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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/R1561    most recent 00485.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Kopp, U. C. Articles by Hökfelt, T. Search for Related Content PubMed PubMed Citation Articles by Kopp, U. C. Articles by Hökfelt, T.

RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE₂-dependent activation of ₁- and ₂-adrenoceptors on renal sensory nerve fibers

¹Departments of Internal Medicine and Pharmacology, Department of Veterans Affairs Medical Center and University of Iowa Carver College of Medicine, Iowa City, Iowa; and ²Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden

Submitted 5 July 2007 ; accepted in final form 15 August 2007

Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA). To test whether the ERSNA-induced increases in ARNA involved norepinephrine activating -adrenoceptors on the renal sensory nerves, we examined the effects of renal pelvic administration of the ₁- and ₂-adrenoceptor antagonists prazosin and rauwolscine on the ARNA responses to reflex increases in ERSNA (placing the rat's tail in 49°C water) and renal pelvic perfusion with norepinephrine in anesthetized rats. Hot tail increased ERSNA and ARNA, 6,930 ± 900 and 4,870 ± 670%·s (area under the curve ARNA vs. time). Renal pelvic perfusion with norepinephrine increased ARNA 1,870 ± 210%·s. Immunohistochemical studies showed that the sympathetic and sensory nerves were closely related in the pelvic wall. Renal pelvic perfusion with prazosin blocked and rauwolscine enhanced the ARNA responses to reflex increases in ERSNA and norepinephrine. Studies in a denervated renal pelvic wall preparation showed that norepinephrine increased substance P release, from 8 ± 1 to 16 ± 1 pg/min, and PGE₂ release, from 77 ± 11 to 161 ± 23 pg/min, suggesting a role for PGE₂ in the norepinephrine-induced activation of renal sensory nerves. Prazosin and indomethacin reduced and rauwolscine enhanced the norepinephrine-induced increases in substance P and PGE₂. PGE₂ enhanced the norepinephrine-induced activation of renal sensory nerves by stimulation of EP4 receptors. Interaction between ERSNA and ARNA is modulated by norepinephrine, which increases and decreases the activation of the renal sensory nerves by stimulating ₁- and ₂-adrenoceptors, respectively, on the renal pelvic sensory nerve fibers. Norepinephrine-induced activation of the sensory nerves is dependent on renal pelvic synthesis/release of PGE₂.

substance P; EP4 receptor; pelvis; prazosin; rauwolscine

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