Abstract
Spontaneously hypertensive rats (SHR), like patients with sleep apnea, have hypertension, increased sympathetic activity, and increased chemoreceptor drive. We investigated the role of carotid chemoreceptors in cardiovascular responses induced by obstructive apnea in awake SHR. A tracheal balloon and vascular cannulas were implanted, and a week later, apneas of 15 s each were induced. The effects of apnea were more pronounced in SHR than in control rats (Wistar Kyoto; WKY). Blood pressure increased by 57±3 mmHg during apnea in SHR and by 28±3 mmHg in WKY (p<0.05, n = 14/13). The respiratory effort increased by 53±6 mmHg in SHR and by 34±5 mmHg in WKY. The heart rate fell by 209±19 bpm in SHR and by 155±16 bpm in WKY. The carotid chemoreceptors were then inactivated by the ligation of the carotid body artery, and apneas were induced two days later. The inactivation of chemoreceptors reduced the responses to apnea and abolished the difference between SHR and controls. The apnea-induced hypertension was 11±4 mmHg in SHR and 8±4 mmHg in WKY. The respiratory effort was 15±2 mmHg in SHR and 15±2 mmHg in WKY. The heart rate fell 63±18 bpm in SHR and 52±14 bpm in WKY. Similarly, when the chemoreceptors were unloaded by the administration of 100% oxygen, the responses to apnea were reduced. In conclusion, arterial chemoreceptors contribute to the responses induced by apnea in both strains, but they are more important in SHR and account for the exaggerated responses of this strain to apnea.
Highlights
Several studies suggest that overactive carotid chemoreceptors can lead to sympathetic activation and hypertension
Behavioral responses to apnea were abolished by bilateral ligation of the carotid body artery, and by inhaling 100% oxygen before induction of apnea
The most interesting new findings of our study were that the cardiovascular responses induced by obstructive apnea were much larger in spontaneously hypertensive rat (SHR) than in normotensive Wistar Kyoto rats (WKY) rats, and that responses to apnea after chemoreceptor inactivation were similar in both
Summary
Several studies suggest that overactive carotid chemoreceptors can lead to sympathetic activation and hypertension. This mechanism may contribute to hypertension induced by obstructive sleep apnea [1,2,3] and by other causes [4,5,6,7,8]. Hypertensive rats are commonly used to study mechanisms of hypertension because of their similarities with hypertensive human patients, including sympathetic activation and chemoreceptor function. Several studies have shown that carotid chemoreceptors are larger and more sensitive in the spontaneously hypertensive rat (SHR) than in normotensive controls [10,11,12]. It has been suggested that increased carotid chemoreceptor activity contributes to the development and maintenance of hypertension in the SHR [13,14], presumably through chemoreceptor-related stimulation of sympathetic activity
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