scholarly journals Role of TLR4 expression in experimental hypertension

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Gisele Facholi Bomfim ◽  
Rita Tostes ◽  
Zuleica Fortes ◽  
Maria Helena Catelli Carvalho
Keyword(s):  
Experimental Hypertension ◽  
Tlr4 Expression

scholarly journals Mild DOCA-salt hypertension: sympathetic system and role of renal nerves

2011 ◽  
Vol 300 (5) ◽  
pp. H1781-H1787 ◽  
Author(s):  
Sachin S. Kandlikar ◽  
Gregory D. Fink
Keyword(s):  
Control Period ◽  
Whole Body ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Sympathetic Activation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Salt Hypertension ◽  
Hypertension Development

Excess sympathetic nervous system activity (SNA) is linked to human essential and experimental hypertension. To test whether sympathetic activation is associated with a model of deoxycorticosterone acetate (DOCA)-salt hypertension featuring two kidneys and a moderate elevation of blood pressure, we measured whole body norepinephrine (NE) spillover as an index of global SNA. Studies were conducted in chronically catheterized male Sprague-Dawley rats drinking water containing 1% NaCl and 0.2% KCl. After a 7-day surgical recovery and a 3-day control period, a DOCA pellet (50 mg/kg) was implanted subcutaneously in one group of rats (DOCA), while the other group underwent sham implantation (Sham). NE spillover was measured on control day 2 and days 7 and 14 after DOCA administration or sham implantation. During the control period, mean arterial pressure (MAP) was similar in Sham and DOCA rats. MAP was significantly increased in the DOCA group compared with the Sham group after DOCA administration ( day 14: Sham = 109 ± 5.3, DOCA = 128 ± 3.6 mmHg). However, plasma NE concentration, clearance, and spillover were not different in the two groups at any time. To determine whether selective sympathetic activation to the kidneys contributes to hypertension development, additional studies were performed in renal denervated (RDX) and sham-denervated (Sham-DX) rats. MAP, measured by radiotelemetry, was similar in both groups during the control and DOCA treatment periods. In conclusion, global SNA is not increased during the development of mild DOCA-salt hypertension, and fully intact renal nerves are not essential for hypertension development in this model.

scholarly journals The Role of Acrolein and NADPH Oxidase in the Granulocyte-Mediated Growth-Inhibition of Tumor Cells

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 292 ◽  
Author(s):  
Morana Jaganjac ◽  
Tanja Matijevic Glavan ◽  
Neven Zarkovic
Keyword(s):  
Nadph Oxidase ◽  
Tumor Cell ◽  
Signaling Pathways ◽  
Tumor Cells ◽  
Redox Homeostasis ◽  
Peroxidation Of Lipids ◽  
Tlr4 Expression ◽  
Antitumor Effects ◽  
Reactive Aldehydes

: Although granulocytes are the most abundant leukocytes in human blood, their involvement in the immune response against cancer is not well understood. While granulocytes are known for their “oxidative burst” when challenged with tumor cells, it is less known that oxygen-dependent killing of tumor cells by granulocytes includes peroxidation of lipids in tumor cell membranes, yielding formation of reactive aldehydes like 4-hydroxynonenal (4-HNE) and acrolein. In the present work, we investigate the role of reactive aldehydes on cellular redox homeostasis and surface toll-like receptor 4 (TLR4) expression. We have further study the granulocyte-tumor cell intercellular redox signaling pathways. The data obtained show that granulocytes in the presence of 4-HNE and acrolein induce excessive ROS formation in tumor cells. Acrolein was also shown to induce granulocyte TLR4 expression. Furthermore, granulocyte-mediated antitumor effects were shown to be mediated via HOCl intracellular pathway by the action of NADPH oxidase. However, further studies are needed to understand interaction between TLR4 and granulocyte-tumor cell intercellular signaling pathways.

scholarly journals Downregulation of Lung Toll-Like Receptor 4 Could Effectively Attenuate Liver Transplantation-Induced Pulmonary Damage at the Early Stage of Reperfusion

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xinjin Chi ◽  
Weifeng Yao ◽  
Ailan Zhang ◽  
Mian Ge ◽  
Jun Cai ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Polymorphonuclear Leukocytes ◽  
Early Stage ◽  
Pulmonary Inflammation ◽  
Toll Like Receptor ◽  
Tlr4 Expression ◽  
Toll Like Receptor 4 ◽  
Pulmonary Damage ◽  
Autologous Liver

