Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake

Chen, Daian; Greca, Luisa La; Head, Geoffrey A.; Walther, Thomas; Mayorov, Dmitry N.

doi:10.1038/hr.2009.59

Cited by 27 publications

(33 citation statements)

References 32 publications

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“…Second, the BP change associated with spontaneous ultradian activity-inactivity bouts, including those in the late-dark period, was not altered by HSD in either group. Third, the pressor response to induced behavioral activation by cage-switch in the present study, or food presentation and feeding in our recent work 19 remained unaffected by HSD in either AT 1A −/− or AT 1A +/+ mice. Finally, the power of spectral LF peaks of BP and HR, which is considered to be a reliable quantifier of autonomic responsiveness, 32,33 was similar between groups on HSD, as were spontaneous baroreflex sensitivity and BP reactivity to a given increase in locomotor activity.…”

Section: Discussionmentioning

confidence: 59%

“…However, our findings that both locomotor activity and the proportion of time spent active were not altered by HSD in either strain do not support this possibility. It should be noted however, that locomotor activity, as measured by DSI telemetry, is primarily an index of gross body movement, and as such may seem less Nonetheless, this appears not to be the case for most stereotypic behaviors in mice, as we found recently that in this species not only eating, 19 but also grooming, orienting-sniffing, rearing, and drinking (D.N. Mayorov, unpublished data) are associated with distinct increases in locomotor activity, as recorded by DSI telemetry.…”

Section: Discussionmentioning

confidence: 82%

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The Day-Night Difference of Blood Pressure Is Increased in AT1A-Receptor Knockout Mice on a High-Sodium Diet

Chen

Greca

Head

et al. 2010

American Journal of Hypertension

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 82%

The Day-Night Difference of Blood Pressure Is Increased in AT1A-Receptor Knockout Mice on a High-Sodium Diet

Chen

Greca

Head

et al. 2010

American Journal of Hypertension

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“…These findings, in conjunction with other studies where we have shown that restraint stress produced a similar degree of reduced pressor responses in AT 1A Ϫ/Ϫ mice with little change in activity (the mice were restrained), suggest that locomotor activity is not confounding the current findings. 30 Our results are also relevant to the autonomic regulation by the baroreflex, because greater c-Fos expression was observed in the caudal ventrolateral medulla and NTS accompanied by an absence of stress-induced baroreflex inhibition in AT 1A Ϫ/Ϫ mice compared with AT 1A ϩ/ϩ mice. These brain regions are important for baroreflex regulation, and the greater c-Fos expression quantitatively reflects a difference in baroreflex responsivity between strains during stress.…”

Section: Discussionmentioning

confidence: 61%

Role of Angiotensin II Type 1A Receptors in Cardiovascular Reactivity and Neuronal Activation After Aversive Stress in Mice

