Document Detail

Involvement of endothelium-derived relaxing factor in the pressure control of renin secretion from isolated perfused kidney.
MedLine Citation:
PMID:  8383697     Owner:  NLM     Status:  MEDLINE    
Using isolated rat kidneys perfused at controlled pressure, we examined a potential role of endothelium-derived relaxing factor (EDRF) in the pressure control of renin secretion. We found that stimulation of EDRF release by acetylcholine (1 mumol/liter) increased mean perfusate flow rates from 15.0 +/- 0.5 to 18.0 +/- 0.5 ml/min per g and average renin secretion rates from 3.5 +/- 0.5 to 16.0 +/- 2.0 ng angiotensin I/h per min per g at a perfusion pressure of 100 mmHg (mean +/- SEM, n = 6). Those effects of acetylcholine were significantly reduced during inhibition of EDRF formation with NG-nitro-L-arginine (100 mumol/liter), but they were not affected with the cyclooxygenase inhibitor indomethacin (10 mumol/liter). Lowering of the perfusion pressure from 100 mmHg to 40 mmHg resulted in an increase of average renin secretion rates from 3.5 +/- 0.5 to 79 +/- 12 ng AngI/h per min per g under control conditions (n = 8), and to 171 +/- 20 ng AngI/h per min per g in the presence of 10 mumol/liter acetylcholine (n = 3). The rise of renin secretion in response to a reduction of the renal artery pressure was markedly attenuated with inhibitors of EDRF formation such as NG-nitro-L-arginine (100 mumol/liter) and related compounds. During inhibition of EDRF formation, addition of sodium nitroprusside (10 mumol/liter) increased mean perfusate flow rates from 12.0 +/- 0.5 to 23.0 +/- 2.0 ml/min per g and average renin secretion rates from 2.0 +/- 0.5 to 18.0 +/- 1.5 ng AngI/h per min per g at 100 mmHg (n = 5). Lowering of the perfusion pressure from 100 mmHg to 40 mmHg under those conditions increased average renin secretion rates to 220 +/- 14 ng AngI/h per min per g (n = 5). Taken together, our findings suggest that EDRF and related activators of soluble guanylate cyclase stimulate renin secretion from isolated kidneys, predominantly at lower perfusion pressure. Moreover, pressure control of renin secretion appears to require the tonical stimulation by intrarenal EDRF.
H Scholz; A Kurtz
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  91     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1993 Mar 
Date Detail:
Created Date:  1993-04-13     Completed Date:  1993-04-13     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1088-94     Citation Subset:  AIM; IM    
Institut für Physiologie, Universität Regensburg, Germany.
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MeSH Terms
Acetylcholine / pharmacology
Angiotensin I / pharmacology*
Arginine / analogs & derivatives,  pharmacology
Atrial Natriuretic Factor / pharmacology
Cyclic GMP / analogs & derivatives,  pharmacology
Diuresis / drug effects
Isoproterenol / pharmacology
Kidney / drug effects,  enzymology,  physiology*
NG-Nitroarginine Methyl Ester
Nitric Oxide / physiology*
Nitroprusside / pharmacology
Rats, Inbred Strains
Renin / secretion*
Reg. No./Substance:
10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 17035-90-4/omega-N-Methylarginine; 2149-70-4/Nitroarginine; 31356-94-2/8-bromocyclic GMP; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-84-3/Acetylcholine; 74-79-3/Arginine; 7665-99-8/Cyclic GMP; 7683-59-2/Isoproterenol; 85637-73-6/Atrial Natriuretic Factor; 9041-90-1/Angiotensin I; EC

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