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We have found that renal artery adenosine infusion produces hypertension associated with increased activity of the sympathetic nervous system in a uninephrectomized conscious dog with intact renal nerves. The objectives of this study were to: 1) compare the hemodynamic responses to renal artery adenosine infusion in the conscious and α–chloralose–anesthetized dog with both kidneys intact; and 2) to correlate the hemodynamic and afferent renal nerve responses to renal artery and renal pelvic adenosine administration. Infusion of adenosine into the renal artery in the conscious animal produced a significant 22 mm Hg rise in mean arterial pressure, while infusion of adenosine into the renal artery in the α–chloralose–anesthetized dog produced a significant 11 mm Hg rise. Nerve traffic studies revealed that an increase in afferent renal nerve activity occurred 80 to 150 seconds after initiation of renal artery adenosine infusion. In contrast, an increase in afferent renal nerve activity was observed within 15 to 20 seconds after initiation of renal pelvic adenosine administration. Despite the difference in onset of afferent renal nerve activity, the degree of hemodynamic responses with renal pelvic or renal artery adenosine administration were the same. The data indicate that: 1) the response to renal artery infusion of adenosine is attenuated by α–chloralose anesthesia; 2) intrarenal adenosine produces increased afferent renal nerve activity; and 3) renal pelvic adenosine infusion produces an earlier but identical hemodynamic response as renal artery adenosine infusion. These observations extend our previous work, suggesting that intrarenal adenosine produces hypertension by activating the sympathetic nervous system via the afferent renal nerves. These observations also suggest that adenosine-sensitive nerve endings are located within or near the renal pelvis.

Hemodynamic and afferent renal nerve responses to intrarenal adenosine in the dog.