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)

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

Diabetic rat models were established with intraperitoneal injection of streptozotocin. The animals were randomly divided into four groups: Group 1, normal control (n = 5); Group 2, diabetic control (n = 4); Group 3, diabetics treated with PZI (n = 5); Group 4, diabetics treated with PZI and captopril (n = 5). Specimens taken from free wall of the left ventricle were observed under electron microscope after 10-week treatment, and the volume density (Vv), numerical density on area (Na), numerical density (Nv) and mean volume (V) of mitochondria were measured with stereological quantitation. The results showed that the myocardial changes in Group 4 were much less severe than those in Group 3 and similar to those in Group 1. There was significant difference in Nv (P < 0.05) but not in Vv, Na and V between Group 4 and Group 1. While the changes of Group 3 were relatively obvious. As comparing Group 3 with Group 1, there were significant differences in all of the four parameters (P < 0.05-0.01). It is implied that the renin-angiotensin system may be involved in the pathogenesis of diabetic cardiomyopathy, since captopril can improve and reverse the cardiomyopathy of diabetic rats.
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PMID:[Effects of captopril on myocardial ultrastructure in diabetic rats]. 822 56