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β-Adrenergic Function in Aging

Basic Mechanisms and Clinical Implications

  • Physiological Aspects Of Aging
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Summary

Catecholamines have an important endocrine and neuroendocrine role in mediating a variety of autonomic functions. One consequence of normal aging, in particular in the cardiovascular system, is a decline in β-adrenergic function associated with an alteration in responsiveness to β-adrenergic therapy. The intrinsic ability for muscle contractility or relaxation is maintained with age and there appears to be an alteration in the process linking the receptor with the contractile or relaxation mechanisms.

In rats, β-adrenergic receptor density decreases with age in adipose tissues and most brain areas, is unchanged in lymphocytes, heart and lung, and increases in the liver. In humans, there are no receptor changes with age in either lymphocytes or brain. In contrast, the number of high-affinity receptors (or coupled receptors) decreases with age in most tissues. In addition, there is a decrease in membrane adenylate cyclase activity or cellular production of cyclic adenosine monophosphate (adenosine 3′,5′-cyclic phosphate; cAMP).

Plasma noradrenaline (norepinephrine) concentration increases with age. The reduced receptor number in some tissues (down-regulation), the reduced high-affinity receptors and the reduced hormone-stimulated adenylate cyclase activity with age suggests receptor desensitisation to increased plasma noradrenaline concentration. The inability of older animals to desensitise to β-adrenergic agonists further supports this hypothesis. However, there is an additional post-receptor reduction in catalytic unit activity with age independent of desensitisation.

Medications directed at the β-adrenergic system are commonly used in the elderly. Many of the data on the impact of age on clinical responses are conflicting or unavailable. Concomitant disease, functional status, nutritional state and polypharmacy may play an even greater role than age. However, the available data can be used to guide the selection of therapy, anticipate side effects, and predict potential interactions with other medications and diseases.

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Acknowledgements

This work was supported by the Medical Research Service of the Department of Veterans Affairs (PJS and NT) and by US Public Health Service grant K08 AG 00387 (SLM). The authors appreciate the assistance of Linda Pritchett in the preparation of the manuscript.

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  1. Geriatric Rcsearch, Education and Clinical Center, Department of Veterans Affairs Medical Center, University of Florida, Gainesville, Florida, 32608-1197, USA

    Philip J. Scarpace & Nihal Turner

  2. Department of Pharmacology, University of Florida, Gainesville, Florida, USA

    Scott L. Mader

  3. Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA

    Philip J. Scarpace & Nihal Turner

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Scarpace, P.J., Turner, N. & Mader, S.L. β-Adrenergic Function in Aging. Drugs & Aging 1, 116–129 (1991). https://doi.org/10.2165/00002512-199101020-00004

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