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10.1016/j.autneu.2017.01.007 http://scihub22266oqcxt.onion/10.1016/j.autneu.2017.01.007 C5530865!5530865!28143710     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Auton+Neurosci 2017 ; 203 (ä): 58-66 Nephropedia Template TP {{tp|p=28143710|t=2017. Hepatic and renal mechanisms underlying the osmopressor response |pdf=|usr=}}{{28143710}} gab.com Text Hepatic and renal mechanisms underlying the osmopressor response JO: Auton Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=28143710 #FOAvip Increased blood pressure (BP) is observed in patients with impaired baroreflexes after water drinking. The stimulus for this effect is low blood osmolality, and it has been termed the osmopressor response (OPR). The BP increase is associated with activation of the sympathetic nervous system and a requirement for transient receptor potential vanilloid 4 (TRPV4) channels. However, the mechanisms underlying the OPR are poorly understood. We tested the hypothesis that hypotonicity is sensed in the portal area to initiate the OPR. Sino-aortic denervated mice were used and BP was monitored for 30 min after fluid infusion while mice were under anesthesia. Infusion of hypotonic fluid (0.45% saline), but not of isotonic 0.9% saline, directly into the portal vein, produced an immediate OPR (increase in BP with saline 0.45%: 15 ± 13 vs. 0.9%: ?7 ± 2 mm Hg, p = 0.003; AUC: 0.45%: 150 ± 99, n = 7 vs. 0.9%: ?74 ± 60 mm Hg · min, n = 5, p = 0.003). However, 0.45% saline was not able to trigger a similar response in TRPV4?/? mice (?BPTRPV4: ?2 ± 5 mm Hg, n = 8, p = 0.009). Hypotonic saline did not raise BP when infused at the same speed and volume into the jugular vein (jugular: ?5 ± 6 mm Hg, p = 0.002, compared to portal). Denervation of the splanchnic nerve by celiac ganglionectomy (CGX) did not abolish the OPR (CGX: 15 ± 11 vs. Sham: 16 ± 6 mm Hg, p = 0.34). Renal denervation diminished the OPR elicited by duodenal water infusion (denervation: 9 ± 4 vs. sham: 31 ± 15 mm Hg, p = 0.016). Therefore, hypotonicity in the portal circulation, probably sensed by TRPV4 channels, triggers the OPR and intact renal nerves are needed for the full response. Twit Text FOAVip Hepatic and renal mechanisms underlying the osmopressor response ????Auton Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=28143710 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28143710 #FOAvip English Wikipedia <ref>{{Cite pmid|28143710}}</ref> Hepatic and renal mechanisms underlying the osmopressor response #MMPMID28143710 Mai TH; Garland EM; Diedrich A; Robertson D Auton Neurosci 2017[Mar]; 203 (ä): 58-66 PMID28143710show ga Increased blood pressure (BP) is observed in patients with impaired baroreflexes after water drinking. The stimulus for this effect is low blood osmolality, and it has been termed the osmopressor response (OPR). The BP increase is associated with activation of the sympathetic nervous system and a requirement for transient receptor potential vanilloid 4 (TRPV4) channels. However, the mechanisms underlying the OPR are poorly understood. We tested the hypothesis that hypotonicity is sensed in the portal area to initiate the OPR. Sino-aortic denervated mice were used and BP was monitored for 30 min after fluid infusion while mice were under anesthesia. Infusion of hypotonic fluid (0.45% saline), but not of isotonic 0.9% saline, directly into the portal vein, produced an immediate OPR (increase in BP with saline 0.45%: 15 ± 13 vs. 0.9%: ?7 ± 2 mm Hg, p = 0.003; AUC: 0.45%: 150 ± 99, n = 7 vs. 0.9%: ?74 ± 60 mm Hg · min, n = 5, p = 0.003). However, 0.45% saline was not able to trigger a similar response in TRPV4?/? mice (?BPTRPV4: ?2 ± 5 mm Hg, n = 8, p = 0.009). Hypotonic saline did not raise BP when infused at the same speed and volume into the jugular vein (jugular: ?5 ± 6 mm Hg, p = 0.002, compared to portal). Denervation of the splanchnic nerve by celiac ganglionectomy (CGX) did not abolish the OPR (CGX: 15 ± 11 vs. Sham: 16 ± 6 mm Hg, p = 0.34). Renal denervation diminished the OPR elicited by duodenal water infusion (denervation: 9 ± 4 vs. sham: 31 ± 15 mm Hg, p = 0.016). Therefore, hypotonicity in the portal circulation, probably sensed by TRPV4 channels, triggers the OPR and intact renal nerves are needed for the full response. äHepatic and renal mechanisms underlying the osmopressor response (epmc).pdf DeepDyve Pubget Overpricing