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Protein kinase C isozymes in hypertension and hypertrophy: insight from SHHF rat hearts.

Authors: Johnsen, DD  Kacimi, R  Anderson, BE  Thomas, TA  Said, S  Gerdes, AM 
Citation: Johnsen DD, etal., Mol Cell Biochem. 2005 Feb;270(1-2):63-9.
Pubmed: (View Article at PubMed) PMID:15792354

Chronic hypertension results in cardiac hypertrophy and may lead to congestive heart failure. The protein kinase C (PKC) family has been identified as a signaling component promoting cardiac hypertrophy. We hypothesized that PKC activation may play a role mediating hypertrophy in the spontaneously hypertensive heart failure (SHHF) rat heart. Six-month-old SHHF and normotensive control Wistar Furth (WF) rats were used. Hypertension and cardiac hypertrophy were confirmed in SHHF rats. PKC expression and activation were analyzed by Western blots using isozyme-specific antibodies. Compared to WF, untreated SHHF rats had increased phospho-active alpha (10-fold), delta (4-fold), and epsilon (3-fold) isozyme expression. Furthermore, we analyzed the effect of an angiotensin II type 1 receptor blocker (ARB) and hydralazine (Hy) on PKC regulation in SHHF rat left ventricle (LV). Both the ARB and Hy normalized LV blood pressure, but only the ARB reduced heart mass. Neither treatment affected PKC expression or activity. Our data show differential activation of PKC in the hypertensive, hypertrophic SHHF rat heart. Regression of hypertrophy elicited by an ARB in this model occurred independently of changes in the expression and activity of the PKC isoforms examined.

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CRRD Object Information
CRRD ID: 1581271
Created: 2006-09-25
Species: All species
Last Modified: 2006-09-25
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.