Presented at the Australian Physiological and Pharmacological Society Symposium Hormonal, Metabolic and Neural Control of the Kidney, September 2003. The papers in these proceedings were peer reviewed under the supervision of the APPS Editor.
NEURAL CONTROL OF RENAL MEDULLARY PERFUSION
Article first published online: 28 MAY 2004
Clinical and Experimental Pharmacology and Physiology
Volume 31, Issue 5-6, pages 387–396, May 2004
How to Cite
Eppel, G. A., Malpas, S. C., Denton, K. M. and Evans, R. G. (2004), NEURAL CONTROL OF RENAL MEDULLARY PERFUSION. Clinical and Experimental Pharmacology and Physiology, 31: 387–396. doi: 10.1111/j.1440-1681.2004.04003.x
The papers are being published with the permission of APPS and were initially published on the APPS website http://www.apps.org.au
- Issue published online: 28 MAY 2004
- Article first published online: 28 MAY 2004
- Received 30 October 2003; revision 21 January 2004; accepted 30 January 2004.
- blood flow;
- innervation density;
- kidney medulla;
- laser Doppler flowmetry;
- nitric oxide;
- sympathetic nervous system
1. There is strong evidence that the renal medullary circulation plays a key role in long-term blood pressure control. This, and evidence implicating sympathetic overactivity in development of hypertension, provides the need for understanding how sympathetic nerves affect medullary blood flow (MBF).
2. The precise vascular elements that regulate MBF under physiological conditions are unknown, but likely include the outer medullary portions of descending vasa recta and afferent and efferent arterioles of juxtamedullary glomeruli, all of which receive dense sympathetic innervation.
3. Many early studies of the impact of sympathetic drive on MBF were flawed, both because of the methods used for measuring MBF and because single and often intense neural stimuli were tested.
4. Recent studies have established that MBF is less sensitive than cortical blood flow (CBF) to electrical renal nerve stimulation, particularly at low stimulus intensities. Indeed, MBF appears to be refractory to increases in endogenous renal sympathetic nerve activity within the physiological range in all but the most extreme cases.
5. Multiple mechanisms appear to operate in concert to blunt the impact of sympathetic drive on MBF, including counter-regulatory roles of nitric oxide and perhaps even paradoxical angiotensin II-induced vasodilatation. Regional differences in the geometry of glomerular arterioles are also likely to predispose MBF to be less sensitive than CBF to any given vasoconstrictor stimulus.
6. Failure of these mechanisms would promote reductions in MBF in response to physiological activation of the renal nerves, which could, in turn, lead to salt and water retention and hypertension.