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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Early potential impairment of renal sensory nerves in streptozotocin-induced diabetic rats: role of neurokinin receptors

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Author(s):
Boer, Patricia Aline [1] ; Rossi, Cintia de Lima [1] ; Mesquita, Flavia Fernandes [1] ; Gontijo, Jose A. R. [1]
Total Authors: 4
Affiliation:
[1] Univ Estadual Campinas, Fac Ciencias Med, Nucleo Med & Cirurgia Expt, Disciplina Med Interna, Lab Metab Hidro Salino, BR-13083970 Campinas, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Nephrology Dialysis Transplantation; v. 26, n. 3, p. 823-832, MAR 2011.
Web of Science Citations: 4
Abstract

Background. Electrophysiological studies in the mammalian kidney have identified two major classes of sensory receptors of the afferent renal nerves; chemoreceptors (CR) and mechanoreceptors (MR). The localization of calcitonin gene-related peptide (CGRP) and substance P (SP) in these renal pelvic sensory neurons provides an anatomical basis for a possible functional interaction between the two neuropeptides and SP receptor. The present study was performed to examine the possible changes in the responsiveness of renal sensory SP and CGRP receptors in rats with streptozotocin (STZ)-induced diabetes mellitus. Due to the crucial role of renal pelvic SP and CGRP receptors in the activation of renal sensory neurons by various stimuli, we examined whether the responsiveness of MR or CR activation and the dorsal root ganglia content of neuropeptides and neurokinin 1 receptors (NK(1)R) were altered in diabetic rats compared with non-diabetic rats. Methods. Afferent renal nerve activity (ARNA) was recorded from the peripheral portion of the cut end of one renal nerve branch placed on a bipolar silver wire electrode. T(13) dorsal root ganglia (DRG) immunoreactivity was performed to NK(1)R, SP and CGRP. Results. The results of the current study confirmed that the stimulation of renal MR and CR elicited a renorenal reflex response, and that the renal pelvic administration of SP and CGRP increased ipsilateral ARNA and contralateral urinary sodium excretion with no changes in arterial pressure. We also found a decrease in NK(1)R expression followed by an increase in SP and CGRP levels in the DRG of diabetic rats. The ARNA response, produced by renal pelvic MR and CR stimulation, was found to be significantly attenuated in the STZ-induced diabetic model. Conclusions. These data may indicate a compensatory synthesis and/or abnormal axonal delivery of neurokinins from the cell body to synaptic portions of the neuron as the underlying reason for attenuated ARNA in renal sensory neurons of diabetic rats. (AU)