The kidney really does tell the brain what to do!

Abstract

‘The brain renin–angiotensin system appears to be upregulated and may be involved in hypertension and sympathetic overactivity in the compensated stage of chronic renal failure rats by subtotal nephrectomy.’ Angiotensin II within the brain is recognized as being involved with autonomic control and regulation of sympathetic outflow to the kidney. Moreover, there is a body of evidence supporting the view that in kidney disease renal sensory receptors are activated and cause a sympatho-excitation contributing to the associated hypertension. The report by Nishimura et al. in this issue brings together these two concepts by providing evidence for a link between them. They have used a model of 5/6th nephrectomy in the spontaneously hypertensive rat, where renal failure develops rapidly, and shown that whereas the exacerbation of the hypertensive state suppresses the peripheral renin–angiotensin system, that existing in the hypothalamus and brain stem is enhanced. This in itself is a significant point in that it demonstrates that the two systems can be modulated independently of each other. Furthermore, the enhanced hypertension and urinary catecholamine excretion in the renal failure rats is prevented by dorsal rhizotomy, which interrupts sensory information from the kidney going to the brain. These observations reinforce the concept that the kidney can determine the level of sympathetic outflow to the periphery.