Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renin activity and aldosterone were evaluated relative to potassium levels and lead intoxication in 33 patients with a history of "moonshine" ingestion. Patients were divided into three groups: I, lead intoxicated with hyperkalemia; II, lead intoxicated without hyperkalemia; and III, not lead intoxicated without hyperkalemia. Those in group I demonstrated suppressed plasma renin activity, baseline and after furosemide, and blunted aldosterone responsiveness to furosemide. Plasma renin activity was not different in groups II and III, whereas aldosterone responsiveness was less in group II than in III. Group I patients tended to be older, had lower creatinine clearances, and six of nine had mild hyperchloremic acidosis. Diabetes and cortisol insufficiency were not present. Chronic lead intoxication due to illicit alcohol ingestion is associated with hyporeninemic hypoaldosteronism and hyperkalemia which appear to develop as the lead nephropathy progresses with duration and/or aging.
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PMID:Renin aldosterone system and potassium levels in chronic lead intoxication. 10 94

Renin substrate (angiotensinogen) in unfractionated human plasma has been shown to exist in multiple forms by DEAE-cellulose chromatography and isoelectric focusing. Two major and 5 to 6 minor peaks were resolved by using a descending pH gradient elution from DEAE-cellulose columns. The two predominant forms were eluted at or near pH 4.8 and 4.4 and usually accounted for 40--50% of the recovered substrate activity. The elution pH values of the various forms were nearly constant among plasmas from normal males and females and in diabetes, early and late pregnancy and estrogen substitution therapy. The relative distribution of components was not affected by prior freezing of the plasma or by dialysis against the column buffer. Eight renin substrate forms were clearly resolved during isoelectric focusing of plasma from a woman on estrogen substitution therapy. Four of these focused at pH 4.79, 4.88, 4.94 and 5.02 in 1% (w/v) ampholytes pH 3.5--5 and were nearly equal in substrate amount. Together these 4 forms constituted 66% of the total recovered activity. A similar pattern but with decreased amounts of each form of substrate was obtained with normal plasma.
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PMID:Multiple forms of renin substrate in human plasma. 62 80

The etiology of the low renin state in DM is not clear. To assess the role of certain growth and regulatory factors in this process, we studied the effects of insulin, IGF-I, and IGF-II on the renin-angiotensin system in normal and 8-wk STZ-induced diabetic rats. Renin secretion was studied both in static incubations and by perifusion of rat renal cortical slices. In diabetic rats, both plasma renin activity (0.65 +/- 1.6 vs. 4.0 +/- 1.2 ng ANG I.ml-1.h-1) and tissue renin concentrations (27 +/- 5 vs. 51 +/- 8 ng ANG I.mg tissue-1.h-1) were reduced. Insulin (0.1-1.0 mu/ml) and IGF-I (10(-9) to 4 x 10(-9) M) stimulated renin secretion in normal tissue (control, 95 +/- 3%; insulin [0.5 mu/ml], 134 +/- 7%; IGF-I [4 x 10(-9) M], 149 +/- 7%). IGF-I stimulated renin secretion in perifusions as early as 30 min, whereas IGF-II had no effect. However, in diabetic renal tissue, neither insulin (0.1-1.0 mu/ml) nor IGF-I (10(-9) to 4 x 10(-9) M) had an effect on renin. This lack of effect was overcome by adding up to 100-fold higher concentrations of these growth factors. ANG II (10(-10) M-10(-8) M) had an exaggerated inhibitory effect on renin secretion in diabetic tissue. This study suggests that the low renin state in DM may be explained by the enhanced inhibitory effect of ANG II and the resistance to the secretogogue actions of insulin and IGF-I.
Diabetes 1992 Sep
PMID:Altered regulation of renin secretion by insulinlike growth factors and angiotensin II in diabetic rats. 138 18

We previously showed that renal prokallikrein synthesis is reduced in streptozotocin (STZ)-diabetic rats. Plasma renin activity is also reduced in diabetic rats. To investigate the molecular mechanisms underlying these changes, we examined the effects of diabetes and insulin treatment on renal kallikrein and renal renin mRNA levels and the activities of these enzymes. Rats made diabetic by STZ were either treated with 1.5 to 1.75 U PZI insulin daily to maintain moderate hyperglycemia (plasma glucose 200 to 300 mg/dl, D + I) or left untreated to produce severe hyperglycemia (plasma glucose greater than 400 mg/dl, D). Control (C) rats were also studied. After three weeks, renal kallikrein mRNA was reduced 50% in D rats. A proportional reduction in immunoreactive kallikrein was also observed (37.8 +/- 2.5 vs. 55.8 +/- 6.8 ng/mg protein, D vs. C, P less than 0.001). Kallikrein mRNA and immunoreactive kallikrein levels in D + I rats were not different from C rats. Renin mRNA level was also markedly reduced in D rats, compared to C rats. This was associated with reduced plasma renin concentration (4.5 +/- 0.2 vs. 10.5 +/- 1.6 ng Ang I/ml/hr, D vs. C, P less than 0.01). However, renal renin concentration was unchanged (0.84 +/- 0.17 vs. 0.84 +/- 1.3 micrograms Ang I/mg protein/hr, D vs. C). In D + I rats, renin mRNA level and plasma renin concentration were not different from C levels. However, renal renin concentration was increased (1.49 +/- 0.27 micrograms Ang I/mg protein/hr) compared to C rats (P less than 0.05). beta-actin mRNA levels were unchanged in either diabetic rat group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of diabetes and insulin on expression of kallikrein and renin genes in the kidney. 151 1

