Drugs online research references
Am J Physiol. 1988 Jun;254(6 Pt 2):F900-6.
Renin and angiotensinogen gene expression and intrarenal renin distribution during ACE inhibition.
Gomez RA, Lynch KR, Chevalier RL, Everett AD, Johns DW, Wilfong N, Peach MJ, Carey RM.
Department of Pediatrics, School of Medicine, University of Virginia, Charlottesville 22908.
To define whether intrarenal renin and angiotensinogen synthesis and distribution are affected by angiotensin-converting enzyme (ACE) inhibition, a control group of adult, male Wistar-Kyoto rats (n = 7) was compared with a group of rats treated with enalapril (n = 8) for 5 days. Kidney renin and angiotensinogen mRNA levels were detected by Northern and dot blot analysis, using full-length rat renin and angiotensinogen cDNAs. Renin mRNA levels in the enalapril-treated group were 4.6-fold higher than in the control group (P less than 0.05). Angiotensinogen mRNA levels were not significantly different. The intrarenal distribution of renin assessed by immunocytochemistry was markedly different between the two groups of rats. Whereas in the control kidney renin was localized in a juxtaglomerular position, in the kidneys from enalapril-treated rats, renin immunoreactivity of the afferent arteriole extended well beyond the juxtaglomerular loci in the direction of the interlobular artery. The percent of afferent arteriolar length immunostained for renin was higher in the enalapril-treated (53 +/- 17%) than in the control (33 +/- 15) group. Similarly, the ratio of immunostained juxtaglomerular apparatuses (JGA) over total number of JGA and the ratio of immunostained arteries over total number of arteries were higher in the enalapril-treated (0.84 +/- 0.017; 0.68 +/- 0.03) than in the control (0.67 +/- 0.034; 0.43 +/- 0.045) group (P less than 0.05). We conclude that chronic ACE inhibition enhances intrarenal renin synthesis and increases renin expression upstream from the glomerulus and in new sites in blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2837909&dopt=Abstract
J Clin Invest. 1986 Jun;77(6):1925-30.
Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension.
Zatz R, Dunn BR, Meyer TW, Anderson S, Rennke HG, Brenner BM.
Two groups of adult male Munich-Wistar rats and a third group of nondiabetic age-matched and weight-matched normal control rats underwent micropuncture study 1 mo, and morphologic studies 14 mo, after induction of streptozotocin diabetes or sham treatment. All animals were fed standard rat chow. Diabetic rats received daily ultralente insulin to maintain stable moderate hyperglycemia (approximately 350 mg/dl). In addition, one group of diabetic rats was treated with the angiotensin I converting enzyme inhibitor, enalapril, 15 mg/liter of drinking water. Average kidney weight, whole kidney and single-nephron glomerular filtration rate, and glomerular plasma flow rate were elevated to similar values in both groups of diabetic rats, relative to normal control rats. Non-enalapril-treated diabetic rats exhibited significant elevations in mean glomerular capillary hydraulic pressure and transcapillary hydraulic pressure gradient, compared with the other groups studied, and only this group eventually developed marked and progressive albuminuria. Likewise, histological examination of the kidneys at 14 mo disclosed a high incidence of glomerular structural abnormalities only in non-enalapril-treated diabetic rats. These findings indicate that prevention of glomerular capillary hypertension in rats with diabetes mellitus effectively protects against the subsequent development of glomerular structural injury and proteinuria. This protection is afforded despite pronounced hyperglycemia and elevated levels of glucosylated hemoglobin, further supporting our view that hemodynamic rather than metabolic factors predominate in the pathogenesis of diabetic glomerulopathy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3011862&dopt=Abstract
J Clin Endocrinol Metab. 1989 Feb;68(2):386-91.
No effect of short term angiotensin II infusion on plasma renin substrate levels in man.
Metsarinne K, Fyhrquist F, Totterman J, Tikkanen I.
Unit of Clinical Physiology, Minerva Foundation Institute for Medical Research, Helsinki, Finland.
We studied the effect of angiotensin II (A-II) infusion (4 ng/kg BW.min) on plasma renin substrate (RS) levels and PRA in five normal men during normal, diuretic-stimulated, and enalapril-interrupted function of the renin-angiotensin system. A-II infusion increased (15-25%) both systolic and diastolic blood pressure in the normal state and during angiotensin-converting enzyme inhibition, whereas the increase during diuretic-stimulated renin-angiotensin system function was less. The plasma RS concentration was measured by both direct and indirect RIA. The mean basal plasma RS levels, measured with direct assay, were 1516 +/- 150 (SE) in the normal state, 1566 +/- 150 after diuretic administration, and 1650 +/- 133 nmol/L after enalapril administration. The corresponding mean basal plasma RS levels measured with the indirect assay were 1073 +/- 100, 1031 +/- 57, and 902 +/- 78 nmol/L, respectively. Plasma RS levels did not change during or after the A-II infusions, whereas PRA decreased significantly in all experimental conditions. The results suggest that A-II exerts no direct stimulatory effect on hepatic release of RS. Thus, A-II appears not to be important in the short term regulation of plasma RS levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2537331&dopt=Abstract
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