scholarly journals Restoration of T-Cell Depression and Suppression of Blood Pressure in Spontaneously Hypertensive Rats (SHR) by Allogeneic Thymus Grafts or Injection of Thymic Hormone

1981 ◽  
Vol 22 (3) ◽  
pp. 494-494 ◽  
Author(s):  
Denian Ba ◽  
Noritoshi Takeichi ◽  
Hiroshi Kobayashi
Keyword(s):  
Blood Pressure ◽  
T Cell ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Thymic Hormone ◽  
Spontaneously Hypertensive

scholarly journals Arrest of T-cell Maturation in Spontaneously Hypertensive Rats Associated with Deficiency of Thymic Hormone

1982 ◽  
Vol 23 (3) ◽  
pp. 426-426
Author(s):  
Noritoshi Takeichi ◽  
Denian Ba ◽  
Kazufumi Suzuki ◽  
Masuo Hosokawa ◽  
Hiroshi Kobayashi
Keyword(s):  
T Cell ◽  
Spontaneously Hypertensive Rats ◽  
Cell Maturation ◽  
Hypertensive Rats ◽  
Thymic Hormone ◽  
Spontaneously Hypertensive ◽  
T Cell Maturation

scholarly journals Transcriptomic signature of gut microbiome-contacting cells in colon of spontaneously hypertensive rats

2020 ◽  
Vol 52 (3) ◽  
pp. 121-132 ◽  
Author(s):  
Tao Yang ◽  
Hongbao Li ◽  
Aline C. Oliveira ◽  
Ruby Goel ◽  
Elaine M. Richards ◽  
...  
Keyword(s):  
Blood Pressure ◽  
T Cell ◽  
Spontaneously Hypertensive Rats ◽  
Colonic Epithelium ◽  
Hypertensive Rats ◽  
Fecal Matter ◽  
Cell Surface Glycoprotein ◽  
Spontaneously Hypertensive ◽  
Functional Changes ◽  
Lower Expression

Fecal matter transfer from hypertensive patients and animals into normotensive animals increases blood pressure, strengthening the evidence for gut-microbiota interactions in the control of blood pressure. However, cellular and molecular events involved in gut dysbiosis-associated hypertension remain poorly understood. Therefore, our objective in this study was to use gene expression profiling to characterize the gut epithelium layer in the colon in hypertension. We observed significant suppression of components of T cell receptor (TCR) signaling in the colonic epithelium of spontaneously hypertensive rats (SHR) when compared with Wistar Kyoto (WKY) normotensive rats. Western blot analysis confirmed lower expression of key proteins including T cell surface glycoprotein CD3 gamma chain (Cd3g) and lymphocyte cytosolic protein 2 (Lcp2). Furthermore, lower expression of cytokines and receptors responsible for lymphocyte proliferation, differentiation, and activation (e.g., Il12r, Il15ra, Il7, Il16, Tgfb1) was observed in the colonic epithelium of the SHR. Finally, Alpi and its product, intestinal alkaline phosphatase, primarily localized in the epithelial cells, were profoundly lower in the SHR. These observations demonstrate that the colonic epithelium undergoes functional changes linked to altered immune, barrier function, and dysbiosis in hypertension.

scholarly journals Female spontaneously hypertensive rats have greater renal anti-inflammatory T lymphocyte infiltration than males

2012 ◽  
Vol 303 (4) ◽  
pp. R359-R367 ◽  
Author(s):  
Ashlee J. Tipton ◽  
Babak Baban ◽  
Jennifer C. Sullivan
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
T Cell ◽  
Spontaneously Hypertensive Rats ◽  
T Regulatory Cells ◽  
Dependent Manner ◽  
Regulatory Cells ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cell Profile

T cells contribute to hypertension in male experimental models; data in females is lacking even though women are more likely to develop immune disorders. The goal of this study was to determine whether immune cells contribute to hypertension in female spontaneously hypertensive rats (SHR) and define the T cell profile in whole blood and kidneys of male and female SHR. We hypothesized that inflammatory cells contribute to hypertension in female SHR; however, male SHR have a higher blood pressure so we hypothesize they will have a heightened inflammatory profile. The lymphocyte inhibitor mycophenolate mofetil (MMF) was administered in a dose-dependent manner to SHR. At the highest dose (50 mg·kg−1·day−1), blood pressure was significantly decreased in both sexes, yet the percent decrease in blood pressure was greater in females (female: 12 ± 1%; males: 7 ± 1%, P = 0.01). Circulating and renal T cell profiles were defined using analytical flow cytometry. Female SHR had more circulating CD3+, CD4+, and pro-inflammatory CD3+CD4+RORγ+ Th17 cells, whereas males had more immune-suppressive CD3+CD4+Foxp3+ T regulatory cells. In the kidney, females had greater numbers of CD8+ and T regulatory cells than males, whereas males had greater CD4+ and Th17 cell infiltration. MMF decreased circulating and renal T cells in both sexes ( P < 0.0001), although the effect of MMF on T cell subtypes was sex specific with females having greater sensitivity to MMF-induced decreases in lymphocytes. In conclusion, there is a lymphocyte contribution to the maintenance of hypertension in the female SHR and sex of the animal impacts the T cell profile.

Abstract 440: Female Spontaneously Hypertensive Rats are More Dependent on Nitric Oxide in Modulating Blood Pressure and Renal Injury Than Males

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ahmed A Elmarakby ◽  
Chelsey Pye ◽  
Krystal Brinson ◽  
Tatsuo Yamamoto ◽  
Jennifer C Sullivan
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
T Cell ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Injury ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Monocyte Chemoattractant Protein 1 ◽  
Spontaneously Hypertensive

We recently demonstrated that female spontaneously hypertensive rats (SHR) have higher nitric oxide (NO) bioavailability in the kidney compared to males. Therefore, we hypothesize that female SHR are more dependent on the NO synthase (NOS) system to modulate their blood pressure, and as a result will have a greater rise in blood presure and renal injury in response to chronic NOS inhibition compared to males. Mean arterial pressure in SHR was very sensitive to NOS inhibition, with both sexes exhibiting a significant increase in blood pressure to the non-specific NOS inhibitor N G -nitro-L-arginine methyl ester (L-NAME) at a dose of 2 mg/kg/day. However, there was not a sex difference in the percent increase in mean arterial pressure. Treatment of female and male SHR with 7 mg/kg/day L-NAME for 2 weeks significantly increased mean arterial pressure and indices of renal injury in both females and males; the percent increases in mean arterial pressure and injury were greater in females during the last three days of L-NAME treatment (% increase in mean arterial pressure was 44± 1.3 in females vs. 35± 2.9 in males, P<0.05). L-NAME treatment also increased indices of inflammation and oxidative stress as urinary monocyte chemoattractant protein-1 (MCP-1) and thiobarbituric acid reactive substances (TBARs) excretion levels were increased by L-NAME; however, the increases were greater in females. Renal cortical macrophage and T cell infiltrations and soluble intracellular adhesion molecule-1 (sICAM-1) were also elevated following L-NAME treatment (cortical sICAM-1 levels increased from 4.7± 0.2 to 9± 0.1 ng/mg in males vs. 4.6± 0.1 to 7.9± 0.3 ng/mg in females, P<0.05). Although renal cortical macrophage infiltration was greater in female SHR vs. males following L-NAME treatment, the increase in cortical T cell infiltration and sICAM-1 were greater in males. These data suggest that the NO system plays an important role in modulating blood pressure, renal injury and inflammation in SHR, with females being more dependent on the NOS system than males.

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