Stimulation of an intermolecular redox reaction by the combined action of high pressure and shear deformation

Author(s):  
V. B. Vol'eva ◽  
T. I. Prokofeva ◽  
E. V. Ivanova ◽  
V. A. Zhorin ◽  
V. V. Ershov ◽  
...  
1987 ◽  
Vol 34 (2) ◽  
pp. 677-687 ◽  
Author(s):  
V. A. Zhorin ◽  
Y. M. Beluza ◽  
V. V. Ivanov ◽  
Y. V. Epstein ◽  
N. S. Enikolopian ◽  
...  

2021 ◽  
pp. 130418
Author(s):  
Anderson J. Caires ◽  
Moara M. Castro ◽  
Luciano A. Montoro ◽  
Augusta Isaac ◽  
Roberto B. Figueiredo

2015 ◽  
Vol 57 (5-6) ◽  
pp. 320-328 ◽  
Author(s):  
A. V. Levina ◽  
L. A. Mal’tseva ◽  
A. A. Arkhangel’skaya ◽  
Yu. N. Loginov ◽  
N. N. Ozerets ◽  
...  

2019 ◽  
Vol 6 (4) ◽  
pp. 046506 ◽  
Author(s):  
A A Yaroslavzev ◽  
I A Evdokimov ◽  
B A Kulnitskiy ◽  
I A Perezhogin ◽  
V D Blank ◽  
...  

2010 ◽  
Vol 298 (3) ◽  
pp. F502-F509 ◽  
Author(s):  
K. Mutig ◽  
T. Saritas ◽  
S. Uchida ◽  
T. Kahl ◽  
T. Borowski ◽  
...  

Vasopressin influences salt and water transport in renal epithelia. This is coordinated by the combined action of V2 receptor-mediated effects along distinct nephron segments. Modulation of NaCl reabsorption by vasopressin has been established in the loop of Henle, but its role in the distal convoluted tubule (DCT), an effective site for fine regulation of urinary electrolyte composition and the target for thiazide diuretics, is largely unknown. The Na+-Cl− cotransporter (NCC) of DCT is activated by luminal trafficking and phosphorylation at conserved NH2-terminal residues. Here, we demonstrate the effects of short-term vasopressin administration (30 min) on NCC activation in Brattleboro rats with central diabetes insipidus (DI) using the V2 receptor agonist desmopressin (dDAVP). The fraction of NCC abundance in the luminal plasma membrane was significantly increased upon dDAVP as shown by confocal microscopy, immunogold cytochemistry, and Western blot, suggesting increased apical trafficking of the transporter. Changes were paralleled by augmented phosphorylation of NCC as detected by antibodies against phospho-threonine and phospho-serine residues (2.5-fold increase at Thr53 and 1.4-fold increase at Ser71). dDAVP-induced phosphorylation of NCC, studied in tubular suspensions in the absence of systemic effects, was enhanced as well (1.7-fold increase at Ser71), which points to the direct mode of action of vasopressin in DCT. Changes were more pronounced in early (DCT1) than in late DCT as distinguished by the distribution of 11β-hydroxysteroid dehydrogenase 2 in DCT2. These results suggest that the vasopressin-V2 receptor-NCC signaling cascade is a novel effector system to adjust transepithelial NaCl reabsorption in DCT.


1957 ◽  
Vol 189 (1) ◽  
pp. 132-136 ◽  
Author(s):  
C. Aravanis ◽  
A. Libretti ◽  
E. Jona ◽  
J. F. Polli ◽  
C. K. Liu ◽  
...  

The mechanism of pulmonary edema caused by stimulation of the central nervous system was studied in 33 dogs. Stimulation was obtained by the intracisternal injection of veratrine, or of air or saline under high pressure, or by electric stimulation of the hypothalamus. Pressure changes in the pulmonary artery, left atrium and left ventricle were recorded by means of three catheters introduced through the right external jugular vein and the left femoral artery. Experiments were performed with closed or open chest, and following ligation of the thoracic aorta and inferior cava. Lung opacity was studied as a means to estimate the blood content of this organ. Data obtained in closed-chest experiments suggest that a blood shift from the systemic to the pulmonary circulation may be a factor in veratrine-induced pulmonary edema. This was confirmed by the observation that, following mechanical exclusion of the systemic circulation, no pulmonary edema occurred while the changes of left ventricular pressure were minimal and inconstant. In these animals, pulmonary artery pressure still rose indicating vasoconstriction while an increase of lung opacity suggested that the vasoconstriction was greater in the pulmonary veins than in the arteries. Injection of air or saline under high pressure into the cisterna magna and faradic stimulation of the hypothalamus caused pulmonary hypertension, even after exclusion of the systemic circulation. In these experiments, a decreased lung opacity suggested that the pulmonary constriction was greater on the arterial than on the venous side. These findings are offered as evidence that the caliber of the pulmonary vessels may be influenced by central nervous system stimulation, an additional element to be considered in the mechanism of pulmonary edema.


2016 ◽  
Vol 7 (1) ◽  
Author(s):  
D. Santamaria-Perez ◽  
C. McGuire ◽  
A. Makhluf ◽  
A. Kavner ◽  
R. Chuliá-Jordan ◽  
...  

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