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Aldosterone (Aldo) Interacts with PKA, MAPKs and PLC Pathway to Sensitize Angiotensin (ANG) II‐Induced Hypertension
Author(s) -
Xue Baojian,
Zhang Zhongming,
Guo Fang,
Johnson Alan Kim
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1091.70
Subject(s) - medicine , endocrinology , creb , phospholipase c , aldosterone , angiotensin ii , renin–angiotensin system , lamina terminalis , kinase , mapk/erk pathway , chemistry , aldo keto reductase , signal transduction , protein kinase a , receptor , transcription factor , enzyme , hypothalamus , biochemistry , gene , blood pressure , reductase
Previous studies using an Induction‐Delay‐Expression (I‐D‐E) experimental design have demonstrated that one‐week Aldo pre‐treatment can sensitize the brain to produce an enhanced hypertensive response to subsequent ANGII. The amplified pressor effects are associated with elevated mRNA expression of RAAS components in the lamina terminalis (LT). The present study was to determine the signaling mechanisms involved in the sensitizing effects of Aldo on the brain. During I Aldo (750 ng/h) or saline was delivered sc for 1 wk. The rats then rested for 1 wk (D). Then the tissues along LT were collected at the end of D for determining activation of PKA, MAPKs or PLC pathway. The week of Aldo treatment during I had no effect on BP during I and D. However, Aldo treatment during I induced a significant increase in phosphorylated cAMP response element‐binding protein (CREB, 1.5 fold), extracellular signal‐regulated kinase (ERK, 1.8 fold), or phospholipase C (PLC, 1.8 fold) in the LT. Moreover, Aldo infusion resulted in a significant increase in mRNA (1.5 fold) and protein (1.3 fold) expression of brain‐derived neurotrophic factor (BDNF) as compared with the saline treated rats. The results indicate that Aldo pre‐treatment may facilitate the development of ANG II‐induced hypertension by acting through a sensitization process involving PKA, MAPKs or PLC pathway.