Fig 1 - uploaded by Zeman Michal
Content may be subject to copyright.
Experimental design. LD, regular 12-h light:12-h dark regimen; PH, prenatal hypoxia; ALAN, artificial light (1-2 lx) during the dark phase of the day; NE, norepinephrine.
Source publication
Prenatal hypoxia (PH) has negative consequences on the cardiovascular system in adulthood and can affect the responses to additional insults later in life. We explored the effects of PH imposed during embryonic day 20 (10.5% O 2 for 12 h) on circadian rhythms of systolic blood pressure (BP) and heart rate (HR) in mature male rat offspring measured...
Contexts in source publication
Context 1
... telemetry, we evaluated daily rhythms of systolic BP and HR in adult, 21-and 27-week-old PH (n = 7, 370 ± 8 g) or control (n = 6, 384 ± 8 g) male offspring. During this period, rats were exposed to regular 12L:12D conditions (Fig. 1). In 28-32-weekold control and PH rats, we determined the response of daily rhythms of BP and HR to ALAN: 12-h L (150 lx) and 12-h of ALAN phases (dim D; 1-2 lx). We evaluated the consequences of ALAN on circadian rhythms of BP and HR via telemetry after 2 and 5 weeks of ALAN exposure (Fig. 1). In 34-week-old rats, we administered ...
Context 2
... rats were exposed to regular 12L:12D conditions (Fig. 1). In 28-32-weekold control and PH rats, we determined the response of daily rhythms of BP and HR to ALAN: 12-h L (150 lx) and 12-h of ALAN phases (dim D; 1-2 lx). We evaluated the consequences of ALAN on circadian rhythms of BP and HR via telemetry after 2 and 5 weeks of ALAN exposure (Fig. 1). In 34-week-old rats, we administered norepinephrine and analysed BP and HR response in the control and PH group (Fig. ...
Context 3
... of daily rhythms of BP and HR to ALAN: 12-h L (150 lx) and 12-h of ALAN phases (dim D; 1-2 lx). We evaluated the consequences of ALAN on circadian rhythms of BP and HR via telemetry after 2 and 5 weeks of ALAN exposure (Fig. 1). In 34-week-old rats, we administered norepinephrine and analysed BP and HR response in the control and PH group (Fig. ...
Similar publications
A comprehensive framework for pervasive telemetry and accelerated networking is presented. The framework is suitable for effective integration of optical, packet, and computing resources, leveraging DPU and P4 programmability in support of edge-to-edge continuum.
Telemetry data acquisition is becoming crucial for efficient detection and timely reaction in the case of network status changes, such as failures. Streaming telemetry data to many collectors might be hindered by scalability issues, causing delay in localization and detection procedures. Providing efficient mechanisms for managing the massive telem...
The demand of aero-engine for non-contact telemetry information transmission is very urgent. Based on the analysis of the characteristics of aero-engine telemetry information transmission system, the rotor disk and stator disk suitable for near-field communication under high centrifugal load are designed in this paper. In order to ensure the stable...
With the development of point cloud-based telemetry technology in recent years, the point cloud data of large field scenes acquired by various sensors have been applied to farmland boundary division, crop growth monitor, area surveying, etc. However, the large field point cloud will cost huge amounts of computational resources in the following tran...
Accurate estimates of abundance and density for geographically open populations must account for the effective sampling area (ESA) of sampling gears. We describe a Marked N-Mixture model to estimate ESA and density (number of individuals/unit area) from repeated counts of unmarked and marked individuals, integrating mark-resight, camera counts, and...
Citations
... Hypoxia impairs the uterus or placenta and causes epigenetic alterations that impact fetal development [18]. A few studies have shown that individuals who experience hypoxia during the embryonic period display adverse effects on their offspring [19]. Recently, we showed that hypoxic exposure during fetal development impaired ovarian function and GC proliferation [20], but the specific mechanism underlying this effect remains unclear. ...