The expression of renin and angiotensinogen genes and their proteins were studied during the progression of diabetes using adult BioBreeding spontaneously diabetic rats at 1 day and 2-12 months of diabetes. The number of renin-stained cells per juxtaglomerular apparatus was determined by immunocytochemistry. Initially, at 2 months of diabetes the number of renin-stained cells per juxtaglomerular apparatus increased significantly (p less than 0.0001, 2 months versus resistant groups) and was followed by a decrease in the number and intensity of renin-stained cells after 12 months of diabetes (p = 0.007, 2 months versus 12 months). A significant negative correlation was observed between the number of renin-containing cells and the duration of diabetes (r = 0.99, p = 0.014). Immunoreactive angiotensinogen was restricted to the proximal tubule and appeared increased after 4 and 8 months of diabetes as compared with the 2- and 12-month diabetic groups. Renin messenger RNA (mRNA) levels increased with the onset of diabetes and decreased markedly during chronic diabetes. At 1 day of diabetes, renin mRNA levels were 700% higher than at 12 months of diabetes. Angiotensinogen mRNA levels were unchanged. We conclude that diabetes results in an initial increase in renin gene expression, and as the duration of diabetes lengthens, there is a progressive decrease in renin gene expression and in the number of cells containing renin. These findings suggest that as the duration of diabetes and the age of the animal lengthens, there is a decrease in the number of cells expressing the renin gene.
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PMID:Renin and angiotensinogen expression during the evolution of diabetes. 173 Apr 42

To determine if insulin has the ability to regulate components of the renin-angiotensin system, renin and angiotensinogen mRNA and plasma concentrations were determined in 4-wk streptozotocin (STZ)-diabetic rats. In another group of STZ-diabetic rats, replacement insulin therapy was given over the 4-wk period, and the above parameters were examined. In STZ-diabetic rats, there was a significant regression of white adipose tissue that was accompanied by an increase in the yield of RNA obtained. Changes in white adipose tissue were reversed by insulin replacement therapy in STZ-diabetic rats. There were no changes in brown adipose tissue weight or RNA yield in STZ-diabetic rats. Plasma renin activity (PRA) was significantly decreased in STZ-diabetic rats; however, plasma angiotensinogen concentration was not significantly affected by diabetes. PRA was restored to control levels in STZ-diabetic rats with insulin replacement. Kidney renin mRNA as well as liver, epididymal, and interscapular fat angiotensinogen mRNA were significantly decreased in STZ-diabetic rats. Renin and angiotensinogen mRNA were not significantly different from control in all tissues examined in STZ-diabetic rats with insulin replacement therapy. Results from this study suggest a downregulation of the renin-angiotensin system in 4-wk STZ-diabetic rats at the level of mRNA expression that is restored by replacement therapy with insulin; therefore, insulin may directly or indirectly regulate the renin-angiotensin system.
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PMID:Downregulation of the renin-angiotensin system in streptozotocin-diabetic rats. 173 40

The value of plasma renin and its inactive precursor, prorenin, were examined as a marker for vasculitis in rheumatoid arthritis (RA). Plasma renin and prorenin rise when the renin-angiotensin system is activated; an isolated increase of prorenin may be a marker for microvascular complications in diabetes mellitus. Renin concentrations in plasma obtained from 34 patients with RA (seven with vasculitis, 27 controls) were measured under standard conditions, before and five days after stopping non-steroidal anti-inflammatory drugs; creatinine clearance was also measured. At first the median renin concentration in the patients with vasculitis was 19 (range 12-63) mU/l (normal less than 61 mU/l) and in the controls 9 (3-43) mU/l. The median prorenin concentration in patients with vasculitis was 233 (144-428) mU/l (normal less than 358 mU/l) and in the controls 144 (25-364) mU/l. Renin and prorenin concentrations increased significantly in both groups after withdrawal of nonsteroidal anti-inflammatory drugs. The creatinine clearance was similar in both groups and did not correlate with renin concentrations. In conclusion, it was found that, unlike patients with diabetes mellitus, patients with RA with vasculitis had slightly raised concentrations of both renin and prorenin. These findings signal activation of the renin-angiotensin system and might indicate early cardiac or renal involvement by vasculitis.
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PMID:Raised plasma renin and prorenin in rheumatoid vasculitis. 220 Mar 59

