1. We have tested in unanaesthetized rabbits two hypotheses regarding a physiological role for cardiogenic chemoreflexes in acute central hypovolaemia. 2. In rabbits, the sympathoinhibitory phase of acute central hypovolaemia depends on the activation of a brain‐stem δ‐opioid receptor mechanism by a signal from the heart. Blockade of this by fourth ventricular injection of the δ‐receptor antagonist ICI 174864 had no effect on the reflex haemodynamic responses to left atrial phenylbiguanide or intrapericardial nicotine. 3. Intravenous administration of the 5‐HT3 receptor antagonist MDL 72222, or intrapericardial administration of the nicotinic ganglionic cholinoceptor antagonist mecamylamine HCl, had no effect on the haemodynamic response to acute central hypovolaemia. 4. We conclude that phenylbiguanide‐sensitive myocardial afferents and nicotine‐sensitive epicardial afferents play no part in the response to acute hypovolaemia in rabbits, and that the reflex effects evoked by chemically exciting these afferents do not depend on a brain‐stem δ‐opioid mechanism.
|Number of pages||5|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 1991|
- Bezold‐Jarisch reflex
- cardiopulmonary chemoreflexes
- receptors nicotinic
- receptors opioid
- receptors serotonergic.