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© 2001 American Heart Association, Inc.

Letter to the Editor

Upregulation of the Nitric Oxide-cGMP Pathway in Aged Myocardium

Saqib Chowdhary, G. Andre Ng, Sarah L. Nuttall, Jonathan N. Townend

Department of Cardiovascular Medicine, University of Birmingham, Birmingham, UK, S.Chowdhary@bham.ac.uk

	Upregulation of the Nitric Oxide–cGMP Pathway in Aged Myocardium

 
To the Editor:

Zieman et al¹ recently assessed the effect of age on the cardiac NO-cGMP pathway postulating that, since NO promotes ventricular relaxation, a reduction in functional NO activity may explain the increased ventricular diastolic dysfunction associating with normal aging. Perhaps surprisingly, the authors observed that elderly male Wistar rats (22 to 25 months old) showed higher constitutive cardiac NOS activity and cardiac endothelial nitric oxide synthase (eNOS) levels than young adult rats (4 to 7 months). Much of this increased activity appeared to take place in the cardiac endothelium rather than the myocytes. The authors concluded that the age-related impairment of ventricular relaxation is mediated by mechanisms other than NO, and, indeed, increased NO production may act as a failed adaptive mechanism in this pathology. This is in notable contrast to the situation in vascular endothelium where impaired endothelial function seems due to reduced eNOS activity as seen in the aorta of the same rat model.^{2 3} We believe that caution should be exercised in applying the results of this model to human aging. Important differences exist in cardiac structural changes associated with aging between Wistar rats and humans. The aged male Wistar rats in this study showed an almost 50% increase in heart weight over younger rats. Such cardiac hypertrophy in the absence of hypertension is a recognized feature of aging in these animals and is not reproduced in the elderly human male.⁴ Zieman et al¹ offer no explanation of how this species-related cardiomyopathy may have influenced their . . . [Full Text of this Article]