Journal of Applied Physiology
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J Appl Physiol 84: 2099-2105, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 6, 2099-2105, June 1998

Hypercapnia-induced long-term depression of respiratory activity requires alpha 2-adrenergic receptors

K. B. Bach and G. S. Mitchell

Department of Comparative Biosciences and Center for Neuroscience, University of Wisconsin, Madison, Wisconsin 53706

We investigated the effects of repeated hypercapnic episodes (inspired CO2 fraction = 0.10) on posthypercapnic respiratory nerve discharge. Anesthetized (urethan), vagotomized, and artificially ventilated rats were presented with three consecutive 5-min episodes of hyperoxic hypercapnia, separated by 5 min of hyperoxic normocapnia (inspired O2 fraction = 0.5). Respiratory nerve discharge and blood gases were recorded before and 30 and 60 min after the final hypercapnic episode. Posthypercapnia, arterial PCO2 was maintained within 1 Torr of initial baseline values. Integrated phrenic and hypoglossal burst amplitudes decreased posthypercapnia by up to 46 ± 17 and 55 ± 13% of baseline values, respectively, and remained reduced for at least 1 h [long-term depression (LTD)]. The protocol was repeated in rats pretreated with the alpha 2-adrenergic antagonists yohimbine HCl (0.5 mg/kg; n = 7) or 2-[2-(2-methoxy-1,4-benzodioanyl)]imidazoline (RX-821002) HCl (0.25 mg/kg; n = 3). Both drugs attenuated LTD in the phrenic and hypoglossal neurograms. Results indicate that episodic hypercapnia elicits a yohimbine- and RX-821002-sensitive LTD of respiratory nerve activity in rats, suggesting that LTD requires alpha 2-receptor activation.

respiratory control; catecholamines; yohimbine; RX-821002; phrenic nerve; hypoglossal nerve; norepinephrine


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