Relaxation evoked by extracellular Ca2+ in rat aorta is nerve-independent and involves sarcoplasmic reticulum and L-type Ca2+ channel.
The perivascular nerve network expresses a Ca2+ receptor that is activated by high extracellular Ca2+ concentrations and causes vasorelaxation in resistance arteries. We have verified the influence of perivascular nerve fibers on the Ca2+-induced relaxation in aortic rings. To test our hypothesis, either pre-contracted aortas isolated from rats after sensory denervation with capsaicin or aortic rings acutely denervated with phenol were stimulated to relax with increasing extracellular Ca2+ concentration. We also studied the role of the endothelium on the Ca2+-induced relaxation, and we verified the participation of endothelial/nonendothelial nitric oxide and cyclooxygenase-arachidonic acid metabolites. Additionally, the role of the sarcoplasmic reticulum, K+ channels and L-type Ca2+ channels on the Ca2+-induced relaxation were evaluated. We have observed that the Ca2+-induced relaxation is completely nerve independent, and it is potentiated by endothelial nitric oxide (NO). In endothelium-denuded aortic rings, indomethacin and AH6809 (PGF2alpha receptor antagonist) enhance the relaxing response to Ca2+. This relaxation is inhibited by thapsigargin and verapamil, while was not altered by tetraethylammonium. In conclusion, we have shown that perivascular nervous fibers do not participate in the Ca2+-induced relaxation, which is potentiated by endothelial NO. In endothelium-denuded preparations, indomethacin and AH6809 enhance the relaxation induced by Ca2+. The relaxing response to Ca2+ was impaired by verapamil and thapsigargin, revealing the importance of L-type Ca2+ channels and sarcoplasmic reticulum in this response.
Rocha
Matheus L
ML
Department of Physics and Chemistry, Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Av do Café s/n, 14040-903, Ribeirão Preto, SP, Brazil. rochaml@usp.br
Bendhack
Lusiane M
LM
D000818:Animals; D001013:Aorta, Thoracic / Q000294:innervation / Q000502:physiology*; D016718:Arachidonic Acid / Q000378:metabolism; D002118:Calcium / Q000008:administration & dosage / Q000502:physiology*; D020746:Calcium Channels, L-Type / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000502:physiology; D045604:Extracellular Fluid / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D009121:Muscle Denervation; D009569:Nitric Oxide / Q000502:physiology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D020746:Calcium Channels, L-Type; D016718:Arachidonic Acid; D009569:Nitric Oxide; D011451:Prostaglandin-Endoperoxide Synthases; D002118:Calcium