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Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats.
Anesthesiology. 2009 Feb; 110(2):361-9.A

Abstract

BACKGROUND

Prostaglandin I2 (PGI2) produced by endothelial cells improves ischemia/reperfusion-induced acute renal injury by inhibiting leukocyte activation in rats. However, the underlying mechanism(s) of increased PGI2 production is not fully understood. Activation of sensory neurons increases endothelial PGI2 production by releasing calcitonin gene-related peptide (CGRP) in rats with hepatic ischemia or reperfusion. We examined here whether activation of sensory neurons increases PGI2 endothelial production, thereby reducing ischemia/reperfusion-induced acute renal injury.

METHODS

Anesthetized rats were subjected to 45 min of renal ischemia/reperfusion. Rats were pretreated with CGRP, capsazepine (a vanilloid receptor-1 antagonist), CGRP(8-37) (a CGRP receptor antagonist), or indomethacin (a cyclooxygenase inhibitor), or subjected to denervation of primary sensory nerves before ischemia/reperfusion.

RESULTS

Renal tissue levels of CGRP and 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2, increased after renal ischemia/reperfusion, peaking at 1 h after reperfusion. Overexpression of CGRP was also noted at 1 h after reperfusion. Increases in renal tissue levels of 6-keto-prostaglandin F1alpha at 1 h after reperfusion were significantly inhibited by pretreatment with capsazepine, CGRP(8-37), and indomethacin. Pretreatment with capsazepine, CGRP(8-37), indomethacin, and denervation of primary sensory nerves significantly increased blood urea nitrogen and serum creatinine levels, renal vascular permeability, renal tissue levels of myeloperoxidase activity, cytokine-induced neutrophil chemoattractant, and tumor necrosis factor-alpha, and decreased renal tissue blood flow. However, pretreatment with CGRP significantly improved these changes.

CONCLUSIONS

Our results suggest activation of sensory neurons in the pathologic process of ischemia/reperfusion-induced acute renal injury. Such activation reduces acute renal injury by attenuating inflammatory responses through enhanced endothelial PGI2 production.

Authors+Show Affiliations

Department of Anesthesiology and Critical Care Medicine, Oita University Faculty of Medicine, Yufu, Oita, Japan. mizutani@med.oita-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19194162

Citation

Mizutani, Akio, et al. "Activation of Sensory Neurons Reduces Ischemia/reperfusion-induced Acute Renal Injury in Rats." Anesthesiology, vol. 110, no. 2, 2009, pp. 361-9.
Mizutani A, Okajima K, Murakami K, et al. Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats. Anesthesiology. 2009;110(2):361-9.
Mizutani, A., Okajima, K., Murakami, K., Mizutani, S., Kudo, K., Uchino, T., Kadoi, Y., & Noguchi, T. (2009). Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats. Anesthesiology, 110(2), 361-9. https://doi.org/10.1097/ALN.0b013e3181942f3c
Mizutani A, et al. Activation of Sensory Neurons Reduces Ischemia/reperfusion-induced Acute Renal Injury in Rats. Anesthesiology. 2009;110(2):361-9. PubMed PMID: 19194162.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of sensory neurons reduces ischemia/reperfusion-induced acute renal injury in rats. AU - Mizutani,Akio, AU - Okajima,Kenji, AU - Murakami,Kazunori, AU - Mizutani,Sachiko, AU - Kudo,Kyosuke, AU - Uchino,Tetsuya, AU - Kadoi,Yuji, AU - Noguchi,Takayuki, PY - 2009/2/6/entrez PY - 2009/2/6/pubmed PY - 2009/3/6/medline SP - 361 EP - 9 JF - Anesthesiology JO - Anesthesiology VL - 110 IS - 2 N2 - BACKGROUND: Prostaglandin I2 (PGI2) produced by endothelial cells improves ischemia/reperfusion-induced acute renal injury by inhibiting leukocyte activation in rats. However, the underlying mechanism(s) of increased PGI2 production is not fully understood. Activation of sensory neurons increases endothelial PGI2 production by releasing calcitonin gene-related peptide (CGRP) in rats with hepatic ischemia or reperfusion. We examined here whether activation of sensory neurons increases PGI2 endothelial production, thereby reducing ischemia/reperfusion-induced acute renal injury. METHODS: Anesthetized rats were subjected to 45 min of renal ischemia/reperfusion. Rats were pretreated with CGRP, capsazepine (a vanilloid receptor-1 antagonist), CGRP(8-37) (a CGRP receptor antagonist), or indomethacin (a cyclooxygenase inhibitor), or subjected to denervation of primary sensory nerves before ischemia/reperfusion. RESULTS: Renal tissue levels of CGRP and 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2, increased after renal ischemia/reperfusion, peaking at 1 h after reperfusion. Overexpression of CGRP was also noted at 1 h after reperfusion. Increases in renal tissue levels of 6-keto-prostaglandin F1alpha at 1 h after reperfusion were significantly inhibited by pretreatment with capsazepine, CGRP(8-37), and indomethacin. Pretreatment with capsazepine, CGRP(8-37), indomethacin, and denervation of primary sensory nerves significantly increased blood urea nitrogen and serum creatinine levels, renal vascular permeability, renal tissue levels of myeloperoxidase activity, cytokine-induced neutrophil chemoattractant, and tumor necrosis factor-alpha, and decreased renal tissue blood flow. However, pretreatment with CGRP significantly improved these changes. CONCLUSIONS: Our results suggest activation of sensory neurons in the pathologic process of ischemia/reperfusion-induced acute renal injury. Such activation reduces acute renal injury by attenuating inflammatory responses through enhanced endothelial PGI2 production. SN - 1528-1175 UR - https://www.unboundmedicine.com/medline/citation/19194162/Activation_of_sensory_neurons_reduces_ischemia/reperfusion_induced_acute_renal_injury_in_rats_ L2 - https://pubs.asahq.org/anesthesiology/article-lookup/doi/10.1097/ALN.0b013e3181942f3c DB - PRIME DP - Unbound Medicine ER -