Influence of neonatal handling on blood pressure, locomotor activity, and preweanling heart rate in spontaneously hypertensive and Wistar Kyoto rats

Tucker, Diane C.; Johnson, Alan Kim

doi:10.1002/dev.420170603

Cited by 26 publications

(15 citation statements)

References 24 publications

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“…The quality of early life, prenatal and/or postnatal, can influence mechanism(s) of metabolic and mental disorders as well as cardiovascular disease in both humans 1-3 and animal models 4-6 . Significant alteration in maternal care is considered a stressful experience associated with modifications in the endocrine response 7, 8 leading to enhanced acute stress-related responses in the offspring later in life.…”

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confidence: 99%

Early Life Stress Enhances Angiotensin II–Mediated Vasoconstriction by Reduced Endothelial Nitric Oxide Buffering Capacity

et al. 2011

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We previously reported that maternal separation (MS) sensitizes adult rats to angiotensin II (AngII)-induced hypertension. The aim of this study was to investigate the vascular reactivity to AngII and the role of renin-angiotensin system components, reactive oxygen species production and nitric oxide synthase (NOS) buffering capacity mediating the exacerbated AngII-induced responses. MS rats were separated from their mothers for 3 hours/day from day 2-14 of life. Controls (C) were non-handled littermates. At 12 weeks of age, aortic AngII-induced constriction was greater from MS rats compared to C (p<0.05), moreover, endothelial denudation abolished this difference. The response to other constrictors was unchanged. Angiotensin type 2 receptor (AT2R) function was reduced in aortic AngII-induced constriction from MS rats compared to C. Angiotensin type 1 receptor (AT1R) function was similarly abolished in both groups. However, protein expression of AT1 and AT2 receptors were similar in aortic rings from MS and C rats. Pre-incubation with superoxide inhibitor or scavenger attenuated the AngII-induced vasoconstriction in C, but not in MS rats. However, acute pre-incubation with a NOS inhibitor enhanced aortic AngII-induced constriction in aorta from C rats, but this effect was significantly reduced in MS rats compared to C. Accordingly, a further increase in AngII-induced hypertension due to chronic NOS inhibition (days 10-13) was blunted in MS rats compared to C. Similar NOS expression and activity was observed in C and MS rats. In conclusion, MS induces a phenotype with reduced endothelial NOS buffering capacity leading to dysfunctional endothelial AngII-mediated signaling and sensitization to AngII-induced vasoconstriction.

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confidence: 99%

Early Life Stress Enhances Angiotensin II–Mediated Vasoconstriction by Reduced Endothelial Nitric Oxide Buffering Capacity

et al. 2011

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“…Acute stressors induce many physiological responses, and greater reactivity to stress or delayed poststress recovery predicts future cardiovascular disease risk (7), such as stroke (14), hypertension (37), and preclinical atherosclerosis (23,52). An acute stress-induced rise in blood pressure results from autonomic and neuroendocrine-mediated changes in cardiac contractility and peripheral vascular resistance (18).…”

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confidence: 99%

Early life stress downregulates endothelin receptor expression and enhances acute stress-mediated blood pressure responses in adult rats

Loria

D’Angelo

Pollock

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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We hypothesized that early life stress enhances endothelin (ET-1)-dependent acute stress responses in adulthood. We utilized a unique rat model, wildtype (WT) and ETB receptor-deficient spotting lethal (sl/sl) rats, as well as pharmacological blockade of ET receptors, in a model of early life stress, maternal separation (MS). MS was performed in male WT and sl/sl rats 3 h/day from day 2 to 14 of life. Acute air jet stress (AJS)-induced responses (elevation in blood pressure, plasma corticosterone, and plasma ET-1) were evaluated in adult MS rats compared with the nonhandled littermate (control) rats. MS significantly augmented the acute AJS-induced blood pressure response (area under the curve) in WT rats compared with control, while the AJS-induced pressor responses were similar in sl/sl MS and control rats. ET receptor blockade significantly blunted the AJS-induced pressor response in WT MS and control rats. Moreover, AJS-induced plasma corticosterone levels in control rats were sensitive to ET receptor blockade, yet, AJS did not alter plasma corticosterone levels in MS rats. MS significantly increased circulating ET-1 levels, and AJS-induced plasma ET-1 levels were similarly increased in control and MS rats. MS induced a significant downregulation in expression of ETA and ETB receptors in aortic tissue compared with control rats. These results indicate that early life stress reduced expression of ETA and ETB receptors, leading to alterations in the ET pathway, and an exaggerated acute stress-mediated pressor response in adulthood.early life stress; maternal separation; air jet stress; blood pressure; endothelin; corticosterone IN HUMANS, THERE IS A LARGE body of epidemiological evidence that early social experiences can promote phenotypic changes that persist in adult life (5,12,28). An adverse environment during early life increases the susceptibility to develop heart disease, as well as depression, drug abuse, obesity, and diabetes (21,24,32).Acute behavioral stress responses in adult life are influenced by early life maternal care in both humans (53) and rodents (36). Maternal separation is a widely used animal model of early life stress and chronic behavioral stress (20). Rat pups separated from their mothers daily for a prolonged period (up to 3 h) during the hyporesponsive period display abnormal anxiety-related behavior (41, 43), as well as increased acute behavioral and endocrine stress reactivity as adults (4,27,38,44).Individuals with increased susceptibility to stressors may also have an exacerbated rise in blood pressure (26). Acute stressors induce many physiological responses, and greater reactivity to stress or delayed poststress recovery predicts future cardiovascular disease risk (7), such as stroke (14), hypertension (37), and preclinical atherosclerosis (23,52). An acute stress-induced rise in blood pressure results from autonomic and neuroendocrine-mediated changes in cardiac contractility and peripheral vascular resistance (18). Particularly relevant to this study, acute stress is associa...

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“…Exposure to sound louder than 85 dB or non-homogenous animal handling can affect blood pressure in small animals like rats as well as in larger animals such as non-human primates [51,52]. Thus, changes in blood pressure might not directly reflect HF, but rather environmental factors.…”

Section: Housing Treatments and Interventionsmentioning

confidence: 97%

Guidelines for Translational Research in Heart Failure

Lara‐Pezzi

Menasché

Trouvin

et al. 2015

J. of Cardiovasc. Trans. Res.

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Heart failure (HF) remains a major cause of death and hospitalization worldwide. Despite medical advances, the prognosis of HF remains poor and new therapeutic approaches are urgently needed. The development of new therapies for HF is hindered by inappropriate or incomplete preclinical studies. In these guidelines, we present a number of recommendations to enhance similarity between HF animal models and the human condition in order to reduce the chances of failure in subsequent clinical trials. We propose different approaches to address safety as well as efficacy of new therapeutic products. We also propose that good practice rules are followed from the outset so that the chances of eventual approval by regulatory agencies increase. We hope that these guidelines will help improve the translation of results from animal models to humans and thereby contribute to more successful clinical trials and development of new therapies for HF.

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Influence of neonatal handling on blood pressure, locomotor activity, and preweanling heart rate in spontaneously hypertensive and Wistar Kyoto rats

Cited by 26 publications

References 24 publications

Early Life Stress Enhances Angiotensin II–Mediated Vasoconstriction by Reduced Endothelial Nitric Oxide Buffering Capacity

Early Life Stress Enhances Angiotensin II–Mediated Vasoconstriction by Reduced Endothelial Nitric Oxide Buffering Capacity

Early life stress downregulates endothelin receptor expression and enhances acute stress-mediated blood pressure responses in adult rats

Guidelines for Translational Research in Heart Failure

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