Key result
Arginine vasopressin triggers local cardiac aldosterone secretion in post-MI rats via V1 receptor activation.
Why the study?
Both aldosterone and arginine vasopressin are produced in the heart and may contribute to cardiac fibrosis, but their relationship remains unknown.
Does arginine vasopressin induce cardiac aldosterone synthesis in rats with myocardial infarction and cardiac microvascular endothelial cells?
Does arginine vasopressin induce cardiac aldosterone synthesis in rats with myocardial infarction and cardiac microvascular endothelial cells?
Arginine vasopressin induces local cardiac aldosterone secretion via V1 receptor activation, CaMK, and CREB phosphorylation, highlighting a potential mechanism for post-MI cardiac fibrosis.
Both aldosterone and arginine vasopressin (AVP) are produced in the heart and may participate in cardiac fibrosis. However, their relationship remains unknown. This study aims to demonstrate the regulation and role of AVP in aldosterone synthesis in the heart. Rats were subjected to a sham operation or myocardial infarction (MI) by ligating the coronary artery. Cardiac function and fibrosis were assessed using echocardiography and immunohistochemical staining, respectively. In addition, the effects of AVP stimulation on cardiac microvascular endothelial cells (CMECs) were studied using ELISA, real-time PCR, and Western blotting. Compared with the rats having undergone a sham operation, the MI rats had an increased LVMI, type I collagen composition, and concentrations of aldosterone and AVP in the heart but decreased cardiac function. As the MI rats aged, the LVMI, type I collagen, aldosterone, and AVP increased, while the LVMI decreased. Furthermore, AVP time-dependently induced aldosterone secretion and CYP11B2 mRNA expression in CMECs. The p-CREB levels were significantly increased by AVP. Nevertheless, these effects were completely blocked by SR49059 or partially inhibited by KN93. This study demonstrated that AVP could induce the secretion of local cardiac aldosterone, which may involve CaMK and CREB phosphorylation and CYP11B2 upregulation through V1 receptor activation.
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Zhai et al. (2022) studied Myocardial Infarction. Arginine vasopressin (AVP) stimulation vs. Sham operation / SR49059 / KN93 was evaluated on Aldosterone secretion and CYP11B2 mRNA expression. Arginine vasopressin induced local cardiac aldosterone secretion in rats with myocardial infarction, involving CaMK and CREB phosphorylation and CYP11B2 upregulation through V1 receptor activation.
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