The borderline hypertensive rat: A model for studying the mechanisms of environmentally induced hypertension.

Lawler, J. E.; Cox, Ray; Sanders, Brian J.; Mitchell, Vicki P.

doi:10.1037/0278-6133.7.2.137

Cited by 20 publications

(15 citation statements)

References 16 publications

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“…Exposure to stress has been found to accelerate hypertension development in SHR (28,29) and several authors have noted the relationship between enhanced cardiovascular activation and enhanced risk in humans (4,5). The mechanism for this relationship is still unclear, although it has been suggested that increased cardiovascular activation is a contributor to hypertension development (5).…”

Section: Discussionmentioning

confidence: 98%

Borderline hypertensives produce exaggerated adrenocortical responses to mental stress.

Al’Absi

Lovallo

McKey

et al. 1994

Psychosomatic Medicine

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Serum cortisol concentrations were compared in 18 borderline hypertensive (BH) and 20 normotensive (NT) men before and after mental stress. Two levels of demand, intermittent reaction time with brief rests and reaction time alternating continuously with mental arithmetic, were used in two consecutive protocols on different days in the laboratory. Continuous, but not intermittent, mental stress produced significant elevations in cortisol levels only in the BH subjects (p < .001). The continuous challenge produced slightly more self-reported distress in both groups than the intermittent condition, and performance on the mental arithmetic task was more strongly correlated with the cortisol response than was performance on the reaction time task, suggesting that the mental arithmetic task was a key contributor to the cortisol response. Therefore, adrenocortical activity appears sensitive to appropriate stressors in BH subjects. These results indicate the importance of including measures of adrenocortical function in studies of reactivity in subjects at high risk for hypertension.

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Section: Discussionmentioning

confidence: 98%

Borderline hypertensives produce exaggerated adrenocortical responses to mental stress.

Al’Absi

Lovallo

McKey

et al. 1994

Psychosomatic Medicine

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“…Previous studies have shown that a genetic predisposition to hypertension is necessary for the development of this pathology in both humans and rats (Lawler and Cox, 1985;Henry et al, 1986;Lawler et al, 1988). An increased sympathetic drive and exaggerated response of the HPA axis may account, in part, for stressinduced hypertension.…”

Section: Figmentioning

confidence: 99%

“…The BHR represents the F 1 offspring between SHR and Wistar-Kyoto (WKY) rats, being very sensitive to external inputs, while still maintaining the nonnotensive phenotype of their WKY parents (Lawler and Cox, 1985). When subjected to chronic intermittent stress (or a diet rich in NaCl), BHRs have been shown to develop a sustainable hypertension (Lawler et al, 1981(Lawler et al, , 1988Fisher and Tucker, 1991;Mansi and Drolet, 1997); otherwise, if left unstressed, they remain in the high normotensive range for arterial pressure (Lawler et al, 1988; Mansi and Drolet, Received November 12, 1997; revised manuscript received November 25, 1997; accepted November 26, 1997. Address correspondence and reprint requests to Dr. G. Drolet at Centre Hospitalier Universitaire de Québec, Pavillon CHUL, Unité de Neuroscience, 2705 Boulevard Laurier, Ste-Foy, Québec,Canada, G1V 4G2.…”

Section: Introductionmentioning

confidence: 99%

Effect of Immobilization Stress on Transcriptional Activity of Inducible Immediate‐Early Genes, Corticotropin‐Releasing Factor, Its Type 1 Receptor, and Enkephalin in the Hypothalamus of Borderline Hypertensive Rats

