Effects of low altitude exposure on 24-hour blood pressure and adrenergic activity

Palatini, Paolo; Businaro, R; Berton, Giuseppe; Mormino, Paolo; Rossi, Gianpaolo; Racioppa, Antonietta; Pessina, Achille C.; Palù, C. Dal

doi:10.1016/0002-9149(89)90587-0

Cited by 37 publications

(19 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…37 In contrast, short visits to modest or high altitudes induce significant increases in systemic blood pressure, 38 and preexisting genetic factors may predispose low altitude residents to altitude-induced hypertension. 39 Our data suggest that the Ahr may represent a candidate gene for altitude-induced hypertension.…”

Section: Perspectivesmentioning

confidence: 99%

Loss of the Aryl Hydrocarbon Receptor Induces Hypoxemia, Endothelin-1, and Systemic Hypertension at Modest Altitude

et al. 2008

View full text Add to dashboard Cite

Abstract-The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix Per-Arnt-Sim transcription factor that mediates induction of metabolic enzymes and toxicity of certain environmental pollutants. Although AHR knockout (KO) mice develop cardiac hypertrophy, conflicting reports associate this pathology with hypotension or endothelin (ET)-1-dependent hypertension. Because hypertension occurred at modest altitude, we tested the hypothesis that loss of AHR increases the sensitivity to hypoxia-induced ET-1, contributing to systemic hypertension. We found that AHR KO mice were hypertensive at modest altitude (1632 m) but hypotensive at low altitude (225 m). When AHR KO mice residing at 1632 m were exposed to the partial pressure of inspired oxygen (PIO 2 ) at sea level for 11 days, blood pressure declined to levels measured at 225 m. Although plasma ET-1 in AHR KO mice was significantly elevated at 1632 m and decreased at 225 m and sea level PIO 2 , pulmonary prepro-ET-1 mRNA was significantly reduced at 1632 m and decreased further at 225 m and sea level PIO 2 . Blood gas analysis revealed that AHR KO mice were hypoxemic, hypercapnic, and acidotic at 1632 m, values that were attenuated and normalized after 24 hours and 11 days under sea level PIO 2 , respectively. Lastly, AHR inactivation in endothelial cells by small interfering RNA significantly reduced basal prepro-ET-1 mRNA but did not alter hypoxia-induced expression. Our studies establish the AHR KO mouse as a model in which modest decreases in PIO 2 lead to hypoxemia, increased plasma ET-1, and systemic hypertension without increased pulmonary prepro-ET-1 mRNA expression. Key Words: blood pressure Ⅲ hypertension Ⅲ endothelin Ⅲ oxygen Ⅲ gene regulation T he aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor belonging to the basic helix-loophelix Per-Arnt-Sim family of DNA binding proteins, which also includes hypoxia-inducible factors. 1 Although the AHR is known to mediate induction of drug-metabolizing enzymes and toxicity after exposure to 2,3,7,8-tetrachlorodibenzo-pdioxin, recent evidence has revealed a physiological role for AHR in cardiovascular homeostasis. AHR knockout (KO) mice develop cardiac hypertrophy, 2,3 which is mediated, in part, by elevated plasma angiotensin II and endothelin-1 (ET-1). 4,5 There are conflicting reports, however, of whether the cardiac hypertrophy is associated with systemic hypertension. Lund et al 4,5 reported that cardiac hypertrophy in AHR KO mice is preceded by hypertension, whereas Vasquez et al 6 and Ichihara et al 7 reported that AHR KO mice are hypotensive and normotensive, respectively. The explanation for the disparate blood pressure values among these studies is unclear.AHR and hypoxia-inducible factor-1␣ share a common dimerization partner, AHR nuclear translocator (hypoxiainducible factor-1␤), as well as other transactivators, and studies have shown that these 2 signal transduction pathways can exhibit reciprocal inhibitory cross-talk. 8,9 The mechanism by which this functional inter...

show abstract

Section: Perspectivesmentioning

confidence: 99%

Loss of the Aryl Hydrocarbon Receptor Induces Hypoxemia, Endothelin-1, and Systemic Hypertension at Modest Altitude

et al. 2008

View full text Add to dashboard Cite

show abstract

“…A rise in BP due to increased sympathetic activity (measured by plasma cathecolamine levels) was described in normotensive and hypertensive subjects after exposure to a moderate altitude of about 1200 m [8] and in normal subjects after a week of exposure to 4300 m [9]. In another study, acute exposure to 3640 m did not change either BP or cathecolamine levels [10].…”

mentioning

confidence: 99%

The effects of exposure to moderate altitude on cardiovascular autonomic function in normal subjects

