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One in every three adults in the United States has hypertension, and the underlying cause of most of these cases is unknown. Therefore, it is imperative to continue the study of mechanisms involved in the pathogenesis of hypertension. Decades ago, studies speculated that elements of an autoimmune response were associated with the development of hypertension based, in part, on the presence of circulating autoantibodies in hypertensive patients. In the past decade, a growing number of studies have been published supporting the concept that self-antigens and the subsequent activation of the adaptive immune system promote the development of hypertension. This manuscript will provide a brief review of the evidence supporting a role for the immune system in the development of hypertension, studies that implicate both cell-mediated and humoral immunity, and the relevance of understanding blood pressure control in an autoimmune disease model with hypertension. [ABSTRACT FROM AUTHOR]

Incretin-based therapies are now well established for diabetes management and are among the frontline agents for control of hyperglycemia. In addition to their antihyperglycemic effects, evidence is emerging on the role of these agents on blood pressure regulation, cardioprotective and renoprotective properties. Because of the pleiotropic nature of these affects, these agents could offer significant benefits with regards to the cardiorenal metabolic complications that are part of the diabetes and obesity epidemic in the United States and worldwide. We review the various known mechanisms or pathways by which incretin based therapy exerts its regulation of blood pressure with emphasis on novel mechanisms such as inflammation/immunomodulation and oxidative stress. [ABSTRACT FROM AUTHOR]

The renin-angiotensin system plays a critical role in the pathogenesis of several cardiovascular diseases, largely through activation of type I angiotensin (AT) receptors by angiotensin II. Treatment with AT receptor blockers (ARBs) is a proven successful intervention for hypertension and progressive heart and kidney disease. However, the divergent actions of AT receptors on individual cell lineages in hypertension may present novel opportunities to optimize the therapeutic benefits of ARBs. For example, T lymphocytes make important contributions to the induction and progression of various cardiovascular diseases, but new experiments indicate that activation of AT receptors on T cells paradoxically limits inflammation and target organ damage in hypertension. Future studies should illustrate how these discrepant functions of AT receptors in target organs versus mononuclear cells can be exploited for the benefit of patients with recalcitrant hypertension and other cardiovascular diseases. [ABSTRACT FROM AUTHOR]