Carotid body (CB) hyperactivity promotes hypertension in response to chronic intermittent hypoxia (CIH). The plasma concentration of adrenaline is reported to be elevated in CIH and our previous work suggests that adrenaline directly activates the CB. However, a role for chronic adrenergic stimulation in mediating CB hyperactivity is currently unknown. This study evaluated whether beta-blocker treatment with propranolol (Prop) prevented the development of CB hyperactivity, vascular sympathetic nerve growth and hypertension caused by CIH. Adult male Wistar rats were assigned into 1 of 4 groups: Control (N), N + Prop, CIH and CIH + Prop. The CIH paradigm consisted of 8 cycles h⁻¹, 8 h day⁻¹, for 3 weeks. Propranolol was administered via drinking water to achieve a dose of 40 mg kg⁻¹ day⁻¹. Immunohistochemistry revealed the presence of both β₁ and β₂-adrenoceptor subtypes on the CB type I cell. CIH caused a 2–3-fold elevation in basal CB single-fibre chemoafferent activity and this was prevented by chronic propranolol treatment. Chemoafferent responses to hypoxia and mitochondrial inhibitors were attenuated by propranolol, an effect that was greater in CIH animals. Propranolol decreased respiratory frequency in normoxia and hypoxia in N and CIH. Propranolol also abolished the CIH mediated increase in vascular sympathetic nerve density. Arterial blood pressure was reduced in propranolol groups during hypoxia. Propranolol exaggerated the fall in blood pressure in most (6/7) CIH animals during hypoxia, suggestive of reduced sympathetic tone. These findings therefore identify new roles for β-adrenergic stimulation in evoking CB hyperactivity, sympathetic vascular hyperinnervation and altered blood pressure control in response to CIH.

颈动脉体（CB）过度活跃会促进慢性间歇性缺氧（CIH）引起的高血压。据报道，CIH 中肾上腺素的血浆浓度升高，我们之前的工作表明肾上腺素直接激活 CB。然而，慢性肾上腺素能刺激在介导 CB 过度活跃中的作用目前尚不清楚。本研究评估了β受体阻滞剂与普萘洛尔 (Prop) 的治疗是否可以预防 CIH 引起的 CB 过度活跃、血管交感神经生长和高血压的发生。成年雄性Wistar大鼠被分配到4组中的一组：对照(N)、N+Prop、CIH和CIH+Prop。CIH范例由8个周期h ^-1 、8 h day ^-1组成，持续3周。通过饮用水施用普萘洛尔以达到40mg kg ^-1天^-1的剂量。免疫组织化学显示 CB I 型细胞上存在_β1和_β2肾上腺素受体亚型。 CIH 导致基础 CB 单纤维化学传入活性升高 2-3 倍，而长期普萘洛尔治疗可以预防这一情况。普萘洛尔减弱了对缺氧和线粒体抑制剂的化学传入反应，这种作用在 CIH 动物中更为明显。普萘洛尔降低常氧和缺氧 N 和 CIH 中的呼吸频率。普萘洛尔还消除了 CIH 介导的血管交感神经密度增加。缺氧期间普萘洛尔组的动脉血压降低。普萘洛尔在缺氧期间夸大了大多数（6/7）CIH 动物的血压下降，表明交感神经张力降低。 因此，这些发现确定了 β-肾上腺素能刺激在诱发 CB 过度活跃、交感血管过度神经支配和 CIH 反应中血压控制改变中的新作用。