Why the study?
Does physiologic (exercise) and pharmacologic (isoproterenol) sympathetic stimulation modify beta-adrenoceptor density in a patient with pure autonomic failure compared to normal subjects?
Does physiologic (exercise) and pharmacologic (isoproterenol) sympathetic stimulation modify beta-adrenoceptor density in a patient with pure autonomic failure compared to normal subjects?
In pure autonomic failure, the inability to upregulate beta-adrenoceptor density during sympathetic stimulation may contribute to the poor circulatory adjustments observed in these patients.
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May underlie hemodynamic instability in pure autonomic failure; case-control data leave open causal role and generalizability.
In a patient with pure autonomic failure, exercise did not modify beta-adrenoceptor density, probably due to an insufficient increase in plasma catecholamines. Isoproterenol infusion increased the number of beta-adrenoceptor by only 17%. Since in control subjects an increased beta-adrenoceptor level was found, following both physical stress and isoproterenol infusion, we suggest that the lack of increased beta-adrenoceptor levels may contribute to the poor circulatory adjustments observed in autonomic dysfunction during activities involving the sympathetic nervous system.
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Perna et al. (1992) studied this question.
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