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Altered Neuronal Activity in the Brain of Cyp1a1‐Ren2 Transgenic Rats with ANG II‐Dependent Malignant Hypertension
Author(s) -
Issa Alexandra T,
Heng Vibol,
Zsombok Andrea,
Mitchell Kenneth D,
Derbenev Andrei V
Publication year - 2011
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.25.1_supplement.843.4
The central nervous system regulates arterial blood pressure largely by controlling the activity of the sympathetic nervous system. Activity of neurons of the rostral ventrolateral medulla (RVLM) and the hypothalamus are critical components of the central pathways mediating sympathetic regulation of cardiovascular function. However, it remains unclear whether or not neuronal activity in these regions of the brain is altered in hypertensive states; in particular, in ANG II‐dependent malignant hypertension. The present study was performe d to determine neuronal activity of brain areas involved in blood pressure regulation in transgenic rats [TGR(Cyp1a1Ren2)] with inducible ANG II‐dependent malignant hypertension. Expression of c‐fos was used as an indirect marker of neuronal activity in brain areas involved in the regulation of blood pressure. Western blot analysis demonstrated that c‐fos expression was increased in the hypothalamus, and decreased in the RVLM compared with non‐induced normotensive control rats (n=2). Additionally, AT 1 receptor total protein expression was decreased in the hypothalamus and brainstem of hypertensive Cyp1a1‐Ren2 rats. The present findings demonstrate that ANG II‐dependent malignant hypertension is associated with a downregulation of AT 1 receptor expression in the hypothalamus and brainstem of Cyp1a1‐Ren2 rats. The data also show that neuronal activity is altered in the brain areas involved in blood pressure regulation in Cyp1a1‐Ren2 transgenic rats with ANG II‐dependent malignant hypertension. Supported by AHA 10GRNT454000, R21HL091293, R21HL091293‐01A1S1.

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