Environmental hypoxia adversely impacts the reproduction of humans and animals. Previously, we showed that fetal hypoxia exposure led to granulosa cell (GC) autophagic cell death via the Foxo1/Pi3k/Akt pathway. However, the upstream regulatory mechanisms underlying GC dysfunction remain largely unexplored. Here, we tested the hypothesis that fetal hypoxia exposure altered gene expression programs in adult GCs and impaired ovarian function. We established a fetal hypoxia model in which pregnant mice were maintained in a high-plateau hypoxic environment from gestation day (E) 0–16.5 to study the impact of hypoxia exposure on the ovarian development and subsequent fertility of offspring. Compared with the unexposed control, fetal hypoxia impaired fertility by disordering ovarian function. Specifically, fetal hypoxia caused mitochondrial dysfunction, oxidant stress, and autophagy in GCs in the adult ovary. RNA sequencing analysis revealed that 437 genes were differentially expressed in the adult GCs of exposed animals. Western blotting results also revealed that fetal exposure induced high levels of hypoxia-inducible factor 1-alpha (Hif1a) expression in adult GCs. We then treated granulosa cells isolated from exposed mice with PX-478, a specific pharmacological inhibitor of Hif1a, and found that autophagy and apoptosis were effectively alleviated. Finally, by using a human ovarian granulosa-like tumor cell line (KGN) to simulate hypoxia in vitro, we showed that Hif1a regulated autophagic cell death in GCs through the Pi3k/Akt pathway. Together, these findings suggest that fetal hypoxia exposure induced persistent Hif1a expression, which impaired mitochondrial function and led to autophagic cell death in the GCs of the adult ovary.
... The impact of artificial light at night on people and dLAN on male mice differs from that of artificial light at night on male rats housed at room temperature 14 . Light at night in rats appears to decrease the relative sympathetic signaling at night to decrease the amplitude of the 24-hour heart rate and blood pressure rhythms 13,36 . One possible reason for the difference between our studies in male mice and previous studies in rats is that we studied the effects of dLAN in mice housed at thermoneutrality to limit coldinduced sympathetic nervous system activation. ...
Shift work and artificial light at night disrupt the entrainment of endogenous circadian rhythms in physiology and behavior to the day-night cycle. We hypothesized that exposure to dim light at night (dLAN) disrupts feeding rhythms, leading to sex-specific changes in autonomic signaling and day-night heart rate and blood pressure rhythms. Compared to mice housed in 12-hour light/12-hour dark cycles, mice exposed to dLAN showed reduced amplitudes in day-night feeding, heart rate, and blood pressure rhythms. In female mice, dLAN reduced the amplitude of day-night cardiovascular rhythms by decreasing the relative sympathetic regulation at night, while in male mice, it did so by increasing the relative sympathetic regulation during the daytime. Time-restricted feeding to the dim light cycle reversed these autonomic changes in both sexes. We conclude that dLAN induces sex-specific changes in autonomic regulation of heart rate and blood pressure, and time-restricted feeding may represent a chronotherapeutic strategy to mitigate the cardiovascular impact of light at night.
... The impact of artificial light at night on people and dLAN on male mice differs from that of artificial light at night on male rats housed at room temperature 14 . Light at night in rats appears to decrease the relative sympathetic signaling at night to decrease the amplitude of the 24-hour heart rate and blood pressure rhythms 13,36 . One possible reason for the difference between our studies in male mice and previous studies in rats is that we studied the effects of dLAN in mice housed at thermoneutrality to limit coldinduced sympathetic nervous system activation. ...
Background: Light input to the suprachiasmatic nucleus entrains circadian rhythms in physiology and behavior to the day-night cycle. Exposure to light at night in people is associated with cardiometabolic disease. Pre-clinical studies show that artificial light at night, including at very low levels, disrupts day-night rhythms in activity, feeding behavior, heart rate, and blood pressure dipping.
Hypothesis: Dim light at night (dLAN) disrupts day-night rhythms in feeding behavior to blunt day-night rhythms in autonomic input to the heart and blood pressure dipping.