et al. 2009

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Abstract-We determined whether genetic deficiency of angiotensin II Type 1A (AT 1A ) receptors in mice results in altered neuronal responsiveness and reduced cardiovascular reactivity to stress. Telemetry devices were used to measure mean arterial pressure, heart rate, and activity. Before stress, lower resting mean arterial pressure was recorded in AT 1AϪ/Ϫ (85Ϯ2 mm Hg) than in AT 1A ϩ/ϩ (112Ϯ2 mm Hg) mice; heart rate was not different between groups. Cage-switch stress for 90 minutes elevated blood pressure by ϩ24Ϯ2 mm Hg in AT 1A ϩ/ϩ and ϩ17Ϯ2 mm Hg in AT 1A Ϫ/Ϫ mice (PϽ0.01), and heart rate increased by ϩ203Ϯ9 bpm in AT 1A ϩ/ϩ and ϩ121Ϯ9 bpm in AT 1A Ϫ/Ϫ mice (PϽ0.001). Locomotor activation was less in AT 1A Ϫ/Ϫ (3.0Ϯ0.4 U) than in AT 1A ϩ/ϩ animals (6.0Ϯ0.4 U), but differences in blood pressure and heart rate persisted during nonactive periods. In contrast to wild-type mice, spontaneous baroreflex sensitivity was not inhibited by stress in AT 1A Ϫ/Ϫ mice. After cage-switch stress, c-Fos immunoreactivity was less in the paraventricular (PϽ0.001) and dorsomedial (Pϭ0.001) nuclei of the hypothalamus and rostral ventrolateral medulla (PϽ0.001) in AT 1AϪ/Ϫ compared with AT 1A ϩ/ϩ mice. Conversely, greater c-Fos immunoreactivity was observed in the medial nucleus of the amygdala, caudal ventrolateral medulla, and nucleus of the solitary tract (PϽ0.001) of AT 1A Ϫ/Ϫ compared with AT 1A ϩ/ϩ mice. Greater activation of the amygdala suggests that AT 1A receptors normally inhibit the degree of stress-induced anxiety, whereas the lesser activation of the hypothalamus and rostral ventrolateral medulla suggests that AT 1A receptors play a key role in autonomic cardiovascular reactions to acute aversive stress, as well as for stress-induced inhibition of the baroreflex. Key Words: receptors Ⅲ angiotensin II Ⅲ stress Ⅲ blood pressure Ⅲ heart rate Ⅲ immunohistochemistry Ⅲ mice C ardiovascular reactivity, a rapid sympathetically mediated increase in blood pressure in response to aversive stress, is considered a risk factor for both hypertension and heart disease. 1,2 To date, the central mechanisms that control cardiovascular reactivity are not fully elucidated. However, it is plausible that the regulation of stress reactivity occurs at least at 3 major central nervous system levels. The first level includes the formation of an emotional reaction to a stimulus by cortico-limbic structures. The second consists of the activation of autonomic and endocrine outputs to the periphery by hypothalamic-brain stem circuits. The third involves suppression of negative feedback signals from baroreceptors, which would otherwise effectively counteract cardiovascular activation.Angiotensin II (Ang II) is increasingly recognized as an important modulator of cardiovascular reactivity to stress at several central nervous system levels. First, Ang II is implicated in modulating anxiety 3 and may thereby influence the integration of emotional and behavioral reactions to aversive stimuli at the limbic level. Second, Ang II is critically involved,...

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“…A piece of almond (ϳ0.5 g), a novel palatable stimulus, was placed in the home cage. This is accompanied by marked increases in BP and HR (Jackson et al, 2007;Chen et al, 2009). The mouse was observed from when it commenced eating until when it ceased eating.…”

Section: Cardiovascular and Stress Responses In Rvlm Lv-prsx8-at 1a Rmentioning

confidence: 99%

Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress

Chen¹,

Jancovski²,

Bassi³

et al. 2012

J. Neurosci.

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The rise in blood pressure during an acute aversive stress has been suggested to involve activation of angiotensin type 1A receptors (AT 1A Rs) at various sites within the brain, including the rostral ventrolateral medulla. In this study we examine the involvement of AT 1A Rs associated with a subclass of sympathetic premotor neurons of the rostral ventrolateral medulla, the C1 neurons. The distribution of putative AT 1A R-expressing cells was mapped throughout the brains of three transgenic mice with a bacterial artificial chromosomeexpressing green fluorescent protein under the control of the AT 1A R promoter. The overall distribution correlated with that of the AT 1A Rs mapped by other methods and demonstrated that the majority of C1 neurons express the AT 1A R. Cre-recombinase expression in C1 neurons of AT 1A R-floxed mice enabled demonstration that the pressor response to microinjection of angiotensin II into the rostral ventrolateral medulla is dependent upon expression of the AT 1A R in these neurons. Lentiviral-induced expression of wild-type AT 1A Rs in C1 neurons of global AT 1A R knock-out mice, implanted with radiotelemeter devices for recording blood pressure, modulated the pressor response to aversive stress. During prolonged cage-switch stress, expression of AT 1A Rs in C1 neurons induced a greater sustained pressor response when compared to the control viral-injected group (22 Ϯ 4 mmHg for AT 1A R vs 10 Ϯ 1 mmHg for GFP; p Ͻ 0.001), which was restored toward that of the wild-type group (28 Ϯ 2 mmHg). This study demonstrates that AT 1A R expression by C1 neurons is essential for the pressor response to angiotensin II and that this pathway plays an important role in the pressor response to aversive stress.

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Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake

Cited by 27 publications

References 32 publications

The Day-Night Difference of Blood Pressure Is Increased in AT1A-Receptor Knockout Mice on a High-Sodium Diet

The Day-Night Difference of Blood Pressure Is Increased in AT1A-Receptor Knockout Mice on a High-Sodium Diet

Role of Angiotensin II Type 1A Receptors in Cardiovascular Reactivity and Neuronal Activation After Aversive Stress in Mice

Angiotensin Type 1A Receptors in C1 Neurons of the Rostral Ventrolateral Medulla Modulate the Pressor Response to Aversive Stress

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