Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1995;25:581-586

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nakamura, A.
Right arrow Articles by Johns, E. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakamura, A.
Right arrow Articles by Johns, E. J.

(Hypertension. 1995;25:581-586.)
© 1995 American Heart Association, Inc.


Articles

Renal Nerves, Renin, and Angiotensinogen Gene Expression in Spontaneously Hypertensive Rats

Akio Nakamura; Edward J. Johns

From the Department of Physiology, The Medical School, Birmingham, UK.

Correspondence to Dr E.J. Johns, Department of Physiology, The Medical School, Birmingham B15 2TT, UK.

Abstract We compared the effect of the renal nerves on renal function, plasma renin activity, and renal renin and angiotensinogen mRNA contents in Wistar rats and spontaneously hypertensive rats (SHR). Rats were anesthetized with sodium pentobarbital, the left kidney was exposed, its nerves were sectioned, the ureter was cannulated, and a flow probe was placed on the renal artery. The renal nerves were stimulated for 1 hour to reduce renal blood flow by 15% and 30%, after which blood was removed for measurement of plasma renin activity, and kidneys were analyzed for renal renin and angiotensinogen mRNA. Frequency-related reductions in filtration rate were similar, from 15% to 50%, as was sodium excretion, from 30% to 70%, in both SHR and Wistar rats. Basal plasma renin activity and responses to nerve stimulation in SHR were approximately half those of Wistar rats (all P<.001). SHR renal renin mRNA concentrations were approximately three quarters those of Wistar rats and were unchanged by either low- or high-level renal nerve stimulation, whereas the higher rate increased renin mRNA approximately threefold (P<.05) in the Wistar rats. SHR renal angiotensinogen mRNA was one quarter that of the Wistar rats and was unaffected by nerve stimulation, whereas in the Wistar rats it was increased threefold (P<.05) by the low but not high level of nerve stimulation. These findings show that whereas the renal nerves are able to modulate hemodynamic and tubular functions relatively normally in SHR, their ability to increase renin release, renal renin, and angiotensinogen mRNA levels is depressed.


Key Words: sympathetic nervous system • gene expression • angiotensinogen • renin • kidney function • RNA, messenger




This article has been cited by other articles:


Home page
HypertensionHome page
M. W. Thompson, S. B. Smith, and C. D. Sigmund
Regulation of Human Renin mRNA Expression and Protein Release in Transgenic Mice
Hypertension, August 1, 1996; 28(2): 290 - 296.
[Abstract] [Full Text]