerebrospinal fluid was measured in 15 dogs and averaged 205 +/- 34 ng/ml. This value was approximately 1/5th of the corresponding plasma angiotensinogen concentration but the ratio of angiotensinogen:total protein in cerebrospinal fluid was approximately 15 times greater than in plasma. Intraventricular injection of hog renin (0.1 Goldblatt units) stimulated drinking in each of 8 dogs; the mean volume drunk in the 15 min period following the injection was 485 +/- 84 ml. When the renin was preceded by intraventricular saralasin acetate, a specific antagonist of angiotensin II, the drinking response was reduced to 8 +/- 6 ml. In eight pentobarbital anesthetized dogs, intraventricular dog or hog renin (0.05-0.25 Goldblatt units) increased systolic pressure from 152 +/- 10 to 168 +/- 10 mm Hg (P less than 0.001) and diastolic pressure from 101 +/- 8 to 116 +/- 7 mm Hg (P less than 0.001). This response, which lasted from 30 min to more than 3 h, was also abolished by saralasin acetate. These data indicate that centrally administered renin increases drinking and blood pressure and that these effects are mediated via the formation of angiotensin II.
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PMID:The effects of intracerebroventricular administration of renin on drinking and blood pressure. 117 5

The presence of the two components of the renin-angiotensin system (RAS) has been systematically investigated in human normal and pathological adrenal tissues with two aims: 1) the detection of renin and especially angiotensinogen, which has not been reported before; and 2) to study possible differences in the coexpression of renin and angiotensinogen in tissue of cortical and medullary origin. The relative levels of renin and angiotensinogen mRNAs were determined by Northern blot analysis in normal (n = 5) and pathological adrenal tissues of cortical (n = 23) and medullary (n = 10) origin. Renin, prorenin, and angiotensinogen levels were also measured. Renin concentrations in normal and pathological adrenals were around 30-fold higher than those in the plasma of normal subjects, except for a Cushing's adenoma, which contains an extremely high renin content. Renin accounted for 56% of the total renin in normal adrenals and up to 87% in neoplastic tissues. This high proportion of renin indicates a likely conversion of prorenin to renin within these tissues. Renin mRNA was detected in each group of adrenal tissues. There was a significant correlation between the concentration of renin and its mRNA (r = 0.75; P less than 0.05). Angiotensinogen and its mRNA were detected in all normal and pathological adrenals. Compared to normal adrenal tissues, the relative amount of angiotensinogen mRNA was significantly higher in pheochromocytomas. However, the increased mRNA level in these tissues was not accompanied by a parallel increase in tissue angiotensinogen levels. Since the translational efficiency of angiotensinogen was verified by in vitro cell-free translation, the low level of angiotensinogen compared to the relatively high amount of its mRNA suggests a lack of storage of this protein in adrenal cells, as in liver cells. This study demonstrates that renin and angiotensinogen are coexpressed in normal and pathological tissues. Tissues of different cellular origin (zona glomerulosa, fasciculata, and medullary tissue), were able to express, store, and process renin and synthesize angiotensinogen. There was no obvious relationship between the expression of these proteins and the pathophysiology of the adrenal gland.
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PMID:Coexpression of renin, angiotensinogen, and their messenger ribonucleic acids in adrenal tissues. 138 71

This report summarizes the present data about the existence of components of the renin-angiotensin system in the rat brain. Angiotensinogen mRNA, mas proto-oncogene mRNA, angiotensin II (Ang II), and Ang II receptors have been mapped in the brain by using in situ hybridization, immunocytochemistry, and receptor autoradiography. These markers turned out to be widely distributed throughout the brain and to be not only restricted to areas related to cardiovascular control, but also to be present in functionally different areas, suggesting also other functions of angiotensin peptides. The distribution patterns of these components were correlated with data on the distribution of angiotensinogen, renin, angiotensin converting enzyme, and angiotensin fragments that revealed substantial topological mismatches. Using the model of "volume transmission," possible explanations for these mismatches are proposed. In this regard, a possible involvement of angiotensin fragments and the mas proto-oncogene in the functioning of the brain renin-angiotensin system is also discussed, demonstrating the increasing complexity of this central regulatory system.
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PMID:The brain renin-angiotensin system: localization and general significance. 138 66

