Role of angiotensin AT1 receptor in the cardiovascular response to footshock

Cierco, Maria; Israel, A

doi:10.1016/0014-2999(94)90450-2

Cited by 21 publications

(15 citation statements)

References 10 publications

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“…5,6 In particular, it has been shown that central or systemic administration of AT 1 receptor antagonists attenuated the increase in blood pressure and plasma catecholamine levels caused by several psycho-and physico-emotional stressors in rats and rabbits. 12,[24][25][26] Our data extend these findings by showing that targeted deletion of the AT 1A receptor gene selectively attenuates the pressor response to stress in mice. Taken together, the above pharmacological and functional genomic studies strongly suggest that AT 1 receptors, and specifically AT 1A subtype for murines, are required for full expression of the cardiovascular component of fight-or-flight response.…”

Section: Stress Responsesupporting

confidence: 79%

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

et al. 2009

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Pharmacological evidence suggests that angiotenisn II type 1 (AT 1 ) receptors are involved in the regulation of cardiovascular response to emotional stress and reinforcing effect of dietary salt on this response. In this study, we examined the effect of genetic deletion of AT 1A receptors on the cardiovascular effects of stress and salt in mice. AT 1A receptor knockout (AT 1A À/À ) and wild-type (AT 1A +/+ ) mice were implanted with telemetry devices and placed on a normal (0.4%) or high (3.1%) salt diet (HSD). Resting blood pressure (BP) in AT 1AÀ/À mice (84 ± 3 mm Hg) was lower than in AT 1A +/+ mice (107 ± 2 mm Hg). Negative emotional (restraint) stress increased BP by 33±3 mm Hg in AT 1A +/+ mice. This response was attenuated by 40% in AT 1AÀ/À mice (18 ± 3 mm Hg). Conversely, the BP increase caused by food presentation and feeding was similar in AT 1AÀ/À (25 ± 3 mm Hg) and AT 1A +/+ mice (26 ± 3 mm Hg). HSD increased resting BP by 14 ± 4 mm Hg in AT 1A À/À mice without affecting it significantly in AT 1A +/+ mice. Under these conditions, the pressor response to restraint stress in AT 1A À/À mice (30±3 mm Hg) was no longer different from that in wild-type animals (28 ± 3 mm Hg). The BP response to feeding was not altered by HSD in either AT 1A À/À or AT 1A +/+ mice (25 ± 2 and 27 ± 3 mm Hg, respectively). These results indicate that AT 1A receptor deficiency leads to a reduction in BP reactivity to negative emotional stress, but not feeding. HSD can selectively reinforce the cardiovascular response to negative stress in AT 1A À/À mice. However, there is little interaction between AT 1A receptors, excess dietary sodium and feeding-induced cardiovascular arousal.

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Section: Stress Responsesupporting

confidence: 79%

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

et al. 2009

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“…5 In the present study we demonstrate that in addition to its inhibitory action on vasopressor response to footshocks, systemic or central angiotensin AT 1 receptors blockade with losartan, caused a vasodepressor response to footshocks. The vasodepressor response unmasked in the presence of losartan was blocked by peripheral or central injection of PD 123319, which is known to be a specific angiotensin AT 2 receptor antagonist, 33 thus supporting the hypothesis that the vasodepressor response is mediated, in part, by activation of the angiotensin Journal of Human Hypertension AT 2 receptor.…”

Section: Discussionsupporting

confidence: 52%

“…The concept of a functional role of angiotensin AT 1 receptor in the regulation of sympathetic activity is supported by our previous findings showing that central or peripheral administration of losartan causes inhibition of the vasopressor response elicited by footshocks. 5 Vascular actions of the angiotensin AT 1 antagonist may not be entirely due to blockade of the angiotensin AT 1 receptor. Angiotensin receptors comprise two major subtypes, AT 1 and AT 2 .…”

Section: Introductionmentioning

confidence: 99%

Role of bradykinins and nitric oxide in the AT2 receptor-mediated hypotension

et al. 2000

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Footshocks increases mean arterial pressure and heart rate. Systemic or intracerebroventricular (IVT) administration of losartan, a specific angiotensin AT 1 receptor antagonist, not only inhibited the pressor response to footshocks but resulted in vasodepression. Peripheral or IVT administration of PD 123319, a specific angiotensin AT 2 receptor antagonist, did not alter the haemodynamic response to footshocks. However, simultaneous blockade of angiotensin AT 1 and AT 2 receptors by combined systemic or central administration of losartan and PD 12319, eliminated the vasodepressor response to footshocks unmasked in losartan pretreated rats. Our data suggest that activation of peripheral or brain angiotensin AT 2 receptor mediated the vasodepressor response to footshocks in the presence

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“…The interaction between Ang II and SNS occurs most likely on sympathetic activity resides at the prejunctional AT 1 receptors located at the sympathetic nerve terminals, where the facilitatory input of endogenous Ang II would be blunted by blockade with losartan. 13 Thus, it is plausible to conceive that the inhibitory action of losartan on the Ang II-induced facilitation of noradrenergic transmission during sympathoadrenal stimulation induced by footshocks could be attributed to the blocking of any interaction between Ang II and its AT 1 receptors.…”

Section: Discussionmentioning

confidence: 99%

“…12,13 After drug treatment, the animals were transferred to a Plexiglas chamber with a copper rod floor where they received mild footshocks (2.0 Hz, 100 V, 5 ms, for 5 min) delivered by a Grass stimulator (Model S48). The rats were placed into the heating oven and after 10 min of heating, footshock-stimulation was performed inside the oven for a period of 5 min.…”

Section: Quantification Of Cardiovascular Responses To Footshocksmentioning

confidence: 99%

Angiotensin II supports sympathetically mediated vasopressor response to footshock-stress

Israel

Sosa-Canache

2002

J Hum Hypertens

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The present study was carried out to assess whether endogenous angiotensin II (Ang II) supports sympathetically mediated cardiovascular response to stress in conscious unrestrained rats, using experimental models in which the renin-angiotensin-system was reduced or blocked. Footshock-stress increased mean arterial pressure (MAP) and heart rate (HR). Inhibition of angiotensin-converting enzyme with captopril or blockade of AT 1 angiotensin receptor with losartan, attenuated vasopressor responses to footshocks, while heart rate response was not altered. Bilateral nephrectomy suppressed vasopressor response as well the elevation of

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Role of angiotensin AT1 receptor in the cardiovascular response to footshock

Cited by 21 publications

References 10 publications

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

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

Role of bradykinins and nitric oxide in the AT2 receptor-mediated hypotension

Angiotensin II supports sympathetically mediated vasopressor response to footshock-stress

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