Methods: Mice (n=5-6/sex) in thermoneutral housing were implanted with telemetry probes to record heart rate, blood pressure, and core body temperature. Autonomic input to the heart was assessed by measuring heart rate and subtracting the temperature-dependent changes in the heart rate after pharmacological inhibition of muscarinic and β-adrenergic receptor activation. Mice were housed in 12 h light: 12 h dark cycles (LD, 200 lux: 0 lux) with ad libitum access to food (LD-ALF), subjected to 12 h light: 12 h dLAN cycles (dLAN-ALF; 200 lux: 5 lux) for two weeks, and then feeding was time-restricted (not calorically restricted) to the dLAN cycle (dLAN-RF). Data were extracted from Ponemah and Clocklab, and statistical analysis was done using GraphPad PRISM software.
Results: Compared to LD-ALF mice, dLAN-ALF mice showed reduced amplitudes in day-night activity, feeding, heart rate, and blood pressure rhythms, with males more affected than females (p<0.001). dLAN-ALF male and female mice had decreased amplitudes in the day-night rhythms in autonomic input to the heart. In addition, dLAN-ALF male mice had less blood pressure dipping. dLAN-RF normalized autonomic input to the heart and heart rate in male and female mice (p<0.05, p<0.01, respectively). dLAN-RF also improved blood pressure dipping in male mice (p<0.001). dLAN-RF did not normalize activity rhythms.
Conclusion: dLAN disrupts day-night rhythms in activity, feeding, heart rate, and blood pressure dipping in mice, with males being more impacted. Time-restricted feeding to the dLAN cycle normalizes autonomic input to the heart and blood pressure dipping. These data suggest that time-restricted feeding counteracts the light-at-night-induced circadian disruption of cardiovascular function.
... In rats, ALAN suppressed the 24-h variability of blood pressure and heart rate and reduced the amplitude and significance of their circadian rhythms [1]. At the same time, some individuals became arrhythmic even after 2 weeks of ALAN [12]. Distinct from humans, in rats, ALAN suppressed sympathetic activity and altered baroreflex sensitivity [1,12], which may be associated with the observed haemodynamic changes. ...
... At the same time, some individuals became arrhythmic even after 2 weeks of ALAN [12]. Distinct from humans, in rats, ALAN suppressed sympathetic activity and altered baroreflex sensitivity [1,12], which may be associated with the observed haemodynamic changes. ...
... These effects are likely mediated through the autonomic nervous system, involving transmission from the SCN to the heart and vasculature [1,22]. Although the effects of ALAN on blood pressure and its rhythm are known from previous studies [1,12], the effects of ALAN on the functionality and structure of blood vessels remain unknown or are often limited to a one-time point or in the light phase of the day. In addition to small resistance vessels, large conduit vessels, such as the thoracic aorta, play an important role in maintaining haemodynamics. ...
Artificial light at night (ALAN) disrupts 24-h variability of blood pressure, but the molecular mechanisms underlying these effects are unknown. Therefore, we analysed the daily variability of pulse pressure, the maximum value of acceleration rate of aortic pressure (dP/dt(max)) measured by telemetry and protein expression in the thoracic aorta of normotensive male rats exposed to ALAN (1-2 lx) for 3 weeks. Daily, 24-h variability of pulse pressure and dP/dt(max) was observed during a regular light/dark regimen with higher values during the dark compared to the light phase of the day. ALAN suppressed 24-h variability and enhanced ultradian (<12-h) periods of pulse pressure and dP/dt(max) in duration-dependent manners. From beat-to-beat blood pressure variability, ALAN decreased low-frequency bands (a sympathetic marker) and had minimal effects on high-frequency bands. At the molecular level, ALAN decreased angiotensin II receptor type 1 expression and reduced 24-h variability. ALAN caused the appearance of 12-h oscillations in transforming growth factor β1 and fibulin 4. Expression of sarco/endoplasmic reticulum Ca2+-ATPase type 2 was increased in the middle of the light and dark phase of the day, and ALAN did not affect its daily and 12-h variability. In conclusion, ALAN suppressed 24-h variability of pulse pressure and dP/dt(max), decreased the power of low-frequency bands and differentially affected the expression of specific proteins in the rat thoracic aorta. Suppressed 24-h oscillations by ALAN underline the pulsatility of individual endocrine axes with different periods, disrupting the cardiovascular control of central blood pressure.
