To test the hypothesis that beta 2 adrenergic receptors mediate the chronotropic more than the inotropic response to endogenous catecholamines the effects on the haemodynamic responses to exercise in dogs of the beta 1 specific antagonist atenolol were compared with those of the non-selective beta antagonist propranolol. Heart rate, left ventricular dP/dt at 40 mmHg developed pressure (dP/dt40), and oxygen consumption (VO2) were determined at seven to eight exercise levels in 16 chronically instrumented adult mongrel dogs with and without beta blockade. In doses that produced equivalent suppression of resting heart rate, propranolol and atenolol affected dP/dt40 similarly at all exercise levels. In contrast to atenolol, which affected heart rate equally at all workloads, propranolol inhibited heart rate more as the workload increased, resulting in a 1.55-fold greater percentage inhibition of chronotropy at a VO2 of 60 ml.Kg-1.min-1 a than at a VO2 of 30 ml.kg-1.min-1. These results are compatible with the hypothesis that, although beta 2 receptors appear to have little influence over cardiac inotropy during exercise, sinoatrial beta 2 receptors may be stimulated by circulating catecholamines and contribute greatly to sympathetic modulation of heart rate during heavy exercise in dogs.

SUMMARYMean arterial pressure (MAP) and heart rate (HR) were measured during static contraction or passive stretch of the triceps surae muscle of chloralose-anaesthetized cats. MAP and HR increased by 46 + 5 mmHg and 17 + 3 beats min-', respectively, during a 1 min contraction.Passive stretch of the same muscle for 1 min reflexly increased MAP and HR by 40 + 7 mmHg and 14 + 3 beats minm , respectively. Microdialysis of 2 mm 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA receptor antagonist, into the dorsal horn at the L7 spinal level attenuated the reflex pressor response to static contraction (2 h of dialysis: AMAP = 23 + 5 mmHg, AHR = 8 + 2 beats min-'). By contrast, there was no attenuation of the pressor response to passive stretch at 2 h of CNQX perfusion. However, the simultaneous microdialysis of 2 mM CNQX into the L6 and S 1 levels blunted the pressor and tachycardic responses to contraction and stretch. These data show that the reflex pressor response to static muscle contraction is partly mediated by activation of non-NMDA receptors at the level of afferent fibre entry into the dorsal horn and through collateral pathways. Further, it appears that the afferent pathways within the dorsal horn for the signal transduction arising from static muscle contraction and passive stretch of the hindlimb are dissimilar.