Mansi

Rivest

Drolet

1998

Journal of Neurochemistry

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Abstract:The effects of immobilization on the expression of immediate-early gene c-fos and nerve growth factorinducible (NGFI)-B mRNAs, corticotropin-releasing factor (CRF) mRNA, CRF heteronuclear RNA (hnRNA), CRF receptor types 1 and 2a mRNA, and enkephalin hn/ mRNA were investigated in the hypothalamic paraventricular nucleus of Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR5). Rats were deeply anesthetized 0, 30, 60, and 180 min after the beginning of the immobilization session (60 min maximum). BHR paraventricular nuclei displayed slight differences in their resting levels of NGFI-B mRNA and CRF hnRNA, both being significantly elevated compared with those of WKY rats. Conversely, basal levels of enkephalin primary transcript were significantly lower in BHRs. Immobilization, however, induced transient variations in the hybridization signals for all evaluated genes within the paraventricular nucleus (except for CRF 2a receptor). Immediate-early gene mRNA levels were higher and more prolonged in BHRs than in WKY rats. This heightened neuronal activation in the BHRs was associated with a more rapid increase in CRF mRNA expression (30 mm) compared with that in WKY rats (60 mm). lt is interesting that a transient rise in CRF hnRNA levels was detected in stressed WKY rats, whereas the BHR group displayed a progressive decline in this transcript, being significantly below resting levels 180 min after the immobilization session. The stress-induced expression of CRF type 1 receptor mRNA was similar in both strains. Moreover, no significant differences were observed for enkephalin hn/mRNA in either strain during the immobilization session. Therefore, the hypothalamic paraventricular nucleus appears to be involved in the functional hyperreactivity of the hypothalamic-pituitaryadrenal and autonomic axes to stress observed in BHRs, which may lead ultimately to a stress-induced hypertensive state. Key Words: Opioids-Paraventricular nucleus-Primary transcript-Gene expression. J. Neurochem. 70, 1556-1566 (1998).Environmental or external stimuli perceived by the mammalian organism as stressful and uncontrollable set into motion a plethora ofbehavioral and physiological events collectively termed as the stress response. The magnitude and extent of this reaction are dependent on the animal's coping or adaptive ability, which may be attributed, at least in part, to the genetic background. Indeed, the spontaneously hypertensive rat (SHR) is hyperresponsive to environmental stimuli, exhibiting an increased behavioral, sympathetic, and cardiovascular responsiveness compared with normotensive rats (Lundin and Thoren, 1982;McCarty, 1983). Lawler et al. (1981) used this genetic trait of the SHR to produce an animal model, the borderline hypertensive rat (BHR), that is suited for studying the effects of environmental stress on adaptation and coping styles. The BHR represents the F 1 offspring between SHR and Wistar-Kyoto (WKY) rats, being very sensitive to external inputs, while still maintaining the nonnotensive phenoty...

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“…Experiments were performed in BHR and Wistar–Kyoto rats (WKY; control strain). BHR are the first generation offspring of spontaneously hypertensive rats (SHR) and WKY; previously only the male offspring have been studied (Lawler et al . 1988).…”

mentioning

confidence: 99%

Genetic predisposition to hypertension sensitizes borderline hypertensive rats to the hypertensive effects of prenatal glucocorticoid exposure

Bechtold¹,

Vernon²,

Hines³

et al. 2008

The Journal of Physiology

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An adverse intrauterine environment can increase the incidence of hypertension and other cardiovascular disease risk factors. However, in clinical and experimental studies the magnitude of the effect is variable. Possibly, the relative influence of the prenatal environment on cardiovascular disease is determined in part by genetic factors that predispose individuals to the development of environmentally induced hypertension. We tested this hypothesis by comparing the effects of prenatal dexamethasone treatment (Dex, 300 μg kg −1 I.P. on days 15 and 16 of gestation) in borderline hypertensive rats (BHR) and control Wistar-Kyoto (WKY) rats. Blood pressure, heart rate and plasma corticosterone values were measured at rest during the middle of the day, and during 1 h of restraint stress in the adult offspring using indwelling arterial catheters implanted at least 4 days prior to data collection. Compared with the saline (vehicle) control treatment, prenatal dexamethasone significantly (P < 0.05) increased baseline mean arterial pressure in male (123 ± 2 versus 131 ± 3 mmHg, saline versus Dex) and female (121 ± 2 versus 130 ± 2 mmHg, saline versus Dex) BHR, but not in male (108 ± 3 versus 113 ± 2 mmHg, saline versus Dex) or female (112 ± 2 versus 110 ± 2 mmHg, saline versus Dex) WKY rats. Relative to saline treatment, prenatal Dex also significantly increased baseline heart rate (328 ± 6 versus 356 ± 5 beats min −1 , saline versus Dex) and plasma corticosterone (5 ± 2 versus 24 ± 4 μg dl −1 , saline versus Dex), and prolonged the corticosterone response to acute stress, selectively in female BHR. However, prenatal Dex significantly enhanced the arterial pressure response to acute stress only in female WKY, while Dex augmented the elevation in heart rate during stress only in male rats. We conclude that prenatal dexamethasone increased baseline arterial pressure selectively in BHR, and plasma corticosterone only in female BHR. In contrast, prenatal Dex enhanced cardiovascular reactivity to stress in both BHR and WKY rats.

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The borderline hypertensive rat: A model for studying the mechanisms of environmentally induced hypertension.

Cited by 20 publications

References 16 publications

Borderline hypertensives produce exaggerated adrenocortical responses to mental stress.

Borderline hypertensives produce exaggerated adrenocortical responses to mental stress.

Effect of Immobilization Stress on Transcriptional Activity of Inducible Immediate‐Early Genes, Corticotropin‐Releasing Factor, Its Type 1 Receptor, and Enkephalin in the Hypothalamus of Borderline Hypertensive Rats

Genetic predisposition to hypertension sensitizes borderline hypertensive rats to the hypertensive effects of prenatal glucocorticoid exposure

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