OPIOID RECEPTORS AND PREJUNCTIONAL MODULATION OF CAPSAICIN-SENSITIVE SENSORY NERVES IN GUINEA-PIG LEFT ATRIUM

1. In the isolated electrically driven left atria from reserpine-pretreated guinea-pigs and in presence of 1 μM atropine, electrical field stimulation (EFS) at 10 Hz produces a delayed positive inotropic response (DPIR) involving activation of capsaicin-sensitive afferents. 2. Opioids inhibited the DPIR with the following order of potency: dermorphin > [d-Ala2, N-MePhe4, Gly5-ol]-enkephalin (DAGO) ≥ [d-Ala2,d-Leu5]-enkephalin (DADLE) > morphine > dynorphin A (1-13) > [d-Pen2, d-Pen5]-enkephalin (DPDPE). U-50488 was ineffective up to 10 μM. 3. Opioids also inhibited resting inotropism (3 Hz) with the following rank order of potency: DADLE > DAGO > U-50488 = dynorphin A (1-13) = morphine = DPDPE. 4. Both inhibition of the DPIR and inhibition of resting inotropism were prevented by 10 μ M naloxone. 5. Neither dermorphin (0.1 μ M) nor DAGO (0.3 μM) or DADLE (1 μM) inhibit responses produced by capsaicin (30 nM) or calcitonin gene-related peptide (3 nM). 6. These findings indicate that capsaicin-sensitive nerves in the guinea-pig atrium are endowed with μ opioid receptors which inhibit transmitter release when sensory nerve terminals are activated by EFS but not by capsaicin. © 1990.