The Autonomic Cardiorenal Crosstalk: Pathophysiology and Implications for Heart Failure Management

Abstract

Excessive sympathetic drive is undoubtedly a major contributing factor to the pathogenesis of hypertension and to the progression of HF. Importantly, much of the excessive sympathetic activity in these conditions targets the kidney, where it leads to inappropriate sodium retention, renin stimulation, and diminished renal function. In addition, the kidney itself is a source of increased sympathetic activation by way of the renal somatic afferent nerves. Various modalities currently allow measurement of sympathetic activation. The clinical relevance of information on autonomic cardiac control is supported by the evidence that increased sympathetic activity is associated with increased mortality in myocardial infarction and heart failure patients, and with an increased risk of sudden arrhythmic death. Many critically important changes occur in the kidney in the setting of cardiac dysfunction and neurohormonal activation. The escalating congestion resulting from these mutually detrimental cardiorenal interactions has profound implications for all abdominal vascular systems, including the splanchnic, intestinal, hepatic, and splenic circulations. The cardiorenal syndrome is therefore a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. On the basis of this definition, five types of the cardiorenal syndrome have been identified and each has unique aspects of autonomic crosstalk between the heart and the kidney. In addition to landmark advances in the pharmacological treatment of neurohormonal activation, innovative non-pharmacological interventions are now evolving that can favorably modulate the cardiac and renal autonomic activities.