Petrosal ganglion responses to acetylcholine and ATP are enhanced by chronic normobaric hypoxia in the rabbit

Icekson, Gabriel; Domínguez, Claudia V.; Dedios, Valentina P.; Arroyo, Jorge G.; Alcayaga, Julio

doi:10.1016/j.resp.2013.07.023

Cited by 8 publications

(6 citation statements)

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“…Animals ( n = 12) were exposed to normoxia ( n = 6), serving as controls for normobaric hypoxia ( n = 6) for 2 weeks as previously described (Icekson et al, 2013). Briefly, three rats were allocated to a cage (D × W × H; 48 cm × 26 cm × 15 cm) and two cages were placed in a 300 L (60 cm × 50 cm × 100 cm) acrylic chamber with a hermetic lid.…”

Section: Methodsmentioning

confidence: 99%

Imbalance in Renal Vasoactive Enzymes Induced by Mild Hypoxia: Angiotensin-Converting Enzyme Increases While Neutral Endopeptidase Decreases

et al. 2018

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Chronic hypoxia has been postulated as one of the mechanisms involved in salt-sensitive hypertension and chronic kidney disease (CKD). Kidneys have a critical role in the regulation of arterial blood pressure through vasoactive systems, such as the renin-angiotensin and the kallikrein–kinin systems, with the angiotensin-converting enzyme (ACE) and kallikrein being two of the main enzymes that produce angiotensin II and bradykinin, respectively. Neutral endopeptidase 24.11 or neprilysin is another enzyme that among its functions degrade vasoactive peptides including angiotensin II and bradykinin, and generate angiotensin 1–7. On the other hand, the kidneys are vulnerable to hypoxic injury due to the active electrolyte transportation that requires a high oxygen consumption; however, the oxygen supply is limited in the medullary regions for anatomical reasons. With the hypothesis that the chronic reduction of oxygen under normobaric conditions would impact renal vasoactive enzyme components and, therefore; alter the normal balance of the vasoactive systems, we exposed male Sprague-Dawley rats to normobaric hypoxia (10% O2) for 2 weeks. We then processed renal tissue to identify the expression and distribution of kallikrein, ACE and neutral endopeptidase 24.11 as well as markers of kidney damage. We found that chronic hypoxia produced focal damage in the kidney, mainly in the cortico-medullary region, and increased the expression of osteopontin. Moreover, we observed an increase of ACE protein in the brush border of proximal tubules at the outer medullary region, with increased mRNA levels. Kallikrein abundance did not change significantly with hypoxia, but a tendency toward reduction was observed at protein and mRNA levels. Neutral endopeptidase 24.11 was localized in proximal tubules, and was abundantly expressed under normoxic conditions, which markedly decreased both at protein and mRNA levels with chronic hypoxia. Taken together, our results suggest that chronic hypoxia produces focal kidney damage along with an imbalance of key components of the renal vasoactive system, which could be the initial steps for a long-term contribution to salt-sensitive hypertension and CKD.

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Section: Methodsmentioning

confidence: 99%

Imbalance in Renal Vasoactive Enzymes Induced by Mild Hypoxia: Angiotensin-Converting Enzyme Increases While Neutral Endopeptidase Decreases

et al. 2018

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“…In each experiment, two rabbits were simultaneously exposed to normobaric hypoxia as previously described [26] (Fig. 1a), with a total of eight rabbits exposed to CNH.…”

Section: Methodsmentioning

confidence: 99%

Effects of vagotomy on cardiovascular and heart rate variability alterations following chronic normobaric hypoxia in adult rabbits

