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Involvement of the cholinergic system of the posterior hypothalamic nucleus (PHN) during the reflex compensatory response to hemorrhage

Stimulation of muscarinic receptors within the PHN of the rat evokes a pressor response. It is not known whether this cholinergic system is activated during a depressor event in an effort to overcome the depressed blood pressure. The goal of the present study was to evaluate whether the PHN cholinergic system is activated during the compensatory reflex response to moderate hemorrhage. Since cannabinoids (CBs) appear to modulate acetylcholine release, the effect of the presence of a CB agonist in the PHN during recovery to hemorrhage was also studied. Carbachol (CCh), a cholinergic agonist, methyl‐atropine (MeATR), a muscarinic receptor antagonist, or CP 55,940, a CB1 receptor agonist, were administered into the PHN of urethane‐anesthetized rats following moderate hemorrhage (20% blood loss). None of the treatments affected the percent MAP recovery or the change in heart rate post‐hemorrhage. While CCh did not affect the rate of recovery of the mean arterial pressure (MAP), both MeATR and CP 55,940 decreased the recovery rate of MAP. The decreased rate of MAP recovery in the presence of CP 55,940 was reversed by pretreatment with AM 251, a CB1 receptor antagonist/inverse agonist. Furthermore, CP 55,940 decreased survival compared to saline‐treated rats. These results suggest that cholinergic activity within the PHN increases during the reflex compensatory response to moderate hemorrhage, and that CBs can decrease this activity through the CB1 cannabinoid receptor. (Supported by a grant from the KCOM Graduate Program Committee.)