The sympathetic nervous system exacerbates carotid body sensitivity in hypertension.
The sympathetic nervous system exacerbates carotid body sensitivity in hypertension.
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DOI：
10.1093/cvr/cvac008
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发表时间：
2023-03-17
影响因子：
10.8
通讯作者：
Paton JFR
中科院分区：
文献类型：
--
作者：
Felippe ISA;Zera T;da Silva MP;Moraes DJA;McBryde F;Paton JFR
自发性高血压（SH）大鼠颈动脉体（CBs）表现出高张力和高反射性，导致外周交感神经流出增加。我们假设脑脊液的高兴奋性是由其自身的交感神经支配驱动的。为了验证这一点，在SH和Wistar大鼠的原位化学反射被激活（NaCN 50-100µL, 0.4µg/µL）前后：(i)电刺激（ES; 30 Hz, 2 ms, 10 V）颈上神经节（SCG），该神经节支配脑后皮层；（ii）单侧切除SCG (SCGx)；（iii） CB注射α1-肾上腺素受体激动剂（苯肾上腺素，50µL, 1 mmol/L）， (iv) α1-肾上腺素受体拮抗剂哌唑嗪（40µL, 1 mmol/L）或坦索罗辛（50µL, 1 mmol/L）。SCG的ES可使cb诱发的交感神经兴奋增强40-50% (P < 0.05)，但不同品系间无差异。单侧SCGx可减弱SH (62%, P < 0.01)，但对Wistar大鼠无影响；它还可以消除SH大鼠化学感受性岩神经元的持续放电，使其变得超极化。在Wistar大鼠中，CB注射苯肾上腺素可增强CB诱发的交感神经兴奋（33%,P < 0.05），而在SH大鼠中，prazosin可抑制CB引起的交感神经兴奋（26%,P < 0.05）。坦索罗辛在SH大鼠体内重现了吡唑嗪的作用，并阻止了ES后SCG的致敏作用。在CB内，α1A-和α 1b -肾上腺素受体在球囊细胞和血管上共定位。在记录血压（BP）的有意识SH大鼠中，SCGx后cbb诱发的降压反应减弱，收缩压下降16±4.85 mmHg。脑脊液的交感神经被紧张性激活，使SH的脑脊液敏感，但Wistar大鼠不敏感。此外，cb诱发的反射交感神经兴奋的增敏似乎是由位于血管和/或血管球细胞上的α - 1肾上腺素受体介导的。SCG是控制高血压CB病理生理的新靶点。
The carotid bodies (CBs) of spontaneously hypertensive (SH) rats exhibit hypertonicity and hyperreflexia contributing to heightened peripheral sympathetic outflow. We hypothesized that CB hyperexcitability is driven by its own sympathetic innervation. To test this, the chemoreflex was activated (NaCN 50–100 µL, 0.4 µg/µL) in SH and Wistar rats in situ before and after: (i) electrical stimulation (ES; 30 Hz, 2 ms, 10 V) of the superior cervical ganglion (SCG), which innervates the CB; (ii) unilateral resection of the SCG (SCGx); (iii) CB injections of an α1-adrenergic receptor agonist (phenylephrine, 50 µL, 1 mmol/L), and (iv) α1-adrenergic receptor antagonist prazosin (40 µL, 1 mmol/L) or tamsulosin (50 µL, 1 mmol/L). ES of the SCG enhanced CB-evoked sympathoexcitation by 40–50% (P < 0.05) with no difference between rat strains. Unilateral SCGx attenuated the CB-evoked sympathoexcitation in SH (62%; P < 0.01) but was without effect in Wistar rats; it also abolished the ongoing firing of chemoreceptive petrosal neurones of SH rats, which became hyperpolarized. In Wistar rats, CB injections of phenylephrine enhanced CB-evoked sympathoexcitation (33%; P < 0.05), which was prevented by prazosin (26%; P < 0.05) in SH rats. Tamsulosin alone reproduced the effects of prazosin in SH rats and prevented the sensitizing effect of the SCG following ES. Within the CB, α1A- and α1B-adrenoreceptors were co-localized on both glomus cells and blood vessels. In conscious SH rats instrumented for recording blood pressure (BP), the CB-evoked pressor response was attenuated after SCGx, and systolic BP fell by 16 ± 4.85 mmHg. The sympathetic innervation of the CB is tonically activated and sensitizes the CB of SH but not Wistar rats. Furthermore, sensitization of CB-evoked reflex sympathoexcitation appears to be mediated by α1-adrenoceptors located either on the vasculature and/or glomus cells. The SCG is novel target for controlling CB pathophysiology in hypertension.
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DOI：
10.1038/s41581-019-0244-2
发表时间：
2020-04
期刊：
Nature reviews. Nephrology
影响因子：
--
作者：
Mills KT;Stefanescu A;He J
通讯作者：
He J
影响因子：
29
作者：
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通讯作者：
Allen, Andrew M.
影响因子：
5.5
作者：
Marcus, Noah J.;Del Rio, Rodrigo;Schultz, Harold D.
通讯作者：
Schultz, Harold D.
DOI：
10.1016/0165-1838(87)90117-2
发表时间：
1987-03-01
期刊：
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
影响因子：
--
作者：
BROKAW, JJ;HANSEN, JT
通讯作者：
HANSEN, JT
DOI：
10.1002/cne.24936
发表时间：
2021-01
期刊：
The Journal of comparative neurology
影响因子：
--
作者：
Bookout AL;Gautron L
通讯作者：
Gautron L