Human vascular antigen complement consumption test of hypertensive patients (preliminary report)

2022

Front. Endocrinol.

In recent studies, primary aldosteronism (PA) has been reported as the most common etiology for secondary hypertension of endocrine origin, accounting for approximately 10% of cases. In PA, excess aldosterone production can lead to deleterious effects at the cardiovascular (CV) and renal levels by activating mineralocorticoid receptors, which involves an increase in pro-inflammatory and pro-fibrotic mediators. Among these mediators, neutrophil gelatinase–associated lipocalin (NGAL), a secretion glycoprotein belonging to the lipocalin superfamily, has been closely linked to CV and renal damage in several pathological conditions. Because NGAL can be detected in biofluids such as plasma and urine, it has been proposed as a damage biomarker for target tissues and has also been studied for its role in hypertension and associated with PA. NGAL is produced by many different cell types, can be carried on extracellular vesicles, and is modulated by microRNAs, which would support its use as a biomarker for endocrine hypertension due to PA. Over the last decade, studies have shown that NGAL is necessary for the development of aldosterone-induced hypertension and that is associated with end-organ damage. In addition, it has been proposed that some mechanisms are dependent on the activation of immune cells, such as dendritic cells and macrophages, where the release of specific cytokines (i.e., interleukin [IL]-23) or chemokines (i.e., CCL-5) induced by aldosterone would depend on NGAL. Subsequently, this activates the T helper (Th) lymphocytes, such as Th17 and Th2, resulting in CV and renal fibrosis due to the high aldosterone levels. Although the immune system has been closely associated with essential hypertension, its participation in endocrine hypertension has not been fully elucidated. This review discusses the link between NGAL and endocrine hypertension, particularly in the context of PA, and their possible regulators and mechanisms, with a focus on its role as an immunomodulator.

Section: The Role Of Ngal In the Immune System During Aldosterone-dep...mentioning

confidence: 99%

Neutrophil gelatinase–associated lipocalin as an immunomodulator in endocrine hypertension

Araos

2022

Front. Endocrinol.

“…The evidence linking the immune system and AH dates from the 1960s [ 6 , 7 ]; however, the hypothesis of a causal role of the immune system in AH was proposed years later by Okuda and Grollman, where the transference of lymph node cells from rats with unilateral renal artery ligation induced AH in recipient rats [ 8 ]. Likewise, splenocytes from rats treated with deoxycorticosterone acetate (DOCA) salt induced AH in normotensive animals [ 9 ].…”

Section: Role Of Immune System In Hypertensionmentioning

confidence: 99%

The Role of Neutrophils in Hypertension

Araos

Figueroa

2020

IJMS

It is well accepted that the immune system and some cells from adaptive and innate immunity are necessary for the initiation/perpetuation of arterial hypertension (AH). However, whether neutrophils are part of this group remains debatable. There is evidence showing that the neutrophil/lymphocyte ratio correlates with AH and is higher in non-dipper patients. On the other hand, the experimental neutrophil depletion in mice reduces basal blood pressure. Nevertheless, their participation in AH is still controversial. Apparently, neutrophils may modulate the microenvironment in blood vessels by increasing oxidative stress, favoring endothelial disfunction. In addition, neutrophils may contribute to the tissue infiltration of immune cells, secreting chemoattractant chemokines/cytokines and promoting the proinflammatory phenotype, leading to AH development. In this work, we discuss the potential role of neutrophils in AH by analyzing different mechanisms proposed from clinical and basic studies, with a perspective on cardiovascular and renal damages relating to the hypertensive phenotype.

“…However, and even when the activation of immune system has been associated to human arterial hypertension (AH) since 60s [12], the implications of increased sodium salt intake on the activation of the immune system have not been clarified. Here, we highlight the effects of sodium and how its distribution may participate on the immune system activation during AH.…”

Section: Introductionmentioning

confidence: 99%

Is the Sodium an Activator of Immune System in Hypertension?

2021

BJSTR

The sodium plays an essential role in human homeostasis and it has been described that a 30-50% of hypertensive patients are sensible to changes in their blood pressure after dietary high sodium intake. The last 20 years have been very active in trying to answer how the immune cells participate in hypertension, where the implications of increased sodium salt intake on the activation of the immune system have not been fully clarified. Even when some described mechanisms for macrophages, dendritic cells and lymphocytes proportion great insight for this understanding, the information concerning the different sodium compartments for its storage arise a new challenge for this area. This mini review highlights recent studies in different experimental settings regarding the effect of sodium as an activator for the immune system in hypertension and the mechanisms involved. We comment also the last studies suggesting the role of sodium as a regulator of immune cells in kidney medulla and extrarenal compartments that possibly may be involved in hypertension.