scholarly journals Wistar Rats Resistant to the Hypertensive Effects of Ouabain Exhibit Enhanced Cardiac Vagal Activity and Elevated Plasma Levels of Calcitonin Gene-Related Peptide

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e108909 ◽  
Author(s):  
Elham Ghadhanfar ◽  
Maie Al-Bader ◽  
Marian Turcani
Neurology ◽  
2000 ◽  
Vol 55 (9) ◽  
pp. 1335-1340 ◽  
Author(s):  
M. Ashina ◽  
L. Bendtsen ◽  
R. Jensen ◽  
S. Schifter ◽  
I. Jansen-Olesen ◽  
...  

2002 ◽  
Vol 25 (3) ◽  
pp. 441-446 ◽  
Author(s):  
Junsuke KAWAI ◽  
Katsuyuki ANDO ◽  
Tatsuo SHIMOSAWA ◽  
Kiyonori HARII ◽  
Toshiro FUJITA

2005 ◽  
Vol 57 (6) ◽  
pp. 799-805 ◽  
Author(s):  
Fumihiko Katagiri ◽  
Shin Inoue ◽  
Yuhki Sato ◽  
Hiroki Itoh ◽  
Masaharu Takeyama

2013 ◽  
Vol 210 (11) ◽  
pp. 2161-2170 ◽  
Author(s):  
Yonatan Ganor ◽  
Anne-Sophie Drillet-Dangeard ◽  
Lucia Lopalco ◽  
Daniela Tudor ◽  
Giuseppe Tambussi ◽  
...  

Upon its mucosal entry, human immunodeficiency virus type 1 (HIV-1) is internalized by Langerhans cells (LCs) in stratified epithelia and transferred locally to T cells. In such epithelia, LCs are in direct contact with peripheral neurons secreting calcitonin gene–related peptide (CGRP). Although CGRP has immunomodulatory effects on LC functions, its potential influence on the interactions between LCs and HIV-1 is unknown. We show that CGRP acts via its receptor expressed by LCs and interferes with multiple steps of LC-mediated HIV-1 transmission. CGRP increases langerin expression, decreases selected integrins, and activates NF-κB, resulting in decreased HIV-1 intracellular content, limited formation of LC–T cell conjugates, and elevated secretion of the CCR5-binding chemokine CCL3/MIP-1α. These mechanisms cooperate to efficiently inhibit HIV-1 transfer from LCs to T cells and T cell infection. In vivo, HIV-1 infection decreases CGRP plasma levels in both vaginally SHIV-challenged macaques and HIV-1–infected individuals. CGRP plasma levels return to baseline after highly active antiretroviral therapy. Our results reveal a novel path by which a peripheral neuropeptide acts at the molecular and cellular levels to limit mucosal HIV-1 transmission and suggest that CGRP receptor agonists might be used therapeutically against HIV-1.


1993 ◽  
Vol 16 (9) ◽  
pp. 662-669 ◽  
Author(s):  
I. Odar-CederlÖf ◽  
E. Theodorsson ◽  
C.G. Eriksson ◽  
B. Hamberger ◽  
B. Tidgren ◽  
...  

Hypotension is a common and sometimes dangerous side effect of hemodialysis. Its etiology is multifactorial and largely unknown. Earlier studies on the role of endogenous blood pressure regulating agents such as catecholamines and renin have rendered conflicting results. We studied the influence of ultrafiltration and isovolemic hemodialysis separately on the plasma concentrations of the following blood pressure regulating agents: adrenaline, noradrenaline, dopamine, neuropeptide Y, calcitonin gene-related peptide (CGRP), renin (PRA), angiotensin II, vasopressin, aldosterone and Cortisol. During isolated ultrafiltration, plasma levels of two strong vasoconstrictors (noradrenaline and angiotensin II) and one strong vasodilator (calcitonin gene-related peptide, CGRP) increased significantly (noradrenaline 3.24 ± 0.60 nM to 4.31 ± 0.55 nM; p = 0.032, angiotensin II 19.74 ± 3.46 pmol/l to 28.49 ± 7.24 pmol/l; p= 0.047) No symptomatic hypotension occurred. At the end of isovolemic hemodialysis, plasma levels of all the vasoconstricting agents had decreased to pretreatment values, but those of CGRP had continued to rise (from 85.3 ± 17.6 pmol/l to 114.5 ± 25.3 pmol/l, p=0.031). During isovolemic hemodialysis, blood pressure fell to symptomatic levels, but was restored at the end of treatment. The study shows that hemodialysis patients respond to fluid removal by ultrafiltration with an increase in plasma levels of CGRP, noradrenaline and angiotensin II. The net effect is an appropriate vasoconstriction and adequate blood pressure is maintained during isolated ultrafiltration. During hemodialysis, the patients’ blood volumes remained unchanged as evident by a stable hematocrit, the vasoconstrictor hormones returned to normal levels, but in several patients there was a continuous release of vasodilating CGRP. Hypotension, then occurred in these patients due to the imbalance between vasoconstricting and vasodilating factors.


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