Key result
The alpha 2-agonist B-HT 920 increased cardiac output in pithed rats but not cats, while the alpha 1-agonist methoxamine increased cardiac output in both species.
Why the study?
Do alpha-1 and alpha-2 adrenoceptor agonists increase cardiac output in pithed rats and cats?
Do alpha-1 and alpha-2 adrenoceptor agonists increase cardiac output in pithed rats and cats?
The study demonstrates species differences in functional venous alpha-2 adrenoceptors, present in rats but absent in cats, and shows that alpha-2 mediated venoconstriction is independent of extracellular calcium.
Species differences in alpha-2 venoconstriction limit rodent data extrapolation; leaves open translational relevance of adrenoceptor effects on cardiac output.
In pithed rats, but not in pithed cats, the alpha 2-/dopamine agonist B-HT 920 (10-300 micrograms kg-1) increased cardiac output. The increase was inhibited by yohimbine (1 mg kg-1), but not by sulpiride (0.3 mg kg-1) and nifedipine (1 mg kg-1). Both in pithed rats and cats, the alpha 1-adrenoceptor agonist methoxamine (30-300 micrograms kg-1 and 30-1000 micrograms kg-1, respectively) increased cardiac output. This increase (rats) was inhibited by prazosin (0.1 mg kg-1). The results indicate the existence of functional venous alpha 2-adrenoceptors in pithed rats, and their absence in pithed cats. Furthermore, alpha 2-adrenoceptor-mediated venoconstriction appears independent of extracellular calcium.
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Kalkman et al. (1984) studied this question. alpha 1- and alpha 2-adrenoceptor agonists (B-HT 920 and methoxamine) was evaluated on Cardiac output. The alpha 2-agonist B-HT 920 increased cardiac output in pithed rats but not cats, while the alpha 1-agonist methoxamine increased cardiac output in both species.
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