Angiotensinogen, the precursor of a vasoactive octapeptide angiotensin II, is the only known natural substrate of renin, and its reaction exhibits strict species specificity and is the rate-limiting step in the renin-angiotensin system that controls the blood pressure. We measured blood pressure and heart rate of the transgenic mice with overproduced human angiotensinogen, and showed no significant difference in these parameters between transgenic and nontransgenic mice. We also provided evidence that mouse renin could not cleave human angiotensinogen, indicating a lack of angiotensin production from the human substrate. These results suggested that the blood pressure of transgenic mice is normally maintained, probably due to the inability of mouse renin to release angiotensin from the transgene products.
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PMID:Species-specific kinetics of mouse renin contribute to maintenance of normal blood pressure in transgenic mice with overexpressed human angiotensinogen. 147 69

Angiotensinogen is the precursor molecule of one of the most potent vasoactive substances, angiotensin-II. Angiotensinogen is normally synthesized in the liver and secreted into the plasma where it is converted into angiotensin-II by the combined proteolytic action of renin and angiotensin converting enzyme. Angiotensinogen levels in the plasma are modulated by a number of pathological and physiological factors. In order to understand the regulation of angiotensinogen gene expression, we have constructed an expression vector in which 688 bp of the 5'-flanking region of the rat angiotensinogen gene were attached to the chloramphenicol acetyl transferase (CAT) coding sequence. We have also obtained 5'-sequential deletion mutants from the rat angiotensinogen promoter attached to the CAT gene, and have identified multiple cis-acting DNA sequences involved in the regulation of angiotensinogen gene expression by transient transfection of these recombinant DNA molecules in human hepatoma cell lines, Hep3B, and HepG2.
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PMID:Identification of cis-acting DNA elements involved in the regulation of angiotensinogen gene expression. 155 46

The local renin-angiotensin system may regulate adrenal cell growth and function. Angiotensinogen, renin, and angiotensin converting enzyme gene expression were studied in four normal adrenal glands (removed from patients with renal carcinomas) and five aldosterone-secreting adenomas. Northern blot analysis showed expression of angiotensinogen messenger RNA (mRNA) in normal adrenals at levels approximately 35-fold lower than liver and sixfold lower than kidney. Similar angiotensinogen mRNA levels were present in two aldosteronomas, whereas a third had levels approximately 50% of those found in kidney. Renin mRNA was detectable in most normal adrenals and in three adenomas, one of which had relatively high renin mRNA levels. Angiotensin converting enzyme gene was expressed in adrenal tissue and in three adenomas. Portions from these normal adrenals and two of these aldosteronomas, as well as samples from two other adrenals and three aldosteronomas, were also studied in an in vitro superfusion system coupled with active renin radioimmunometric assay, angiotensin II/III, and aldosterone radioimmunoassay. Total amounts of active renin and angiotensin II/III released from normal adrenals during 270 minutes of superfusion were higher than the amounts released from aldosteronomas (312 +/- 35 versus 187 +/- 43 and 823 +/- 100 versus 436 +/- 55 pg/100 mg tissue, respectively; mean +/- SEM, p less than 0.05), whereas aldosterone release from the adenomatous tissue was approximately threefold higher (320 +/- 21 versus 115 +/- 18 ng/100 mg tissue; mean +/- SEM, p less than 0.01). Total amounts of active renin and angiotensin II/III released by normal or adenomatous adrenal samples exceeded threefold to fourfold the amounts extracted from similar samples of the same surgical specimen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local renin-angiotensin system in human adrenals and aldosteronomas. 159 71


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