The incidence and prevalence of hypertension are increasing as a consequence of the obesity epidemic. Adipocytes and their variety of factors make contributions to the long-term regulation of blood pressure. The pathophysiologic states of hypertension, including obesity, are regulated by the production of adipocytederived factors. Increased body mass index was closely linked to elevated blood pressure. Mostly the hypertensive subjects were obese as well as overweight. There are numerous adipokines, however, this review article only focuses on the major adipokines including chemerin, visfatin, retinol-binding protein 4, plasminogen activator inhibitor-1, monocyte chemotactic protein-1, omentin-1, lipocalin-2, vaspin, progranulin, complement c1q tumor necrosis factor-related protein, and nesfatin-1 role in the pathogenesis of hypertension. This review article concludes the significant association of major adipokines in the pathogenesis of hypertensives. New research should be focused on other newly reported adipokine roles in hypertensive subjects and the management of these adipokines in hypertensive subjects. The discovery of this information could result in the creation of antihypertensive medications, particularly those that focus on obesity-related hypertension.
High blood pressure (BP), known as hypertension, is a major contributing factor to the development of cardiovascular disease. The development and pathogenesis of hypertension involve a wide array of factors including genetics, environment, hormones, hemodynamics, and inflammation. There is a significantly positive association between higher levels of colonization by Aggregatibacter actinomycetemcomitans , Porphyromonas gingivalis , Tannerella forsythia , and Treponema denticola (etiologic bacterial burden) below the gum line, and the presence of hypertension. The use of antibiotics during pregnancy, which is likely indicative of bacterial infections severe enough to require antibiotic treatment, is associated with a slight increase in average arterial BP. Cytomegalovirus infection is a risk factor for heightened arterial BP and acts as a co-factor in the development of aortic atherosclerosis. The relationship between hypertension and coronavirus disease 2019 involves endothelial dysfunction and dysregulation of the renin-angiotensin system. The effects of gut microbiota on BP, whether beneficial or harmful, are influenced by multiple factors including genetics, epigenetics, lifestyle choices, and antibiotic usage. These variables collectively contribute to overall BP levels and the control of hypertension. Several reports have examined the BP levels of patients infected with the Zika virus. In regions with a high incidence of nasopharyngeal carcinoma, hypertension has been linked to a higher risk of Epstein-Barr virus reactivation. Also, a potential causal link has been found between malaria and elevated BP. Also, the elevated prevalence of hypertension among dengue patients during their initial visit suggests that relying solely on BP measurements to predict severe infection may not be clinically reliable.
Cardiac biomarkers may play unique roles in the prognostic evaluation of patients with hypertension, as many cardiac biomarker levels become abnormal long before the onset of obvious cardiovascular disease（CVD）. There are numerous cardiac markers. However, this review article only reported the roles of creatinine kinase-MB, cardiac troponins, lipoprotein a, osteopontin, cardiac extracellular matrix, C-reactive protein, cardiac matrix metalloproteinases, cardiac natriuretic peptides, myoglobin, renin, and dynorphin in the pathogenesis of hypertension. This article explained recent major advances, as well as discoveries, significant gaps, and current debates and outlined possible directions for future research. Further studies are required to determine the association between myoglobin and other cardiac markers in hypertension. Moreover, therapeutic approaches are required to determine the early control of these cardiac markers, which ultimately reduce the prevalence of CVDs.