... Moreover, significant increases in blood pressure and heart rate during the transitions between the light and dark phases were lost [74]. ALAN (1-2 lx) had the most pronounced effects on blood pressure and heart rate after two weeks of exposure, and day-night variability was partially restored after five weeks of exposure [55,82]. In contrast, in rats (28 weeks old) prenatally exposed to hypoxia, a significant decrease in day-night variability of blood pressure and heart rate was not present until 5 weeks of ALAN (1-2 lx) [82]. ...
... ALAN (1-2 lx) had the most pronounced effects on blood pressure and heart rate after two weeks of exposure, and day-night variability was partially restored after five weeks of exposure [55,82]. In contrast, in rats (28 weeks old) prenatally exposed to hypoxia, a significant decrease in day-night variability of blood pressure and heart rate was not present until 5 weeks of ALAN (1-2 lx) [82]. A similar dampening of the blood pressure rhythms was observed after the shift of the light cycle [71]. ...
... Studies in spontaneously hypertensive rats [74] and rats exposed prenatally to hypoxia, which experimentally increases sympathetic nerve activity [82], suggest that the sympathetic nervous system is essential in transmitting information from the SCN to the cardiovascular system [83]. The sympathetic nervous system acts on the cardiovascular system through noradrenaline, released from the nerve terminals. ...
Artificial light at night (ALAN) affects most of the population. Through the retinohypothalamic tract, ALAN modulates the activity of the central circadian oscillator and, consequently, various physiological systems, including the cardiovascular one. We summarised the current knowledge about the effects of ALAN on the cardiovascular system in diurnal and nocturnal animals. Based on published data, ALAN reduces the day-night variability of the blood pressure and heart rate in diurnal and nocturnal animals by increasing the nocturnal values of cardiovascular variables in diurnal animals and decreasing them in nocturnal animals. The effects of ALAN on the cardiovascular system are mainly transmitted through the autonomic nervous system. ALAN is also considered a stress-inducing factor, as glucocorticoid and glucose level changes indicate. Moreover, in nocturnal rats, ALAN increases the pressure response to load. In addition, ALAN induces molecular changes in the heart and blood vessels. Changes in the cardiovascular system significantly depend on the duration of ALAN exposure. To some extent, alterations in physical activity can explain the changes observed in the cardiovascular system after ALAN exposure. Although ALAN acts differently on nocturnal and diurnal animals, we can conclude that both exhibit a weakened circadian coordination among physiological systems, which increases the risk of future cardiovascular complications and reduces the ability to anticipate stress.
... [3][4][5] It is reported that offspring of pregnant rats exposed to hypoxic environment show elevated blood pressure and blood glucose compared to those exposed to normal oxygen level. 6,7 In addition, some animal models of mid-to-late-pregnancy hypoxia have shown that ICH leads to lung and nerve damage, reduction in ovarian primordial follicle count, telomere length shortening, and accelerated aging in offspring of rodents. [8][9][10][11] ICH caused by various factors will induce fetal blood flow to be preferentially supplied to the heart and brain and other vital organs, possibly at the expense of others, 12 thus affecting fetal development. ...
Background:
Intrauterine chronic hypoxia (ICH) can lead to pancreatic dysmetabolism in offspring. This study aimed to determine the changes in islet function of offspring through a rat ICH model and detect the factors affecting islet function.
Methods:
Twenty couples of healthy Sprague - Dawley adult rats were randomly mated, and the pregnant rats were randomly allocated to ICH and normal control (NC) groups. Pregnant rats in the ICH group were placed in a hypoxic chamber with 13% oxygen concentration for hypoxia treatment twice a day for 4 h until delivery at 21 days. NC group is inlet with normal air from beginning to end. After delivery, blood was taken from the heart of pregnant rats for blood gas analysis. The weight of the offspring rats was measured at 12 h after birth and 16 weeks after birth. At 16 weeks, the immunohistochemical results of β-cell total, islet area, insulin (INS), and glucose transporter 2 (GLUT2) proteins were obtained from the islets. The mRNA data of INS and pancreatic and duodenal homeobox 1 (PDX-1) genes were obtained from pancreas.