et al. 2018

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Backgroundchronic hypoxia increases basal ventilation and pulmonary vascular resistance, with variable changes in arterial blood pressure and heart rate, but it’s impact on heart rate variability and autonomic regulation have been less well examined. We studied changes in arterial blood pressure, heart rate and heart rate variability (HRV) in rabbits subjected to chronic normobaric hypoxia (CNH; PB ~ 719 mmHg; FIO2 ~ 9.2%) for 14 days and assess the effect of autonomic control by acute bilateral vagal denervation.Resultsexposure to CNH stalled animal weight gain and increased the hematocrit, without affecting heart rate or arterial blood pressure. Nevertheless, Poincaré plots of the electrocardiographic R–R intervals showed a reduced distribution parallel to the line of identity, which interpreted as reduced long-term HRV. In the frequency domain, CNH reduced the very-low- (< 0.2 Hz) and high-frequency components (> 0.8 Hz) of the R–R spectrograms and produced a prominent component in the low-frequency component (0.2–0.5 Hz) of the power spectrum. In control and CNH exposed rabbits, bilateral vagotomy had no apparent effect on the short- and long-term HRV in the Poincaré plots. However, bilateral vagotomy differentially affected higher-frequency components (> 0.8 Hz); reducing it in control animals without modifying it in CNH-exposed rabbits.ConclusionsThese results suggest that CNH exposure shifts the autonomic balance of heart rate towards a sympathetic predominance without modifying resting heart rate or arterial blood pressure.

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“…Type I cells are known to respond to stimulatory inputs by releasing ATP, which binds to P2X2 and P2X3 purinoreceptors (organized in homomeric or heteromeric complexes) located in sensory endings tightly surrounding clusters of type I cells (Prasad et al, ; Piskuric and Nurse, ; Yokoyama et al, 2016). Acetylcholine is also released by type I cells and cholinergic receptors are present on CB afferent nerves (Icekson et al, ). Dopamine D2 receptors have also been reported in type I cells, petrosal ganglion cells and nerve bundles in the CB (Wakai et al, ).…”

Section: Targets Of the Csnmentioning

confidence: 99%

“…Acetylcholine has been considered to be a neurotransmitter involved in increased O2 sensitivity in chronic hypoxia, due to increased numbers of nicotinic cholinergic receptors on CB afferent nerves (Icekson et al, ).…”

Section: Targets Of the Csnmentioning

confidence: 99%

The Carotid Sinus Nerve—Structure, Function, and Clinical Implications

Porzionato

Macchi

Stecco

et al. 2018

The Anatomical Record

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Interest has been renewed in the anatomy and physiology of the carotid sinus nerve (CSN) and its targets (carotid sinus and carotid body, CB), due to recent proposals of surgical procedures for a series of common pathologies, such as carotid sinus syndrome, hypertension, heart failure, and insulin resistance. The CSN originates from the glossopharyngeal nerve soon after its appearance from the jugular foramen. It shows frequent communications with the sympathetic trunk (usually at the level of the superior cervical ganglion) and the vagal nerve (main trunk, pharyngeal branches, or superior laryngeal nerve). It courses on the anterior aspect of the internal carotid artery to reach the carotid sinus, CB, and/or intercarotid plexus. In the carotid sinus, type I (dynamic) carotid baroreceptors have larger myelinated A-fibers; type II (tonic) baroreceptors show smaller A- and unmyelinated C-fibers. In the CB, afferent fibers are mainly stimulated by acetylcholine and ATP, released by type I cells. The neurons are located in the petrosal ganglion, and centripetal fibers project on to the solitary tract nucleus: chemosensory inputs to the commissural subnucleus, and baroreceptor inputs to the commissural, medial, dorsomedial, and dorsolateral subnuclei. The baroreceptor component of the CSN elicits sympatho-inhibition and the chemoreceptor component stimulates sympatho-activation. Thus, in refractory hypertension and heart failure (characterized by increased sympathetic activity), baroreceptor electrical stimulation, and CB removal have been proposed. Instead, denervation of the carotid sinus has been proposed for the "carotid sinus syndrome." Anat Rec, 2018. © 2018 Wiley Periodicals, Inc.

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Petrosal ganglion responses to acetylcholine and ATP are enhanced by chronic normobaric hypoxia in the rabbit

Cited by 8 publications

References 56 publications

Imbalance in Renal Vasoactive Enzymes Induced by Mild Hypoxia: Angiotensin-Converting Enzyme Increases While Neutral Endopeptidase Decreases

Imbalance in Renal Vasoactive Enzymes Induced by Mild Hypoxia: Angiotensin-Converting Enzyme Increases While Neutral Endopeptidase Decreases

Effects of vagotomy on cardiovascular and heart rate variability alterations following chronic normobaric hypoxia in adult rabbits

The Carotid Sinus Nerve—Structure, Function, and Clinical Implications

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