title: Effect of renal perfusion pressure on renal function, renin release and renin and angiotensinogen gene expression in rats.
abstract: 1. A study was undertaken to examine the influence of acute renal perfusion pressure (RPP) reduction on renin release, renal renin and angiotensinogen gene expression and the role played by angiotensin II in these responses. 2. In chloralose-urethane anaesthetised rats, reduction of RPP to 60 mmHg for 3 h in vehicle or losartan-treated (5 days at 10 mg kg-1 bis in die (b.i.d.)) rats decreased renal blood flow by 46 and 29 % (both P < 0.001), respectively, glomerular filtration rate by 45 and 57 % (both P < 0.001), respectively, and sodium excretion by 96 and 98 % (both P < 0.01). 3. Chloralose-urethane anaesthesia and surgery caused a rise in plasma renin activity but was associated with a suppression of renal renin (50 %, P < 0.01) and angiotensinogen (40 %, P < 0.05) gene expression. Following reduction of RPP to 60 mmHg for 3 h, plasma renin activity was increased more than 7-fold (P < 0.001) and renal renin gene expression about 2-fold (P < 0.05). 4. Chronic (5 days) blockade of angiotensin II receptors with losartan elevated plasma renin activity some 29-fold (P < 0.001) and caused a marked increase (30-fold, P < 0.05) in renal renin gene expression, compatible with angiotensin II exerting a negative feedback control on renin release and gene expression. Reduction of RPP to 60 mmHg for 3 h in these animals had little effect on renal renin gene expression. 5. From these findings it can be concluded that (a) chloralose-urethane anaesthesia and surgery had a stimulatory effect on renin release but suppressed basal levels of renal renin and angiotensinogen gene expression; (b) acute reduction of RPP for 3 h could stimulate renin gene expression in the renin producing cells; and (c) the negative feedback control of angiotensin II on renin release and synthesis which was evident following chronic losartan treatment was not apparent during short-term reduction of RPP.
authors.affiliation: Department of Physiology, The Medical School, Birmingham B15 2TT, UK.
authors.forename: S M
authors.initials: SM
authors.lastname: Moosavi
authors.forename: E J
authors.initials: EJ
authors.lastname: Johns
mesh_terms: D000804:Angiotensin II / Q000502:physiology; D057911:Angiotensin Receptor Antagonists; D000808:Angiotensinogen / Q000096:biosynthesis* / Q000235:genetics*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D015152:Blotting, Northern; D005246:Feedback / Q000502:physiology; D015870:Gene Expression / Q000502:physiology; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D017403:In Situ Hybridization; D007444:Inulin; D007668:Kidney / Q000502:physiology*; D019808:Losartan / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000502:physiology*; D012083:Renin / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000808:Angiotensinogen; D000804:Angiotensin II; D007444:Inulin; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D012083:Renin; D019808:Losartan