Results:
We found the β-cell total, islet area, and the positive cell area of INS and GLUT2 of offspring rats in ICH group were lower than those of NC group, while the levels of INS and PDX-1 genes were higher in ICH group than in NC group.
Conclusions:
ICH can lead to islet hypoplasia in adult male offspring rats. However, this is within the compensatory range.
... Circadian variability was assessed from the basic measurements (3day weekend measurements; 72 equally sampled data points per 24 h) using Chronos-Fit software [17,18]. The presence and significance of 24h variability were quantified by the percentage of rhythm (the coefficient of determination multiplied by 100; represents the percentage of variation in the data that can be explained by the 24-h model used), mesor (midline-estimating statistic of rhythm), amplitude (amplitude of the sinewave), and acrophase (a time when the monitored parameter reaches the highest value). ...
Aldosterone regulates blood pressure (BP) through water and sodium balance. In our study, we studied if continuous treatment with a mineralocorticoid receptor antagonist, spironolactone (30 mg/kg/day) for 20 days can: 1) attenuate hypertension development and restore inverted 24-h BP rhythm in hypertensive transgenic (mRen-2)27 rats (TGR) measured by telemetry; 2) improve function of the kidneys and heart; 3) be protective against high salt load (1% in water) by mitigating oxidative injury and improving kidney function. Spironolactone decreased albuminuria and 8-isoprostane in normal and salt load conditions in BP-independent effects. Salt load increased BP, impaired autonomic balance, suppressed plasma aldosterone level and increased natriuresis, albuminuria and oxidative injury in TGR. Spironolactone did not restore the inverted 24-h rhythm of BP in TGR, therefore, mineralocorticoids are not crucial in regulation of BP daily profile. Spironolactone improved kidney function, decreased oxidative stress and was protective against high salt load in the BP-independent manner.
... Moreover, a study associated with intrauterine growth restriction induced by intermittent hypoxia from ED 14 to ED 18 showed no changes in dP/dt max on ED 22 and postnatally; however, these rats had an increased inotropic response [50]. On the other hand, in rats exposed to 12 h of hypoxia on ED 20, no differences in heart rate and blood pressure response to noradrenaline compared with the control rats were observed [132], thus, it seems that changes are prenatal hypoxia duration dependent. ...
... Exposure of rats to intermittent 4 h periods of hypoxia on ED 19 and ED 20 during the daytime (passive phase for rats) increased the blood pressure in adult male offspring but did not affect the circadian rhythms of blood pressure and heart rate [14]. Similarly, prenatal hypoxia (12 h, ED 20) during the light phase did not change the circadian rhythms of blood pressure and heart rate in male offspring, as well as the response of the cardiovascular system to vasoconstriction drugs [30,132]; however, these animals had an altered response to artificial light at night [132], which is considered as a risk factor for the disruption of circadian control and the development of cardiovascular diseases [225]. ...
... Exposure of rats to intermittent 4 h periods of hypoxia on ED 19 and ED 20 during the daytime (passive phase for rats) increased the blood pressure in adult male offspring but did not affect the circadian rhythms of blood pressure and heart rate [14]. Similarly, prenatal hypoxia (12 h, ED 20) during the light phase did not change the circadian rhythms of blood pressure and heart rate in male offspring, as well as the response of the cardiovascular system to vasoconstriction drugs [30,132]; however, these animals had an altered response to artificial light at night [132], which is considered as a risk factor for the disruption of circadian control and the development of cardiovascular diseases [225]. ...
