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Intracarotid norepinephrine infusions inhibit ventilation in goats.
J Pizarro1, M M Warner, M Ryan
1Department of Comparative Biosciences, University of Wisconsin, Madison 53706.
Respiration Physiology
|December 1, 1992
Summary
Norepinephrine (NE) inhibits ventilation in goats by acting on carotid chemoreceptors, particularly during normoxia. This effect involves alpha-adrenergic and D2-dopaminergic receptors and is independent of blood pressure changes.
Area of Science:
- Physiology
- Neuroscience
- Respiratory Control
Background:
- Plasma norepinephrine increases during exercise, especially under hypoxic conditions.
- The carotid body (CB) plays a crucial role in mediating ventilatory responses to physiological stimuli.
- Understanding norepinephrine's effect on ventilatory control is essential for respiratory physiology.
Purpose of the Study:
- To investigate the carotid body-mediated effects of norepinephrine on ventilatory control in goats.
- To determine the specific receptors involved in norepinephrine-induced ventilatory changes.
- To differentiate the effects of norepinephrine from baroreceptor feedback and blood pressure changes.
Main Methods:
- Infusion of norepinephrine (NE) into the carotid artery of awake goats, both with intact and denervated carotid bodies.
- Measurements of pulmonary ventilation (VI), arterial blood gases, and blood pressure under normoxic and hypoxic conditions.
- Administration of alpha-adrenergic (phenoxybenzamine), beta-adrenergic (propranolol), and D2-dopamine receptor (domperidone) antagonists.
Main Results:
- NE infusion into the CB-intact carotid artery significantly decreased VI and increased PaCO2 in normoxia, but not in hypoxia.
- NE infusion into the CB-denervated carotid artery did not affect VI or PaCO2, despite increasing blood pressure.
- Ventilatory inhibition by NE was blocked by domperidone and partially blocked by phenoxybenzamine, but unaffected by propranolol.
Conclusions:
- Norepinephrine inhibits ventilation in goats through a mechanism involving carotid chemoreceptors.
- This NE-induced ventilatory inhibition is independent of blood pressure changes and baroreceptor reflexes.
- The effect appears to be mediated by both alpha-adrenergic and D2-dopaminergic receptors on the carotid body.