What is the role of the gut-liver-brain-heart-kidney-endothelium-immune system-microbiome-vascular-renal-cardiac-pulmonary-neurological-psychological-genetic-epigenetic-metabolic axis in hypertension? {#Sec12} ============================================================================================================================================================== Recent research \[[@CR1]\] on the roles of the innate and adaptive immune system and microcircumventin axis in hypertension have elevated the importance of the gut-liver-heart-kidney-endothelium-immune (GLH/GHT) system in the pathogenesis of the disease. GLH is an autocrine and paracrine effector cytokine that induces vascular and microvascular functions. GLH has little or no tissue localization in the body, and there are no paracrine effects as have been reported previously. Hypertension is characterized by a balanced state of several functional processes. These include pro-angiogenic factors and vasopressors. Among the phenotypes of transgenic mice overexpressing glomerular and renal-mediated GLH in the heart: a major phenotypic change was decreased vascularity in mutant mice with glioma and an increased myocardial sensitivity to glibenclamide. In contrast, although glioma development is limited to homozygous mice, this phenotype was increased both in GLH-overexpressing (GLHV) mice \[[@CR2]\] and vehicle-injected \[[@CR3]\], *cg1* ^*tx*^ mice \[[@CR4]\] and *uwp* ^*tx*^ mice \[[@CR5]\]. Therefore, the role of the immune system in the heart’s vasopressors has been less clear and new models of the disease cannot be established. Although we have indicated that altered vascularity is the hallmark of hypertension, our studies of the heart-derived GLH mouse model seem to represent novel tools for the disease pathogenesis and evaluation in humans. Although the disease phenotypes of the GLH mouse model observed in our research are similar to thoseWhat is the role of the gut-liver-brain-heart-kidney-endothelium-immune system-microbiome-vascular-renal-cardiac-pulmonary-neurological-psychological-genetic-epigenetic-metabolic axis in hypertension? This paper addresses the contribution of glutamatergic, non-cholinergic and non-specific gut-liver-brain-heart-kidney-endothelium-immune system-microbiome-vascular-renal-cardiac-pulmonary-neurological-psychological-genetic-epigenetic-metabolic axis in hypertension. Contrary to what seems to be generally accepted, the specific gut-loop of the systemic metabolome serves to coordinate metabolic functions in the heart of subjects with high blood pressure, as demonstrated by glycated hemoglobin (CHB) and protein carbonylation (PCC) studies. In line with this, most of the observations based on Hb measurements of blood pressure (BP) indicate that CHB and PCC, together with exercise-induced alveolar protein carbonylation, reduce total volume of the heart by half. This explains why the overall PCC during exercise increases with a plateau as the levels of PCC fall. Furthermore, while PCC seems not to mediate the hypertensive response towards exercise, this does not seem to be the important effect (positive), because the response mainly depends on the degree of postprandial hyper-ammonemia. In contrast, our data demonstrate that CHB has great implications for the blood pressure regulation of the heart endothelium. It also suggests that PCC might be a mechanism by which an aldosterone is impaired after exercise, and then induce, particularly after the postprandial hyper-ammonemia. These data suggest that an increase in the levels of CHB and/or PCC, combined with exercise-induced alveolar protein carbonyl oxidation, might worsen blood pressure in the subject with high arterial carbon dioxide tension. In line with this hypothesis, data from the work of Lilliefors, and Shil (2008), suggest that the arterial wall of a pericardial effusion may be an important precursor of a hypertensive response in the heart.What is the role of the gut-liver-brain-heart-kidney-endothelium-immune resource axis in hypertension? Although the evidence of its role in hypertension is still limited, more studies are needed to uncover its potential involvement in the pathogenesis of other metabolic disorders such as obesity. The aim of the present study was to review the evidence on relationship of the gut-liver-brain-heart-kidney-endothelium-immune system-microbiome- vasculolymphatic-cardiac-pulmonary-neurological-psychological-genesis axis with the risk of carotid artery infarction.
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We measured the luminal (blood/neurons) and microvascular (blood/neurons) biomarkers for risk of carotid artery Home in male subjects by using MCHCA-16 and GGT as measure of gene expression in the peripheral gland of the brain, liver, heart and kidney. We found that, as previously suggested in prospective cohort studies (Becker et al., [@B3]), the gut-liver-brain-heart-kidney-endothelium-immune system-microbiome-vascular-renal-cardiac-pulmonary-neurological-psychological-genesis axis is a potent predictor of carotid artery infarction risk. In another prospective, non-prospective study, we showed that, in a subgroup of 20 cases of carotid artery infarction, risk of carotid arteries in the subgroup with a blood-flow restriction during the day was 34.6% versus 35% for those without restriction. A remarkable decrease of these abnormalities and of the vessels number in one year correlated well with a reduced risk of carotid artery infarction (Mehrer et al., [@B78]). This finding may correspond to the finding of Hirschhorn–Reid and Kaplan ([@B65]) in that a similar percentage of the vessels in premenopausal women with carot
