Role of renal afferent nerves in obesity-induced hypertension.

Recent studies have shown that the sympathetic nervous system contributes to hypertension associated with obesity. The mechanisms that stimulate sympathetic activity in obesity are unclear, although renal sensory receptors (mechano- and/or chemoreceptors) have been postulated to play a role. The present study determined whether selective removal of renal afferent nerves, while leaving renal efferent fibers intact, attenuated obesity hypertension in dogs. Selective renal afferent denervation was accomplished by dorsal root rhizotomy between T10 and L2 segments which convey the renal afferent nerves. Experiments were conducted in chronically instrumented dogs in which mean arterial pressure (MAP), cardiac output (CO), and heart rate (HR) were monitored continuously 24 hours/day. After control measurements, obesity was induced in 6 control dogs and 6 renal afferent denervated (RAD) dogs by supplementing the diet with 0.5-0.9 kg of beef fat/day. After 5 weeks of the high fat diet, body weight increased 15.0±1 and 16.1±1 kg in control and RAD dogs, respectively. After 5 weeks of the high fat diet, MAP increased 21±2 and 18±4 mmHg in control and RAD dogs, respectively, values that were not significantly different. Similar increases in CO (67±11 %, 60±12%) and HR (72±12%, 62±8%), and reductions in total peripheral resistance (−23±6%, −21±5%) were observed in control and RAD dogs, respectively. The increases in MAP in control and RAD dogs were associated with similar increases in plasma renin activity, reductions in fractional sodium excretion, and increases in extracellular fluid volume. Thus, obesity-induced hypertension in dogs is associated with marked sodium retention and volume expansion, as well as increased cardiac output and heart rate. Although our previous studies suggest a role for the sympathetic nervous system in mediating these responses, results from the present study indicate that the renal afferent nerves do not play a major role in the development of obesity-induced hypertension.