Reflex control of renal sympathetic nervous activity in heart failure

It is not completely clear if the renal sympathetic nerves are essential for normal renal function, however, it has been reasonably well established that the renal nerves can influence renal function under experimental conditions. These influences are manifested as changes in sodium excretion, urine flow, renin release, renal blood flow and glomerular filtration rate. Under conditions of stress the renal nerves can have powerful influences on renal function and, as a result, on systemic hemodynamics. Because renal sympathetic outflow is under central control, the reflex modulation of renal nerve activity is an extremely important factor in the control of salt and water balance. We have shown that cardiac and arterial baroreflex control of renal nerve activity is abnormal in chronic congestive heart failure. The mechanisms for this abnormality can reside in any arm of the reflex arc. The evidence from this and other laboratories has clearly implicated the afferent limb of these reflexes as being abnormal. Experiments done in anesthetized dogs with pacing induced heart failure have indicated that the central component of these reflexes are probably normal. The experiments described above cannot differentiate between abnormal afferent mechanisms and abnormal end organ responses to renal nerve stimulation. Several humoral mechanisms may be operative in heart failure to modulate renal nerve activity. These include bradykinin, prostaglandins and the renin-angiotensin aldosterone axis. Future work should be directed towards a further understanding of the role played by these and other humoral factors in the control of renal sympathetic outflow in heart failure.