In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring

Ye, Zhengmeng; Lu, Xi; Deng, Yi; Wang, Xinquan; Zheng, Shuo; Ren, Hongmei; Zhang, Miao; Chen, Tingting; José, Pedro A.; Yang, Jian; Zeng, Chunyu

doi:10.1159/000488418

Cited by 23 publications

(21 citation statements)

References 54 publications

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“…Blood lipids, including total cholesterol and triglycerides, were measured by the ELISA kit (Jiancheng, Nanjing, China). The blood pressure and heart rate were also measured at 4, 8, 12, 16, 20, and 24 weeks of age in conscious rats using a computerized noninvasive tail-cuff manometry (BP-98A; Softron, Tokyo, Japan) as described in previous studies [22,23]. Blood pressure and heart rate were measured five times between 3:00–5:00 PM; the average of the five measurements was used in the calculations.…”

Section: Methodsmentioning

confidence: 99%

Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system

Chen

Sun

et al. 2019

Clinical Science

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Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α2 adrenergic receptor agonist, lowered blood pressure to a greater degree in the prenatal cold-exposed than control offspring. Moreover, these prenatal cold-exposed offspring had hypothalamic paraventricular nucleus (PVN) disorder because magnetic resonance spectroscopy showed decreased N-acetylaspartate and increased choline and creatine ratios in the PVN. Additional studies found that prenatal cold exposure impaired the balance between inhibitory and excitatory neurons. This led to PVN overactivation that was related to enhanced PVN-angiotensin II type 1 (AT1) receptor expression and function. Microinjection of the AT1 receptor antagonist losartan in the PVN lowered blood pressure to a greater extent in prenatal cold-exposed that control offspring. The present study provides evidence for overactive peripheral and central sympathetic nervous systems in the pathogenesis of prenatal cold-induced hypertension. Central AT1 receptor blockade in the PVN may be a key step for treatment of this type hypertension.

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Section: Methodsmentioning

confidence: 99%

Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system

Chen

Sun

et al. 2019

Clinical Science

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“…The computerized non-invasive tail-cuff manometry system (MODEL MK-2000, Muromachikikai Co. Ltd, Tokyo, Japan) was used to measure the systolic and diastolic blood pressure of conscious SD rats (18). The blood pressures were measured for 15 min between 8:00 AM and 12:00 PM in rats individually restrained in a clear acrylic restrainer at an ambient temperature of 37°C.…”

Section: Non-invasive Blood Pressure Measurementmentioning

confidence: 99%

“…To investigate the effect of a low salt diet on the blood pressure, SD rats were randomly divided into low salt (0.04% NaCl) diet group and normal salt (0.4% NaCl) diet group. After 8 weeks, the systolic and diastolic blood pressures of conscious SD rats were measured using a non-invasive tail-cuff manometry system (18). The results showed that the blood pressures of the low salt diet group (SBP: 143 ± 6.0 mmHg, DBP: 92 ± 7.4 mmHg) were significantly higher than the normal salt diet group (SBP: 121 ± 7.0 mmHg, DBP: 74 ± 8.5 mmHg) (Figures 1(a) and 1(b)).…”

Section: Low Salt Diet Increases the Blood Pressure Of Sd Ratsmentioning

confidence: 99%

Long-term low salt diet increases blood pressure by activation of the renin-angiotensin and sympathetic nervous systems

Wang

Deng

Zou

et al. 2018

Clinical and Experimental Hypertension

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Background-The aim of this study was to investigate the effect of long-term low salt diet on blood pressure and its underlying mechanisms. Methods-Male Sprague-Dawley (SD) rats were divided into normal salt diet group (0.4%) and low salt diet group (0.04%). Blood pressure was measured with the non-invasive tail-cuff method. The contractile response of isolated mesenteric arteries was measured using a small vessel myograph. The effects on renal function of the intrarenal arterial infusion of candesartan (10 µg/kg/min), an angiotensin II receptor type 1 (AT 1 R) antagonist, were also measured. The expressions of renal AT 1 R and mesenteric arterial α 1A , α 1B , and α 1D adrenergic receptors were quantified by immunoblotting. Plasma levels of angiotensin II were also measured. Results-Systolic blood pressure was significantly increased after 8 weeks of low salt diet. There were no obvious differences in the renal structure between the low and normal salt diet groups. However, the plasma angiotensin II levels and renal AT 1 R expression were higher in low than normal salt diet group. The intrarenal arterial infusion of candesartan increased urine flow and sodium excretion to a greater extent in the low than normal salt diet group. The expressions of α 1A and α 1D , but not α 1B , adrenergic receptors, and phenylephrine-induced contraction were increased in mesenteric arteries from the low salt, relative to the normal salt diet group. Conclusion-Activation of the renin-angiotensin and sympathetic nervous systems may be involved in the pathogenesis of long-term low salt diet-induced hypertension.

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“…2017). Evidence of prenatal reprogramming by PM2.5 also extends to the renal system; research in rats suggests that adult offspring of dams exposed to PM2.5 via oropharyngear drip during pregnancy have impaired renal dopamine D1 receptor-mediated sodium excretion and increased blood pressure (Ye et al. 2018).…”

Section: Discussionmentioning

confidence: 99%

Prenatal Exposure to PM2.5 and Cardiac Vagal Tone during Infancy: Findings from a Multiethnic Birth Cohort

Cowell

Brunst

Malin

et al. 2019

Environ Health Perspect

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Background:The autonomic nervous system plays a key role in maintaining homeostasis and responding to external stimuli. In adults, exposure to fine particulate matter (PM2.5) has been associated with reduced heart rate variability (HRV), an indicator of cardiac autonomic control.Objectives:Our goal was to investigate the associations of exposure to fine particulate matter (PM2.5) with HRV as an indicator of cardiac autonomic control during early development.Methods:We studied 237 maternal–infant pairs in a Boston-based birth cohort. We estimated daily residential PM2.5 using satellite data in combination with land-use regression predictors. In infants at 6 months of age, we measured parasympathetic nervous system (PNS) activity using continuous electrocardiogram monitoring during the Repeated Still-Face Paradigm, an experimental protocol designed to elicit autonomic reactivity in response to maternal interaction and disengagement. We used multivariable linear regression to examine average PM2.5 exposure across pregnancy in relation to PNS withdrawal and activation, indexed by changes in respiration-corrected respiratory sinus arrhythmia (RSAnormalc)—an established metric of HRV that reflects cardiac vagal tone. We examined interactions with infant sex using cross-product terms.Results:In adjusted models we found that a 1-unit increase in PM2.5 (in micrograms per cubic meter) was associated with a 3.53% decrease in baseline RSAnormalc (95% CI: −6.96, 0.02). In models examining RSAnormalc change between episodes, higher PM2.5 was generally associated with reduced PNS withdrawal during stress and reduced PNS activation during recovery; however, these associations were not statistically significant. We did not observe a significant interaction between PM2.5 and sex.Discussion:Prenatal exposure to PM2.5 may disrupt cardiac vagal tone during infancy. Future research is needed to replicate these preliminary findings. https://doi.org/10.1289/EHP4434

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In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring

Cited by 23 publications

References 54 publications

Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system

Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system

Long-term low salt diet increases blood pressure by activation of the renin-angiotensin and sympathetic nervous systems

Prenatal Exposure to PM2.5 and Cardiac Vagal Tone during Infancy: Findings from a Multiethnic Birth Cohort

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