To clarify the relationship between kallikrein-kinin and renin-angiotensin systems, glandular kallikrein, renin and angiotensin converting enzyme in the submandibular gland, the kidney and plasma were investigated in streptozotocin diabetic and spontaneously hypertensive rats. Kallikrein content in the submandibular gland, the kidney and plasma of diabetic rats was found to be decreased compared with nondiabetic controls. Renin activity in diabetic rats was also reduced in the submandibular gland, but the activity showed no significant changes in the kidney and plasma. The activity of angiotensin converting enzyme (ACE) in plasma significantly increased in diabetic rats. On the other hand, kallikrein content in hypertensive rats was depressed in the kidney, while the content was unchanged in the submandibular gland and plasma. Renin activity in hypertensive rats was found to be higher than that of normotensive rats in the submandibular gland, but the activity showed no remarkable changes in the kidney and plasma. ACE activity in plasma markedly decreased in hypertensive rats in contrast to diabetic rats. In hypertensive-diabetic rats, changes in the levels of these enzymes in tested materials were similar to those of diabetic rats. From these results it is reasonable to assume that (1) reduced kallikrein generation and elevated ACE activity may induce impaired kinin formation and contribute to the development of diabetes mellitus apart from the presence of hypertension and (2) low kallikrein content in the kidney could cause hypertension.
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PMID:Glandular kallikrein, renin and angiotensin converting enzyme of diabetic and hypertensive rats. 255 14

Renin and prorenin, the latter after conversion to renin, are usually measured by indirect RIA using antibodies against angiotensin I. They can now also be measured by direct RIA using monoclonal antibodies reacting with total immunoreactive renin (renin plus prorenin) or with renin alone. Results of measurements in renal and peripheral venous plasma indicate that normally a large proportion of prorenin in plasma is of renal origin and they support the concept of separate pathways for prorenin and renin secretion by the JG-cells. Acute stimulation causes a prompt increase of plasma renin without any change in prorenin. During chronic stimulation both renin and prorenin are increased, in such a way that the ratio between the two is higher the stronger the stimulus. Thus, with acute stimulation only the release of stored renin appears to be increased (regulated pathway), whereas during chronic stimulation the synthesis and secretion of prorenin are also (constitutive pathway). During pregnancy, in the early luteal phase of the menstrual cycle and after ovarian hyperstimulation with gonadotropins, a normal or somewhat elevated plasma level of renin is associated with a disproportionally high level of prorenin. This is an indication of extrarenal production of prorenin and in these conditions the ovary, probably corpus luteum, seems to be the main source. In most patients with renin-producing tumors plasma prorenin is also disproportionally high. In diabetes mellitus complicated by micro-angiopathy plasma prorenin is also elevated whereas renin is normal or even low. In diabetics with end-stage nephropathy we found no significant veno-arterial difference in prorenin across the kidneys, despite high circulating prorenin and a very low blood flow through these kidneys, suggesting that also in these patients part of the increased prorenin in plasma is of extrarenal origin. Thus, measurements of prorenin in plasma in various pathological conditions may contribute to a better understanding of the physiological role of the renal and extrarenal renin-angiotensin systems.
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PMID:Human prorenin: pathophysiology and clinical implications. 306 28

Possible factors involved in the control of plasma renin activity (PRA) and concentration (PRC) have been analysed in 49 patients with long-standing Type 1 diabetes and in 40 healthy controls matched for age and sex. Eighteen of the diabetic subjects were clinically free of all microvascular and macrovascular complications of their disease (Group A); 31 had proliferative retinopathy (Group B). Both lying and standing PRA and PRC were similar in Group A and healthy controls. Mean PRA was 50-115% higher in Group B diabetics than in controls (P less than 0.001 supine and erect) and 50-70% higher than in Group A diabetics (P less than 0.05 supine and erect); PRC also was 60% higher in Group B than in Group A (P less than 0.05 supine and erect). Control subjects showed significant falls in both PRA and PRC with increasing age, while Groups A and B showed significant falls in PRA or PRC with age. Group A showed a significant inverse correlation between systolic blood pressure and supine PRC (r = -0.57), but this was not significant in the controls and was completely absent in Group B. With correction for the effect of age there were significant relationships of PRA and PRC with sodium excretion in the controls and in Group A, but not in Group B. PRA and PRC are thus normal in uncomplicated long-standing Type 1 diabetes, but regulation of renin secretion appears to be impaired in patients with microvascular disease. Renin secretion inappropriate to their blood pressure and sodium status may contribute to maintenance of their relative hypertension.
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PMID:Factors in the control of plasma renin activity and concentration in Type 1 (insulin-dependent) diabetes. 637 34


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