Abstract

Aging leads to progressive pathophysiological changes in blood vessels of the brain and periphery. The aim of this study was to evaluate the effects of aging on cerebral vascular function and structure. Basilar arteries were isolated from male Fischer 344 cross Brown Norway (F344xBN) rats at 3, 8, and 24 months of age. The basilar arteries were cannulated in the pressurized system (90 cm H2O). Contractile responses to KCl (30–120 mmol/L) and endothelin‐1 (10−11–10−7 mol/L) were evaluated. Responses to acetylcholine (ACh) (10−10–10−4 mol/L), diethylamine (DEA)‐NONO‐ate (10−10–10−4 mol/L), and papaverin (10−10–10−4 mol/L) were assessed to determine both endothelium‐dependent and endothelium‐independent responsiveness. Advanced aging (24 months) decreased responses of the basilar artery to both the contractile and relaxing agents; whereas, DEA‐induced dilation was significantly higher in the 8‐month‐old group compared with the younger and older groups. The arterial wall‐to‐lumen ratio was significantly increased in 24‐month‐old rats. Smooth muscle cell count was also decreased in old rats. These findings indicate that aging produces dysfunction of both the endothelium and the vascular smooth muscle in the basilar artery. Aging also alters wall structure of the basilar artery, possibly through decreases in smooth muscle cell number and concomitant hypertrophy.

Highlights

  • Aging is associated with increased risk of cardiovascular disease

  • Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society

  • KCl contracted the basilar arteries in a concentrationdependent manner with decreased sensitivity and diminished maximal response demonstrated in arteries from aged rats (Fig. 1A)

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Summary

Introduction

Aging is associated with increased risk of cardiovascular disease. The prevalence of hypertension, atherosclerosis, and other cardiovascular complications increase with age. The increase in intima-media thickness and vascular stiffness; the reduced number of smooth muscle cells and production/ availability of endothelial nitric oxide (NO) and other vasoactive agents; and the increased oxidative stress are proposed mechanisms that impair vascular homeostasis. These subtle changes conspire to trigger vascular dysfunction and a 2014 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society

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