| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Medicine, Division of Nephrology-Hypertension University of California, San Diego, CA, USA; Medical Research, VA San Diego Health Care System, San Diego, CA, USA
2 Department of Medicine, Division of Nephrology-Hypertension University of California, San Diego, CA, USA
* To whom correspondence should be addressed. E-mail: sthomson{at}ucsd.edu.
Dysregulation of kidney NOS-I may alter renal hemodynamics in diabetes. Four types of studies were performed in anesthetized 1-2 week streptozotocin diabetic rats: 1) GFR was measured before and during NOS-I blockade. Subsequent addition of non-specific NOS blocker tested for residual NO from other isoforms. Acute systemic NOS-I blockade reduced GFR only in diabetics. Non-specific NOS blockade had no additional effect in NOS-I blocked diabetics. 2) RBF was monitored for evidence that tubuloglomerualr feedback (TGF) resets during one hour of continuous activation with benzolamide. NOS-I blockade was added to test for the role of NOS-I in TGF resetting. During one hour of TGF activation in controls, RBF initially declined then returned to baseline. In diabetic and NOS-I blocked rats, RBF declined and remained low. 3) The ability of NOS-I blockade to increase the homeostatic efficiency of TGF in diabetes was tested by micropuncture in free flowing nephrons. Adding NOS-I blocker to the tubular fluid increased TGF efficiency in control and diabetic rats. 4) The influence of distal salt delivery on local NOS-I activity was tested by micropuncture. Henle's loop was perfused at varying rates with NOS-I blocker while measuring single nephron GFR (SNGFR) from the late proximal tubule. In controls, NOS I blockade mainly reduced SNGFR when flow through Henle's loop was high. In diabetics, NOS I blockade reduced SNGFR independent of flow through Henle's loop. Conclusions- Normally, salt delivered to the macula densa (MD) exerts immediate control over MD NOS-I activity. In diabetes there is ongoing overactivity of NOS-I that is not regulated by MD salt.
This article has been cited by other articles:
|
|
 |
|
  T. D. Bell, G. F. DiBona, R. Biemiller, and M. W. Brands Continuously measured renal blood flow does not increase in diabetes if nitric oxide synthesis is blocked Am J Physiol Renal Physiol, November 1, 2008; 295(5): F1449 - F1456. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. W. Brands and H. Labazi Role of Glomerular Filtration Rate in Controlling Blood Pressure Early in Diabetes Hypertension, August 1, 2008; 52(2): 188 - 194. [Full Text] [PDF]
|
|
|
|
 |
|
 R. Faulhaber-Walter, L. Chen, M. Oppermann, S. M. Kim, Y. Huang, N. Hiramatsu, D. Mizel, H. Kajiyama, P. Zerfas, J. P. Briggs, et al. Lack of A1 Adenosine Receptors Augments Diabetic Hyperfiltration and Glomerular Injury J. Am. Soc. Nephrol., April 1, 2008; 19(4): 722 - 730. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. L. Onozato, A. Tojo, J. Leiper, T. Fujita, F. Palm, and C. S. Wilcox Expression of NG,NG-Dimethylarginine Dimethylaminohydrolase and Protein Arginine N-Methyltransferase Isoforms in Diabetic Rat Kidney: Effects of Angiotensin II Receptor Blockers Diabetes, January 1, 2008; 57(1): 172 - 180. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Palm, M. L. Onozato, Z. Luo, and C. S. Wilcox Dimethylarginine dimethylaminohydrolase (DDAH): expression, regulation, and function in the cardiovascular and renal systems Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3227 - H3245. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Zhang, H. Meng, Z.-H. Li, Z. Shu, X. Ma, and B.-X. Zhang Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells Am J Physiol Renal Physiol, March 1, 2007; 292(3): F1054 - F1064. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. D. Bell, G. F. DiBona, Y. Wang, and M. W. Brands Mechanisms for Renal Blood Flow Control Early in Diabetes as Revealed by Chronic Flow Measurement and Transfer Function Analysis J. Am. Soc. Nephrol., August 1, 2006; 17(8): 2184 - 2192. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Kang, I. Toma, A. Sipos, F. McCulloch, and J. Peti-Peterdi Quantitative imaging of basic functions in renal (patho)physiology Am J Physiol Renal Physiol, August 1, 2006; 291(2): F495 - F502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Z. Levine, M. Iacovitti, S. J. Robertson, and G. A. Mokhtar Modulation of single-nephron GFR in the db/db mouse model of type 2 diabetes mellitus Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R975 - R981. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Shi, X. Wang, K. H. Chon, and W. A. Cupples Tubuloglomerular feedback-dependent modulation of renal myogenic autoregulation by nitric oxide Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R982 - R991. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Just and W. J. Arendshorst Nitric oxide blunts myogenic autoregulation in rat renal but not skeletal muscle circulation via tubuloglomerular feedback J. Physiol., December 15, 2005; 569(3): 959 - 974. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Palm, D. G. Buerk, P.-O. Carlsson, P. Hansell, and P. Liss Reduced Nitric Oxide Concentration in the Renal Cortex of Streptozotocin-Induced Diabetic Rats: Effects on Renal Oxygenation and Microcirculation Diabetes, November 1, 2005; 54(11): 3282 - 3287. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Herrera and J. L. Garvin Recent Advances in the Regulation of Nitric Oxide in the Kidney Hypertension, June 1, 2005; 45(6): 1062 - 1067. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
