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No Decrease in Blood Pressure After an Acute Bout of Intermittent Hyperpnea and Hypoxia in Prehypertensive Elderly.

ABSTRACT: Prevalence of hypertension, subjective sleep complaints and snoring increases with age. Worse sleep and snoring, in turn, are independent risk factors to develop hypertension. Both respiratory muscle training (RMT) and intermittent hypoxia (IH) are suggested to have positive effects on these physiological and behavioral variables. This study therefore aimed to test the acute effects of a single bout of RMT, with and without IH, on resting blood pressure (BP) and sleep. Fourteen prehypertensive elderly performed a 60-min session of (a) intermittent voluntary normocapnic hyperpnea (HYP) alone, (b) HYP in combination with IH (HYP&IH) and (c) a sham intervention in randomized order. BP, hemodynamics, heart rate variability (HRV), cardiac baroreflex sensitivity (BRS) and pulse wave velocity (PWV) were assessed before and 15, 30 and 45 min after each intervention. Variables of sleep were assessed with actigraphy, pulse oximetry and with questionnaires during and after the night following each intervention. Neither HYP nor HYP&IH resulted in a decrease in BP. Repeated measures ANOVA revealed no significant interaction effect for systolic BP (p = 0.090), diastolic BP (p = 0.151), HRV parameters, BRS and PWV (all p > 0.095). Fragmentation index was lower after both HYP (-6.5 units) and HYP&IH (-8.4 units) compared to sham, p(ANOVA) = 0.046, although pairwise comparisons reveal no significant differences. There were no other significant effects for the remaining sleep variables. We conclude that one bout of intermittent hyperpnea, alone or in combination with IH, is not effective in lowering blood pressure or improving sleep in prehypertensive elderly.

SUBMITTER: Stutz J

PROVIDER: S-EPMC7566905 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Cyclooxygenases 1 and 2 differentially regulate blood pressure and cerebrovascular responses to acute and chronic intermittent hypoxia: implications for sleep apnea.

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Cardiac Sympathetic Denervation Suppresses Atrial Fibrillation and Blood Pressure in a Chronic Intermittent Hypoxia Rat Model of Obstructive Sleep Apnea.

Project description:Background Chronic intermittent hypoxia ( CIH ) is a distinct pathological mechanism of obstructive sleep apnea ( OSA ), which is recognized as an independent risk factor for cardiovascular diseases. The aims of this study were to ascertain whether CIH induces atrial fibrillation ( AF ), to determine whether cardiac sympathetic denervation ( CSD ) can prevent it and suppress blood pressure, and to explore the potential molecular mechanisms involved. Methods and Results Sixty Sprague-Dawley male rats were randomly divided into 4 groups: sham, CSD , CIH , CIH + CSD . The rats were exposed either to CIH 8 hours daily or normoxia for 6 weeks. Cardiac pathology and structure were analyzed by hematoxylin and eosin staining and echocardiogram. ECG, blood pressure, body weight, and blood gas were recorded. Connexin 43 and tyrosine hydroxylase were detected by western blot, immunohistochemistry, and immunofluorescence. CIH induced atrial remodeling, and increased AF inducibility. CSD treatment reduced postapneic blood pressure rises and AF susceptibility, which could attenuate CIH -associated structural atrial arrhythmogenic remodeling. In addition, CIH -induced sympathetic nerve hyperinnervation and CSD treatment reduced sympathetic innervation, which may affect CIH -induced AF -associated sympathovagal imbalance. Connexin 43 was specifically downregulated in CIH , whereas CSD treatment increased its expression. Conclusions These results suggested CIH induces atrial remodeling, increases AF inducibility, results in sympathetic nerve hyperinnervation, and decreases connexin 43 expression, but CSD treatment reduces AF susceptibility, postapneic blood pressure increase, sympathetic innervation, and the alteration of Cx43, which may be a key point in the genesis of CIH -induced AF .

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GNPS_2018 Mouse intermittent hypoxia (IH) - Blood plasma

Project description:2018 Mouse intermittent hypoxia (IH) - Blood plasma Contains LC/MS data for 10-week experiments involving mice raised in environments with normal oxygen, intermittent hypoxia (IH) and intermittent hypercapnia (IC)

2019-02-25 | MSV000083482 | GNPS

GNPS_2017 Mouse intermittent hypoxia (IH) - Blood plasma

Project description:2017 Mouse intermittent hypoxia (IH) - Blood plasma Contains LC/MS data for 10-week experiments involving mice raised in environments with normal oxygen, intermittent hypoxia (IH).

2019-02-25 | MSV000083481 | GNPS

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Project description:BackgroundInflammation has been implicated in the development of cardiovascular disease. We determined whether nod-like receptor with pyrin domain containing 3 (NLRP3) involved in the process of prehypertension, central blockade of NLRP3 decreased inflammation reaction, regulated neurohormonal excitation, and delayed the progression of prehypertension.MethodsPrehypertensive rats were induced by 8% salt diet. The rats on high-salt diet for 1 month were administered a specific NLRP3 blocker in the hypothalamic paraventricular nucleus (PVN) for 4 weeks. ELISA, western blotting, immunohistochemistry, and flow cytometry were used to measure NLRP3 cascade proteins, pro-inflammation cytokines (PICs), chemokine ligand 2 (CCL2), C-X-C chemokine receptor type 3 (CXCR3), vascular cell adhesion molecule 1 (VCAM-1), neurotransmitters, and leukocytes count detection, respectively.ResultsNLRP3 expression in PVN was increased significantly in prehypertensive rats, accompanied by increased number of microglia, CD4+, CD8+ T cell, and CD8+ microglia. Expressions of PICs, CCL2, CXCR3, and VCAM-1 significantly increased. The balance between 67-kDa isoform of glutamate decarboxylase (GAD67) and tyrosine hydroxylase (TH) was damaged. Plasma norepinephrine (NE) in prehypertensive rats was increased and gamma-aminobutyric acid (GABA) was reduced. NLRP3 blockade significantly decreased blood pressure, reduced PICs, CCL2, VCAM-1 expression in PVN, and restored neurotransmitters. Blood pressure and inflammatory markers were upregulated after termination of central blockage NLRP3.ConclusionsSalt-induced prehypertension is partly due to the role of NLRP3 in PVN. Blockade of brain NLRP3 attenuates prehypertensive response, possibly via downregulating the cascade reaction triggered by inflammation and restoring the balance of neurotransmitters.

| S-EPMC5866519 | biostudies-literature

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