caa a22 4500 445883715 CHVBK 20180317145552.0 cr unu---uuuuu 170323e20110401xx s 000 0 eng 10.1007/s10157-010-0382-0 doi (NATIONALLICENCE)springer-10.1007/s10157-010-0382-0 Effects of connexin-mimetic peptides on perfusion pressure in response to phenylephrine in isolated, perfused rat kidneys [Elektronische Daten] [Honglan Piao, Ayako Sato, Yukiko Nozawa, Wei Sun, Tetsuo Morioka, Takashi Oite] Background: Gap junction intercellular communication plays a fundamental role in various tissues and organs. Gap junctions transfer ions and molecules between adjacent cells and are formed by connexins (Cx). It is supposed that vascular conducted responses, which most likely spread through gap junctions in vascular beds, regulate microcirculatory blood flow and maintain vascular resistance. This study provides functional evidence supporting the critical role of gap junctions in a physiological setting and in phenylephrine (PE)-induced vasoconstriction using an ex vivo kidney perfusion technique. Methods: Using the isolated, perfused kidney model, infusion of gap junction inhibitors and PE, we examined the local effect of gap junction communication. Additionally, gap junction proteins Cx37, Cx40 and Cx43 were detected by immunofluorescence. Results: First, changes in the perfusion pressure were analyzed by infusing the nonselective gap junction uncoupler, 18α-glycyrrhetinic acid (18α-GA), and specific connexin-mimetic peptide inhibitors, 37,43Gap27, 40Gap27 and 43Gap26. Administration of 18α-GA and 43Gap26 significantly elevated perfusion pressure while infusion of 40Gap27 and 37,43Gap27 had no effect. Second, we examined the effect of infusing gap junction inhibitors on PE-induced vasoconstriction. Infusion of 18α-GA and 40Gap27 significantly suppressed the increase in perfusion pressure induced by PE, while 43Gap26 and 37,43Gap27 had no effect. Third, we confirmed by immunofluorescence that Cx37, Cx40 and Cx43 were found in the endothelial cells of interstitial microvessels and that Cx40 was localized in glomerular mesangial cells as well as in smooth muscle cells of the juxtaglomerular area. Conclusions: This study showed that Cx43 plays a pivotal role in regulating renal vascular resistance and that Cx40 attenuates PE-induced vasoconstriction. These results provide new evidence that gap junctions may control renal circulation and vascular responses. Japanese Society of Nephrology, 2010 Connexin nationallicence Gap junction nationallicence Phenylephrine nationallicence Resistant artery nationallicence Piao Honglan Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut Sato Ayako Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut Nozawa Yukiko Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut Sun Wei Department of Nephrology, Affiliated Hospital of Nan Jing University of Traditional Chinese Medicine, Nanjing, China aut Morioka Tetsuo Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut Oite Takashi Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut Clinical and Experimental Nephrology Springer Japan 15/2(2011-04-01), 203-211 1342-1751 15:2<203 2011 15 10157 https://doi.org/10.1007/s10157-010-0382-0 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s10157-010-0382-0 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Piao Honglan Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut NATIONALLICENCE 700 1- Sato Ayako Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut NATIONALLICENCE 700 1- Nozawa Yukiko Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut NATIONALLICENCE 700 1- Sun Wei Department of Nephrology, Affiliated Hospital of Nan Jing University of Traditional Chinese Medicine, Nanjing, China aut NATIONALLICENCE 700 1- Morioka Tetsuo Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut NATIONALLICENCE 700 1- Oite Takashi Department of Cellular Physiology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University, 1-757 Asahimachi-dori, 951-8510, Niigata, Japan aut NATIONALLICENCE 773 0- Clinical and Experimental Nephrology Springer Japan 15/2(2011-04-01), 203-211 1342-1751 15:2<203 2011 15 10157 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer