beta-Adrenoceptor mRNA is expressed in the human heart, but corresponding receptor protein has not yet consistently been demonstrated. Furthermore, their physiological role remains highly controversial. For example, in human atria these receptors apparently do not promote cAMP formation. Evidence presented in this issue of the BJP suggests that a previously reported beta-adrenoceptor-mediated stimulation of Ca(2+) channels at room temperature is absent at physiological temperatures, and that beta-adrenoceptors have no effect on atrial contraction. Drugs classified as beta-adrenoceptor agonists cause contraction in human atria but in most cases this involves beta- and/or beta-adrenoceptors. In contrast, in human ventricles beta-adrenoceptor agonists can exhibit negative inotropic effects, potentially involving Pertussis toxin-sensitive G-proteins and activation of a NO synthase. However, firmer pharmacological evidence is required that these effects indeed occur via beta-adrenoceptors. Whether the expected future use of beta-adrenoceptor agonists in the treatment of urinary bladder dysfunction is associated with adverse events related to cardiac function remains to be determined from clinical studies.
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