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- W785566648 abstract "In many hypertension (Htn) models, myogenic tone (MT) in isolated small arteries is increased. MT is regulated mainly by Ca2+ transporters. Arterial transporter expression is “reprogrammed” in many Htn models: e.g., Na/Ca exchanger (NCX) and SR Ca2+ pumps (SERCA2) are increased; this enhances constriction and MT. In heart failure (HF), cardiac Ca2+ transporter “reprogramming” impairs contraction: e.g., NCX1 is increased, and SERCA2 expression or function is reduced. Do these cardiovascular (CV) changes in Htn and HF have a common trigger? The brain RAAS is activated in both Htn and HF. Central Ang II infusion increases BP, circulating endogenous ouabain (EO), and arterial NCX and SERCA2 expression; brain RAAS blockade prevents all effects (Hamlyn et al., PloS one 9: e108916, 2014). Here we induced Htn in rats (mean BP = 124 vs Control = 99 mm Hg) and mice (139 vs C = 110 mm Hg) with sc low dose Ang II (150-350 ng/kg/min) and a high (2-6%) salt diet. Also, in mice, coronary artery ligation caused ~45% LV myocardial infarction (MI) and HF: a 38±4% fall in LV ejection fraction at 8 wks post-MI. In both Htn and HF, plasma EO increased (1.31-2.59 nM vs C = 0.07-0.53 nM) as did expression of arterial NCX (1.7-1.8xC) and SERCA2 (2.0-2.3xC) and cardiac NCX (1.7-1.9xC), but cardiac SERCA2 expression declined (0.58-0.74xC). In vitro 48-72 hr treatment with 50-100 nM ouabain, but not digoxin, increased NCX and SERCA2 protein in primary cultured arterial myocytes (published), and NCX (1.3-1.7xC) in cardiomyocytes. Conclusion plasma EO is the signal from the brain that triggers Ca2+ transporter reprogramming in both Htn and HF. The novel slow brain RAAS-plasma EO-CV system modifies responses to the rapid RAAS-activated sympathetic nerve pathway, and both modulate CV function in Htn and HF." @default.
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- W785566648 date "2015-04-01" @default.
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- W785566648 title "How Does the Brain Talk to the Arteries and Heart?" @default.
- W785566648 doi "https://doi.org/10.1096/fasebj.29.1_supplement.984.3" @default.
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