Neurotransmitter Release from the Rabbit Carotid Body: Differential Effects of Hypdxia on Substance P and Acetylcholine Release

Abstract

The mechanism(s) by which carotid body senses low oxygen remains to be an active area of investigation. It is currently believed that hypoxia causes membrane depolarization, activation of voltage-dependent Cat+ channel(s), elevation in the cytosolic calcium, and release of neurotransmitter(s) leading to increase in the sensory discharge of the carotid body6’7. Multiple neurotransmitters are expressed in the carotid body including acetylcholine, catecholamines, substance P-like neuropeptides and gas molecules (see Ref. [7] for review). While acetylcholine (ACh) and substance P (SP) augment the sensory response of the carotid body, dopamine, enkephalins, and atrial natriuretic peptide inhibit the carotid body activity. Based on a variety of observations reported in the literature, it has been postulated that hypoxia facilitates the concurrent release of several neurotransmitters from the carotid body and potential interactions among these neurotransmitters are of importance in shaping the sensory response of the carotid body to hypoxia7. As a first step toward testing this hypothesis, in the present study, we have determined the release of SP and ACh from the carotid body in response to hypoxia and assessed whether the magnitude of their release is comparable or differs from each other.