Transfer of Arterial Hypertension by Splenic Cells From Doca‐salt Hypertensive and Renal Hypertensive Rats to Normotensive Recipients

Olsen, Finn

doi:10.1111/j.1699-0463.1980.tb00065.x

Cited by 49 publications

(45 citation statements)

References 7 publications

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“…Moreover, the transfer of lymph nodes from male hypertensive rats into normotensive rats caused the development of hypertension in the recipient rat 33 , while, a thymus transplant from a normotensive male WKY rat into a male SHR reduced BPin the SHR recipient 27 . Similarly, the transfer of spleen cells from hypertensive DOCA-salt rats into normotensive rats increased BP in recipient rats 34 and anti-thymocyte serum decreases BP in SHR to normal levels 28 . These early studies implicated the adaptive immune system in BP control and hypertension since both the spleen and thymus are sites of lymphocyte activation and maturation, and laid the foundation for more mechanistic studies to come.…”

Section: Linking Inflammation and Hypertensionmentioning

confidence: 98%

Sex Differences in T Cells in Hypertension

Tipton

Sullivan

2014

Clinical Therapeutics

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Purpose Hypertension is a major risk factor for the development of cardiovascular disease, stroke and end-organ damage. There is a sex difference in blood pressure (BP) that begins in adolescence and continues into adulthood, where men have a higher prevalence of hypertension compared to women until the sixth decade of life. Less than 50% of hypertensive adults in the United States taking medication manage to control their BP to recommended levels using current therapeutic options, and women are more likely than men to have uncontrolled high BP. This is despite the fact that more women compared to men are aware that they have hypertension and women are more likely to seek treatment for the disease. Novel therapeutic targets need to be identified in both sexes to increase the percentage of hypertensive individuals with controlled BP. The purpose of this article is to review the available literature on the role of T cells in BP control in both sexes, and the potential therapeutic application/implications of targeting immune cells in hypertension. Methods A search of PUBMED was conducted to determine the impact of sex and gender on T cell-mediated control of BP. The search terms included sex, gender, estrogen, testosterone, inflammation, T cells, T regulatory cells, Th17 cells, hypertension and blood pressure. Additional data were included from our laboratory examining cytokine expression in the kidney of male and female SHR and differential genes expression in both the renal cortex and mesenteric arterial bed of male and female SHR. Findings There is a growing basic science literature regarding the role of T cells in the pathogenesis of hypertension and BP control, however, the majority of this literature has been performed exclusively in males despite the fact that both men and women develop hypertension. There is increasing evidence that while T cells also mediate BP in females, there are distinct differences in both the T cell profile and the functional impact of “male” vs. “female” T cells on cardiovascular health, although more work is needed to better define the relative impact of different T cell subtypes on BP in both sexes. Implications The challenge now is to fully understand the molecular mechanisms by which the immune system regulates BP and how the different components of the immune system interact so that specific mechanisms can be targeted therapeutically without compromising natural immune defenses.

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Section: Linking Inflammation and Hypertensionmentioning

confidence: 98%

Sex Differences in T Cells in Hypertension

Tipton

Sullivan

2014

Clinical Therapeutics

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“…9 Subsequent experiments by Finn Olsen showed that transfer of splenocytes from rats with deoxycorticosterone (DOCA)-salt hypertension raises blood pressure in recipient rats. 10 …”

Section: Historical Perspectivesmentioning

confidence: 99%

Inflammation, Immunity, and Hypertensive End-Organ Damage

McMaster

Kirabo

Madhur

et al. 2015

Circulation Research

595

459

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For more than 50 years, it has been recognized that immunity contributes to hypertension. Recent data have defined an important role of T cells and various T cell-derived cytokines in several models of experimental hypertension. These studies have shown that stimuli like angiotensin II, DOCA-salt and excessive catecholamines lead to formation of effector like T cells that infiltrate the kidney and perivascular regions of both large arteries and arterioles. There is also accumulation of monocyte/macrophages in these regions. Cytokines released from these cells, including IL-17, IFN-γ, TNFα and IL-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. The renal effects of these cytokines remain to be fully defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption and increased renal fibrosis. Very recent experiments have defined a link between oxidative stress and immune activation in hypertension. These have shown that hypertension is associated with formation of reactive oxygen species in dendritic cells that lead to formation of gamma ketoaldehydes, or isoketals. These rapidly adduct to protein lysines and are presented by dendritic cells as neoantigens that activate T cells and promote hypertension. Thus, cells of both the innate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension. Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension including myocardial infarction, heart failure, renal failure and stroke.

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“…The link between systemic inflammation and high blood pressure has been well described by human [5][6][7] and animal data [8][9][10][11][12][13][14]. However, the effects of hypertension on the pathogenesis of cerebral inflammation are less understood.…”

Section: Introductionmentioning

confidence: 99%

Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice

Iulita

Vallerand

Beauvillier

et al. 2018

J Neuroinflammation

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Background: Angiotensin II (Ang II), a peptide hormone involved in the development of hypertension, causes systemic and cerebral inflammation, affecting brain regions important for blood pressure control. The cause-andeffect relationship between hypertension and inflammation is two-way, but the role of blood pressure in the induction of cerebral inflammation is less clear. The vulnerability of specific brain regions, particularly those important for memory, is also of interest. Methods: We used molecular biology approaches, immunohistochemistry, and electron microscopy to examine the interdependence between the hypertensive and pro-inflammatory effects of Ang II. We examined the effect of blood pressure by administering a subpressive (200 ng/kg/min) or a pressive Ang II dose (1000 or 1900 ng/kg/min) with and without hydralazine (150 mg/L) for 1 week and used phenylephrine to increase blood pressure independently of the renin-angiotensin system.

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Transfer of Arterial Hypertension by Splenic Cells From Doca‐salt Hypertensive and Renal Hypertensive Rats to Normotensive Recipients

Cited by 49 publications

References 7 publications

Sex Differences in T Cells in Hypertension

Sex Differences in T Cells in Hypertension

Inflammation, Immunity, and Hypertensive End-Organ Damage

Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice

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