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Chronic catecholamine depletion in rats and guinea-pigs increased [3H]dihydroalprenolol binding sites by 1.41- and 1.52-fold, though calculated requirements for observed supersensitivity were higher.
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The observed increase in beta-adrenoceptor number following catecholamine depletion is insufficient to fully explain the degree of cardiac supersensitivity to isoprenaline.
Chronic catecholamine depletion induced by reserpine pretreatment of rats, or 6-hydroxydopamine pretreatment of guinea-pigs, resulted in an enhanced sensitivity of isolated papillary muscles to isoprenaline. This hypersensitivity was accompanied by 1.41-(rats) and 1.52-fold (guinea-pigs) increases in the number of [3H]dihydroalprenolol binding sites, without changes in binding affinity. An equation was derived for calculation of increases in receptor number. Application of this showed that substantially greater increases in receptor number were required (2.32- to 4.04-fold) to account for the degree of supersensitivity observed.
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Chess‐Williams et al. (1986) studied this question. Chronic catecholamine depletion (reserpine or 6-hydroxydopamine pretreatment) was evaluated on Number of [3H]dihydroalprenolol binding sites and cardiac sensitivity to isoprenaline. Chronic catecholamine depletion in rats and guinea-pigs increased [3H]dihydroalprenolol binding sites by 1.41- and 1.52-fold, though calculated requirements for observed supersensitivity were higher.
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