Prenatal hypoxia during the prenatal period can interfere with the developmental trajectory and lead to developing hypertension in adulthood. Prenatal hypoxia is often associated with intrauterine growth restriction that interferes with metabolism and can lead to multilevel changes. Therefore, we analysed the effects of prenatal hypoxia predominantly not associated with intrauterine growth restriction using publications up to September 2021. We focused on: (1) The response of cardiovascular regulatory mechanisms, such as the chemoreflex, adenosine, nitric oxide, and angiotensin II on prenatal hypoxia. (2) The role of the placenta in causing and attenuating the effects of hypoxia. (3) Environmental conditions and the mother’s health contribution to the development of prenatal hypoxia. (4) The sex-dependent effects of prenatal hypoxia on cardiovascular regulatory mechanisms and the connection between hypoxia-inducible factors and circadian variability. We identified that the possible relationship between the effects of prenatal hypoxia on the cardiovascular regulatory mechanism may vary depending on circadian variability and phase of the days. In summary, even short-term prenatal hypoxia significantly affects cardiovascular regulatory mechanisms and programs hypertension in adulthood, while prenatal programming effects are not only dependent on the critical period, and sensitivity can change within circadian oscillations.
... In addition to phase shifts, constant dim light of 5 lx (Witte et al., 1998a) and artificial light at night (ALAN) of 2 lx also significantly reduce circadian rhythms of the heart rate in normotensive Wistar rats within a few days Sutovska et al., 2020). ...
... ALAN exposure is a phenomenon of modern society and affects blood pressure and heart rate in humans (Obayashi et al., 2014(Obayashi et al., , 2019 and rats, probably through the sympathetic nervous system Rumanova et al., 2019;Sutovska et al., 2020). The sympathetic nervous system accelerates heart rate, heart contractility and heart relaxation (lusitropy), which is mediated by SERCA2. ...
... Therefore, we hypothesize that ALAN can also be related to a decrease in ryanodine receptor 2 expression. Decreased expression of ryanodine receptor 2 is responsible for reduced calcium release from the sarcoplasmic reticulum to the cytosol, probably due to reduced adrenergic stimulation of the heart after ALAN ( Figure 6) Sutovska et al., 2020). Therefore, we propose a longterm decrease in calcium release that can adaptively decrease SERCA2 expression (Oh et al., 2010;Sallinen et al., 2007). ...
New findings:
What is the central question of this study? Artificial light at night decreases blood pressure and heart rate in rats. Are mentioned changes in heart rate accompanied by changes in protein expression in the heart's left ventricle? What is the main finding and its importance? For the first time, we reported that five weeks of artificial light at night affected protein expression in the heart's left ventricle in normotensive and hypertensive rats. Artificial light at night decreased expression of the sarco/endoplasmic reticulum Ca2+ -ATPase, angiotensin II receptor type 1, and endothelin-1.
Abstract:
Artificial light at night (ALAN) affects the circadian rhythm of the heart rate in normotensive Wistar (WT) and spontaneously hypertensive rats (SHR) through the autonomic nervous system, which regulates the heart's activity through calcium handling, an important regulator in heart contractility. We analysed the expression of the sarco/endoplasmic reticulum Ca2+ -ATPase (SERCA2) and other selected regulatory proteins involved in the regulation of heart contractility, angiotensin II receptor type 1 (AT1 R), endothelin-1 (ET-1) and tyrosine hydroxylase (TH) in the left ventricle of the heart in WT and SHR after two and five weeks of ALAN with intensity 1-2 lx. Expression of SERCA2 was decreased in WT (control: 0.53 ± 0.07; ALAN: 0.46 ± 0.10) and SHR (control: 0.72 ± 0.18; ALAN: 0.56 ± 0.21) after five weeks of ALAN (p = 0.067). Expression of AT1 R was significantly decreased in WT (control: 0.51 ± 0.27; ALAN: 0.34 ± 0.20) and SHR (control: 0.38 ± 0.07; ALAN: 0.23 ± 0.09) after two weeks of ALAN (p = 0.028) and in SHR after five weeks of ALAN. Expression of ET-1 was decreased in WT (control: 0.51 ± 0.27; ALAN: 0.28 ± 0.12) and SHR (control: 0.54 ± 0.10; ALAN: 0.35 ± 0.23) after five weeks of ALAN (p = 0.015). ALAN did not affect the expression of TH in WT or SHR. In conclusion, ALAN suppressed the expression of SERCA2, AT1 R and ET-1, which are important for the regulation of heart contractility, in a strain-dependent pattern in both WT and SHR. This article is protected by copyright. All rights reserved.
