Rabbit Anti-Human ADRB2 (Phospho-Ser346) polyclonal antibody

Hypertension (HTN) is a prevalent condition with complex etiology and pathophysiology. Evidence exists of significant communication between the nervous system and the immune system (IS), and there appears to be a direct role for inflammatory bone marrow (BM) cells in the pathophysiology of hypertension. However, the molecular and neural mechanisms underlying this interaction have not been characterized. Here, we transplanted whole BM cells from the beta 1 and 2 adrenergic receptor (AdrB1(tm1Bkk)AdrB2(tm1Bkk)/J) knockout (KO) mice into near lethally irradiated C57BL/6J mice to generate a BM AdrB1. B2 KO chimera. This allowed us to evaluate the role of the BM beta 1 and beta 2 adrenergic receptors in mediating BM IS homeostasis and regulating blood pressure (BP) in an otherwise intact physiological setting. Fluorescence-activated cell sorting demonstrated that a decrease in systolic and mean BP in the AdrB1. B2 KO chimera is associated with a decrease in circulating inflammatory T cells, macrophage/monocytes, and neutrophils. Transcriptomics in the BM identified 7,419 differentially expressed transcripts between the C57 and AdrB1. B2 KO chimera. Pathway analysis revealed differentially expressed transcripts related to several cell processes in the BM of C57 compared with AdrB1. B2 KO chimera, including processes related to immunity (e.g., T-cell activation, T-cell recruitment, cytokine production, leukocyte migration and function), the cardiovascular system (e.g., blood vessel development, peripheral nerve blood flow), and the brain (e.g., central nervous system development, neurite development) among others. This study generates new insight into the molecular events that underlie the interaction between the sympathetic drive and IS in modulation of BP.

Purpose: The purpose of the current study was to characterize the role of aerobic exercise in the gene expression of the angiotensin-converting enzyme (ACE) and the beta(2)-adrenergic receptor (ADRB2) in untrained men. Methods: Twenty untrained middle-aged men were randomly assigned to exercise (Exe) and control (Con) groups. The Exe group performed aerobic exercises for eight weeks. ACE mRNA and ADRB2 mRNA were determined by PCR. Results: The expression of ACE in week 4 and in the Exe group decreased significantly (p < .001). ADRB2 in the Exe group, in week 4 and in week 8, was markedly higher, and blood pressure was significantly lower than in the Con group (p < .001). In the Con group ADRB2 mRNA decreased. Conclusion: These results suggest that moderate intensity exercise promotes the leukocyte expression of gene markers that may affect blood pressure by improving cardiovascular fitness levels in middle-aged men.