Acute lung injury (ALI) is a severe complication of orthotopic liver transplantation (OLT) with unclear underline mechanism. Toll-like receptor 4 (TLR4) has been identified as a key receptor mediating inflammation. We hypothesized that TLR4-mediated pulmonary inflammation may contribute to development of ALI during OLT. Patients with or without ALI were observed for serum cytokines and expression of TLR4 on peripheral blood polymorphonuclear leukocytes (PMNs). Next, rats which underwent orthotopic autologous liver transplantation (OALT) were divided into sham and model groups. Pulmonary function and the level of TLR4 expression and cytokines were analyzed. Furthermore, the role of TLR4 in OALT-mediated ALI was assessed in rats treated with TLR4-siRNA before OALT. The PMNs TLR4 expression and the serum TNF-αand IL-βlevel were higher in patients with ALI than those with non-ALI. Interestingly, lung TLR4 expression was significantly increased after 8 hours of OALT with increased levels of TNF-αand IL-β, which lead to lung pathological damage and an increase of lung myeloperoxidase content. Moreover, knockdown of TLR4 reduced lung cytokines release and reversed the above pathologic changes after OALT and finally improved rats’ survival rate. In conclusion, TLR4 overexpression, potentially by stimulating proinflammatory cytokine overproduction, contributes to the development of ALI after OLT.

scholarly journals The ANG-(1–7)/ACE2/mas axis in the regulation of nephron function

2010 ◽  
Vol 298 (6) ◽  
pp. F1297-F1305 ◽  
Author(s):  
Carlos M. Ferrario ◽  
Jasmina Varagic
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Therapeutic Interventions ◽  
Experimental Hypertension ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
A Site

The study of experimental hypertension and the development of drugs with selective inhibitory effects on the enzymes and receptors constituting the components of the circulating and tissue renin-angiotensin systems have led to newer concepts of how this system participates in both physiology and pathology. Over the last decade, a renewed emphasis on understanding the role of angiotensin-(1–7) and angiotensin-converting enzyme 2 in the regulation of blood pressure and renal function has shed new light on the complexity of the mechanisms by which these components of the renin angiotensin system act in the heart and in the kidneys to exert a negative regulatory influence on angiotensin converting enzyme and angiotensin II. The vasodepressor axis composed of angiotensin-(1–7)/angiotensin-converting enzyme 2/mas receptor emerges as a site for therapeutic interventions within the renin-angiotensin system. This review summarizes the evolving knowledge of the counterregulatory arm of the renin-angiotensin system in the control of nephron function and renal disease.

Studies on thyroid activity in deoxycorticosterone-salt and Goldblatt two-kidney, one-clip hypertensive rats

1988 ◽  
Vol 118 (1) ◽  
pp. 22-30 ◽  
Author(s):  
F. Vargas ◽  
C. Garcia del Rio ◽  
J. D. Luna ◽  
J. M. Haro ◽  
C. Osorio
Keyword(s):  
Serum Levels ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Thyroid Activity ◽  
Thyroid Gland Function ◽  
Suppressor Effect ◽  
Serum Aldosterone ◽  
Gland Function ◽  
2K1c Hypertension

Abstract. In this paper we studied the role of thyroid gland function in two experimental hypertension models with different pathophysiological mechanisms: deoxycorticosterone-salt (DOCA-salt, volume dependent) and Goldblatt 2-kidney, 1-clip (2K1C, renin dependent). DOCA-salt hypertensive rats showed lower T3 and T4 serum levels by the third week of induced hypertension. Goldblatt 2K1C hypertensive rats, however, exhibited normal values for both hormones. Treatment with thyroxine accelerated the evolution of hypertension and did not affect the PRA of DOCA-salt rats. Radiothyroidectomy inhibited DOCA-salt and Goldblatt 2K1C hypertension, and prevented the suppression of PRA in DOCA-salt rats, without altering PRA or serum aldosterone in Goldblatt 2K1C rats. These results suggest that: a) a thyroid depressing factor is not activated in Goldblatt 2K1C rats; b) thyroidectomy interferes with the suppressor effect of mineralocorticoid on renin secretion; and c) normal thyroid activity is required for the hypertensive effect of the renin-angiotensin-aldosterone system in Goldblatt 2K1C rats.

Role of the kidney in the pathogenesis of experimental hypertension

1949 ◽  
Vol 7 (2) ◽  
pp. 251
Author(s):  
Arthur Grollman ◽  
John Vanatta ◽  
E.E. Muirhead
Keyword(s):  
Experimental Hypertension
Sign in / Sign up

Export Citation Format

Share Document