Veglio

Maule

Cametti

et al. 1999

Clinical Autonomic Research

View full text Add to dashboard Cite

Cardiovascular responses to altitude have been studied on well-trained young subjects, generally at high altitudes (>4000 m). Less known are the effects of exposure to lower altitudes, easily reached by the general population. The aim of the study was to evaluate the effects of exposure to a moderate altitude (2950 m) on heart rate (HR), blood pressure (BP) profile, and cardiovascular autonomic function, and their correlation with hemoglobin oxygen saturation (HbO2S), in untrained subjects of a wide age range. Twenty-seven healthy normotensive subjects (age range 6-83; 8 children, 9 adults, and 10 elderly subjects) underwent a battery of noninvasive cardiovascular reflex tests and 24-h ambulatory BP monitoring. Corrected QT interval was also calculated. HbO2S was measured with a transcutaneous oxymeter. All measurements were performed at about 200 m (s.l.) and repeated at 2950 m. 24-h HR and systolic/diastolic BP mean values increased at 2950 m in children (% change respectively: 6.4 +/- 6.4, p<0.05; 6.5 +/- 4.0/13.5 +/- 6.9, p < 0.05), adults (4.9 +/- 8.1, NS; 6.0 +/- 5.1/8.1 +/- 5.8, p < 0.05), and elderly subjects (7.2 +/- 4.8, p < 0.05; 5.1 +/- 2.3/2.8 +/- 4.1, p < 0.05 for systolic BP only). Standard deviation of BP mean values increased during night-time in the adult group (p < 0.05). All subjects scored normal cardiovascular test results and no differences were observed after exposure to 2950m, at both 1 hour and 24 hours from arrival. After exposure to altitude, HbO2S decreased significantly in the three groups, both on arrival and after 24 hours. No correlation was found between changes in HbO2S and BP/HR responses, and cardiovascular test results. In conclusion, exposure to moderate altitudes, easily and often reached by the general population, causes a small but significant increase in BP and HR in healthy untrained subjects of a wide age range (6-83 years). Some physiological factors (eg, lower environmental temperature and lifestyle modification) together with hypoxia, possibly more than altered cardiovascular reactivity, seem responsible for this cardiovascular change. In terms of end-organ damage, the clinical relevance of this increase in BP and BP variability for repeated exposure is not known.

show abstract

“…However, most studies report that, for hypertensive subjects ascending high altitude moderate increase in BP is more common [32,50,51]. However, the individual differences still have importance [51,52].…”

Section: Hypertension At High Altitudementioning

confidence: 99%

“…At lower height, the average increase of BP is minimal. Palatini et al [32] examined 12 normotensive subjects and 12 patients with mild hypertension using 24 h ambulatory BP monitoring, at sea level, 12 h after arrival at 1,210 m and 1.5-3 h after arrival at 3,000 m. BP was higher at 1,210 m in all subjects during the day but not at night, and BP elevation was similar in both groups compared with sea-level figures (6.1 mmHg for systolic/ 1.5 mmHg for diastolic BP in normotensive subjects and 5.5 mmHg for systolic/4.3 mmHg for diastolic blood pressure in hypertensive ones). However, the marked interindividual variability was observed.…”

Section: Hypertension At High Altitudementioning

confidence: 99%

Hypertension at High Altitude

Sarybaev

Mulajkar

Sikri

et al. 2014

Translational Research in Environmental and Occupational Stress

View full text Add to dashboard Cite

Systemic hypoxia is associated with conditions like anemia, lung diseases, sleep disorders, breathing, and exposure to high altitude. The physiological responses including blood pressure regulation to acute, chronic, intermittent normobaric, and hypobaric hypoxia have been under intense investigation for the past many years; however, the regulatory mechanisms are incompletely understood. The available literature indicates a differential response to hypoxia in pulmonary versus systemic circulation. Multiple physiological and metabolic changes contribute towards high-altitude acclimatization; yet, in some individuals, exposure to high altitude could be life threatening due to maladaptation. There are a few studies on the prevalence of hypertension in high-altitude natives and sea-level dwellers exposed to high altitude (acute and chronic). Elevated blood pressure is an established risk factor for different cardiovascular disease and the evidence suggests that the blood pressure rises to a modest extent in patients with mild to moderate hypertension upon acute ascent to high altitude (Luks et al., Congenit Heart Dis 5:220-232, 2010), but there is no clear evidence on increased risk of complications due to increased systemic blood pressures. This book chapter reviews available literature on systemic blood pressure responses to high altitude. A. Sarybaev (*)

show abstract

Effects of low altitude exposure on 24-hour blood pressure and adrenergic activity

Cited by 37 publications

References 10 publications

Loss of the Aryl Hydrocarbon Receptor Induces Hypoxemia, Endothelin-1, and Systemic Hypertension at Modest Altitude

Loss of the Aryl Hydrocarbon Receptor Induces Hypoxemia, Endothelin-1, and Systemic Hypertension at Modest Altitude

The effects of exposure to moderate altitude on cardiovascular autonomic function in normal subjects

Hypertension at High Altitude

Contact Info

Product

Resources

About