Aging and Vasodilation to Atrial Peptides

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Abstract
Alterations in the levels or activity of atrial peptides may be associated with cardiovascular pathologies such as hypertension and congestive heart failure that are more common in the elderly. In the present study, we examined the possibity that vascular relaxation to atrial peptides may be affected by animal age. In vitro evaluation of the relaxation produced by atrial peptide-25 (AP-25) in serotonin-contracted rat aorta, carotid artery and mesenteric artery indicated that relaxation was greatest in tissues from rats 1-2 months of age. Nevertheless, roughly 80% of the maximal possible relaxation to AP-25 occurred in arteries from older rats (up to 18-19 months of age). A similar profile of relaxant responsiveness occurred with AP-21 (atriopeptin I). Unlike the arterial preparations examined, portal veins from rats of all ages relaxed similarly to AP-25, consistent with the lack of age-related changes in relaxation to β-agonists in the rat portal vein. In vivo, AP-25 given intravenously lowered blood pressure to a similar extent in rats of all ages. Thus, the greater In vitro sensitivity of arteries from rats 1-2 months of age did not result in a greater reduction in blood pressure in these young rats. This latter observation is consistent with the possibility that the effect of atrial peptides on blood pressure may not be associated with an arterial event, but rather with an alteration in venous return and/or cardiac output as previously proposed. Since arteries from older rats were able to respond to atrial peptides, our studies add further support to the impetus to develop clinical agents that might either enhance atrial peptide levels or mimic the action of atrial peptides since no major decline in receptor function of atrial peptides occurred with advanced age.