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An analysis of renal nitric oxide contribution to hyperfiltration in diabetic rats.
J Lab Clin Med. 2001 Feb; 137(2):107-14.JL

Abstract

We have investigated whether nitric oxide (NO) generation is increased in diabetes and whether specific NO synthase (NOS) isoforms are up-regulated in 4-week diabetic male Wistar rats. Glomerular filtration rate (GFR), kidney weight, and urinary nitrate (NOx) generation were measured in the following groups (n = 6): normal control animals, diabetic animals, diabetic animals given L -NIL (a selective iNOS inhibitor)(D + L -NIL), diabetic animals given L -NAME (a nonselective NOS inhibitor)(D + L -NAME), and control animals given L -NAME (C + L -NAME). Diabetes increased GFR (0.78 +/- 0.05 mL/min/100 g body wt vs 1.49 +/- 0.07 mL/min/100 g body wt, P <.01). L -NIL did not affect hyperfiltration, while L -NAME decreased GFR to values that were lower than those in normal control animals, a response identical to that in non-diabetic control rats. L -NIL did not affect urinary NOx values, but L -NAME completely abolished the increase in urinary nitrates. Kidney weight was not affected by L -NIL, but L -NAME significantly attenuated kidney growth. Inducible NOS (iNOS) and endothelial NOS (eNOS) mRNA levels measured by reverse transcription-polymerase chain reaction in diabetic rats were not changed as compared with levels in controls. Cyclic guanosine monophosphate responses to carbachol (an index of eNOS activity) in glomeruli from diabetic rats were significantly reduced as compared with those in controls, and guanylate cyclase responses to sodium nitroprusside were significantly decreased. Therefore, renal NO generation, at least via eNOS and iNOS, is not the primary cause of glomerular hyperfiltration in diabetes.

Authors+Show Affiliations

Division of Nephrology and Hypertension, University of California San Diego, and the Veterans Affairs Medical Center, San Diego, CA, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11174467

Citation

Schwartz, D, et al. "An Analysis of Renal Nitric Oxide Contribution to Hyperfiltration in Diabetic Rats." The Journal of Laboratory and Clinical Medicine, vol. 137, no. 2, 2001, pp. 107-14.
Schwartz D, Schwartz IF, Blantz RC. An analysis of renal nitric oxide contribution to hyperfiltration in diabetic rats. J Lab Clin Med. 2001;137(2):107-14.
Schwartz, D., Schwartz, I. F., & Blantz, R. C. (2001). An analysis of renal nitric oxide contribution to hyperfiltration in diabetic rats. The Journal of Laboratory and Clinical Medicine, 137(2), 107-14.
Schwartz D, Schwartz IF, Blantz RC. An Analysis of Renal Nitric Oxide Contribution to Hyperfiltration in Diabetic Rats. J Lab Clin Med. 2001;137(2):107-14. PubMed PMID: 11174467.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - An analysis of renal nitric oxide contribution to hyperfiltration in diabetic rats. AU - Schwartz,D, AU - Schwartz,I F, AU - Blantz,R C, PY - 2001/2/15/pubmed PY - 2001/3/17/medline PY - 2001/2/15/entrez SP - 107 EP - 14 JF - The Journal of laboratory and clinical medicine JO - J Lab Clin Med VL - 137 IS - 2 N2 - We have investigated whether nitric oxide (NO) generation is increased in diabetes and whether specific NO synthase (NOS) isoforms are up-regulated in 4-week diabetic male Wistar rats. Glomerular filtration rate (GFR), kidney weight, and urinary nitrate (NOx) generation were measured in the following groups (n = 6): normal control animals, diabetic animals, diabetic animals given L -NIL (a selective iNOS inhibitor)(D + L -NIL), diabetic animals given L -NAME (a nonselective NOS inhibitor)(D + L -NAME), and control animals given L -NAME (C + L -NAME). Diabetes increased GFR (0.78 +/- 0.05 mL/min/100 g body wt vs 1.49 +/- 0.07 mL/min/100 g body wt, P <.01). L -NIL did not affect hyperfiltration, while L -NAME decreased GFR to values that were lower than those in normal control animals, a response identical to that in non-diabetic control rats. L -NIL did not affect urinary NOx values, but L -NAME completely abolished the increase in urinary nitrates. Kidney weight was not affected by L -NIL, but L -NAME significantly attenuated kidney growth. Inducible NOS (iNOS) and endothelial NOS (eNOS) mRNA levels measured by reverse transcription-polymerase chain reaction in diabetic rats were not changed as compared with levels in controls. Cyclic guanosine monophosphate responses to carbachol (an index of eNOS activity) in glomeruli from diabetic rats were significantly reduced as compared with those in controls, and guanylate cyclase responses to sodium nitroprusside were significantly decreased. Therefore, renal NO generation, at least via eNOS and iNOS, is not the primary cause of glomerular hyperfiltration in diabetes. SN - 0022-2143 UR - https://www.unboundmedicine.com/medline/citation/11174467/An_analysis_of_renal_nitric_oxide_contribution_to_hyperfiltration_in_diabetic_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2143(01)22996-5 DB - PRIME DP - Unbound Medicine ER -