Premium
Modulation of the cannabinoid‐1 receptor by angiotensin II in astrocytes isolated from spontaneously hypertensive rats (1140.8)
Author(s) -
Haspula Dhanush,
Clark Michelle
Publication year - 2014
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.28.1_supplement.1140.8
Subject(s) - astrocyte , endocrinology , angiotensin ii , neuroinflammation , medicine , messenger rna , neuroprotection , receptor , spontaneously hypertensive rat , chemistry , cannabinoid , inflammation , cannabinoid receptor , central nervous system , blood pressure , antagonist , gene , biochemistry
Objective: To determine whether a mediator of neuroprotection, the Cannabinoid Type 1 receptor (CB1R), is altered by Angiotensin (Ang) II in astrocytes. Background: Along with an elevated Ang II level, neuroinflammation in the brainstem (BS) has been shown to shift the balance towards an augmented sympathetic drive, the latter being associated with hypertension. Astrocytes play a central role in the bidirectional modulation of inflammation Methods: BS astrocytes isolated from Spontaneously Hypertensive Rats (SHR) were used as a hypertension model to determine whether Ang II induces CB1R protein and mRNA expression. The results were compared to normotensive Wistar rats. The cells were treated with 100nM Ang II in a time‐dependent manner, and the effect of Ang II on CB1R protein and mRNA levels were measured using Western blotting and qt‐PCR techniques, respectively. Results: In Wistar cells, Ang II increased the CB1R protein and mRNA levels in a time‐dependent manner. In SHR astrocytes, Ang II down‐regulated or had no effect on CB1R protein and mRNA levels. Compared with Wistar astrocytes, the CB1R protein and mRNA levels in SHR astrocytes were significantly different. Conclusion: Our findings suggest that the CB1R is differentially regulated in SHR versus normotensive astrocytes. This interaction may serve as a potential target to restore an elevated sympathetic drive in hypertension. Grant Funding Source : NSU PFRDG 2013‐14: Grant # 335309