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Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
Published on: June 29, 2014
Multiple polyamine regulatory pathways control compensatory cardiovascular hypertrophy in coarctation hypertension
D W Lipke1, P S Newman, S Tofiq
1Division of Pharmacology and Experimental Therapeutics College of Pharmacy, University of Kentucky Lexington 40536, USA.
Abstract:
While a number of factors may initiate structural alterations within the cardiovascular system in response to hypertension, there are obligate cellular signaling mechanisms, such as the polyamines, through which they must operate. This study examined the effects of polyamine synthesis inhibition using eflornithine, a suicide inhibitor of ornithine decarboxylase on blood pressure, compensatory remodeling of the cardiovascular system, and cardiac and aortic polyamine contents using an aortic coarctation model in rats. Eflornithine treatment failed to reduce carotid arterial blood pressure and actually significantly elevated vascular pressure above and below the coarctation site by 14 days of hypertension. Eflornithine only transiently reduced aortic polyamine content of hypertensive rats while this agent reduced coarctation-induced aortic medial wall thickening and the synthesis/deposition of fibronectin and laminin in the hypertensive aorta. Increases in left ventricular mass and polyamine content were concomitantly reduced in hypertensive rats administered eflornithine. These results suggest that multiple polyamine regulatory pathways may maintain vascular polyamine content in response to aortic coarctation; however de novo polyamine synthesis is essential for select aspects of vascular remodeling, including matrix synthesis. Cardiac tissue, in contrast, may rely principally on de novo polyamine synthesis.
Insights
Inhibiting polyamine synthesis with eflornithine did not lower blood pressure in hypertensive rats but did reduce vascular remodeling and matrix synthesis. Cardiac polyamine levels were also reduced.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Pharmacology
Background:
- Hypertension induces cardiovascular structural changes via cellular signaling pathways.
- Polyamines are critical signaling molecules involved in cellular processes.
Purpose of the Study:
- To investigate the role of polyamine synthesis in hypertension-induced cardiovascular remodeling.
- To assess the effects of eflornithine, a polyamine synthesis inhibitor, on blood pressure and vascular structure in a rat model.
Main Methods:
- Utilized an aortic coarctation model in rats to induce hypertension.
- Administered eflornithine, an ornithine decarboxylase inhibitor, to assess its impact on polyamine levels, blood pressure, and cardiovascular remodeling.
- Quantified polyamine content, vascular wall thickness, fibronectin, laminin, and left ventricular mass.
Main Results:
- Eflornithine treatment did not reduce blood pressure; instead, it elevated vascular pressure.
- Eflornithine transiently decreased aortic polyamine content but reduced aortic medial wall thickening and matrix protein synthesis (fibronectin, laminin).
- Left ventricular mass and polyamine content increases were reduced in eflornithine-treated hypertensive rats.
Conclusions:
- De novo polyamine synthesis is crucial for specific vascular remodeling processes, including matrix synthesis, in response to hypertension.
- Multiple polyamine regulatory pathways may contribute to maintaining vascular polyamine levels.
- Cardiac tissue appears to rely primarily on de novo polyamine synthesis for its polyamine content.
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