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This Article Full Text Full Text (PDF) All Versions of this Article: 90/2/163    most recent expphysiol.2004.029025v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Johns, E. J Search for Related Content PubMed PubMed Citation Articles by Johns, E. J Related Collections Symposia Papers Cardiovascular control

¹ Department of Physiology, University College Cork, Ireland

Abstract

The kidney plays a central role in ensuring cardiovascular homeostasis, in that it functions to ensure that the variation in fluid intake is matched to that lost through normal everyday metabolism. The autonomic nervous system, via the renal sympathetic nerves, allows kidney function to be adjusted dynamically in response to changes in sensory information arising from the cardiovascular system, the soma, viscera and the higher cortical centres. At the level of the kidney, the sympathetic nerves innervate the vascular and tubular components, thereby regulating renal haemodynamics and fluid reabsorption. The processing of sensory information by the central nervous system involves nuclei associated with cardiovascular control and it is these nuclei which are influenced by angiotensin II generated locally in the brain. The angiotensin II appears to act in a neuromodulatory fashion or as a neurotransmitter. There is now sound evidence that the baroreflex control of sympathetic outflow to the kidney, at least, is under tonic inhibitory control by brain angiotensin II, which also facilitates the impact of the somatosensory system in mediating sympatho-excitation. The significance of brain angiotensin II in mediating reflex activation of the sympathetic nerves from other sensory systems has not yet been defined and needs to be resolved. Interestingly, it may be that deficits in the production of brain angiotensin II at these nuclei could contribute in part to the genesis of hypertension.

(Received 3 November 2004; accepted after revision 9 December 2004; first published online 16 December 2004)
Corresponding author E. J. Johns: Sir Bertram Windle Building, University College Cork, College Road, Cork, Ireland. Email: e.j.johns{at}ucc.i.e

This article has been cited by other articles:

				C. Huang, M. Yoshimoto, K. Miki, and E. J. Johns The contribution of brain angiotensin II to the baroreflex regulation of renal sympathetic nerve activity in conscious normotensive and hypertensive rats J. Physiol., July 15, 2006; 574(2): 597 - 604. [Abstract] [Full Text] [PDF]