What is the clinical evidence from this study?

Population: Acute immobilization stress. Intervention: Losartan (intracerebroventricular injection) vs. Controls. Primary outcome: Plasma catecholamines (epinephrine, norepinephrine, dopamine) after 5 and 20 min stress (p=<0.05 for norepinephrine, <0.01 for epinephrine and dopamine).

What question did this study set out to answer?

This research investigates the role of brain angiotensin II type-1 receptors in stress-related activation of the HPA axis and sympathetic system.

January 1, 1998Journal of Neuroendocrinology

Brain Angiotensin II Modulates Sympathoadrenal and Hypothalamic Pituitary Adrenocortical Activation during Stress

Q: What are the key findings of this study?

Central AT1 receptor blockade with Losartan blunted the increases in plasma catecholamines during immobilization stress (P<0.05 for norepinephrine, P<0.01 for epinephrine and dopamine) in rats.

Q: What question did this study set out to answer?

This research investigates the role of brain angiotensin II type-1 receptors in stress-related activation of the HPA axis and sympathetic system.

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Key result

Central AT1 receptor blockade with Losartan blunted the increases in plasma catecholamines during immobilization stress (P<0.05 for norepinephrine, P<0.01 for epinephrine and dopamine) in rats.

Why the study?

Does central AT1 receptor blockade with Losartan blunt sympathoadrenal and HPA axis activation during acute immobilization stress in rats?

Key Points

This research investigates the role of brain angiotensin II type-1 receptors in stress-related activation of the HPA axis and sympathetic system.
Used acute immobilization stress on rats to assess catecholamines, ACTH, corticosterone, and mRNA levels.
Administered Losartan, a central AT1 receptor antagonist, to evaluate its effects on stress responses.
Analyzed plasma and tissue samples to measure biochemical and gene expression changes.
Catecholamine increases after 5 and 20 minutes of stress were significantly blunted in Losartan-treated rats (P < 0.05 for norepinephrine, P < 0.01 for epinephrine and dopamine).
No significant changes were observed in plasma ACTH and corticosterone due to Losartan treatment.
Losartan prevented increases in CRH mRNA levels post-stress, indicating a regulatory role within the PVN.

Structured PICO

Does central AT1 receptor blockade with Losartan blunt sympathoadrenal and HPA axis activation during acute immobilization stress in rats?

Population

Rats subjected to acute immobilization stress to evaluate the effects of central AT1 receptor blockade.

Intervention

Losartan 10 microg via i.c.v. injection (central AT1 receptor blockade)

Comparator

Controls

Outcome

Plasma catecholamines (epinephrine, norepinephrine, dopamine), ACTH, corticosterone, and mRNA levels of CRH and CRH receptors in the PVNsurrogate

Main Result

p-value: p=<0.05 for norepinephrine, <0.01 for epinephrine and dopamine

Endogenous brain Angiotensin II is required for sympathoadrenal activation and regulates CRH expression in the PVN during immobilization stress in rats.

Discussion

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Implication

Central AT1 blockade attenuates sympathetic stress responses in rats; leaves open clinical translation to human cardiovascular stress modulation.

Cite This Study

Ježová et al. (1998) studied Acute immobilization stress. Losartan (intracerebroventricular injection) vs. Controls was evaluated on Plasma catecholamines (epinephrine, norepinephrine, dopamine) after 5 and 20 min stress (p=<0.05 for norepinephrine, <0.01 for epinephrine and dopamine). Central AT1 receptor blockade with Losartan blunted the increases in plasma catecholamines during immobilization stress (P<0.05 for norepinephrine, P<0.01 for epinephrine and dopamine) in rats.

synapsesocial.com/papers/6a56d0e793d190d1bc09515d https://doi.org/10.1046/j.1365-2826.1998.00182.x

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Implication

Central AT1 blockade attenuates sympathetic stress responses in rats; leaves open clinical translation to human cardiovascular stress modulation.

Brain Angiotensin II Modulates Sympathoadrenal and Hypothalamic Pituitary Adrenocortical Activation during Stress

Key Points

Structured PICO

Main Result

Discussion

Implication

Cite This Study

Brain Angiotensin II Modulates Sympathoadrenal and Hypothalamic Pituitary Adrenocortical Activation during Stress

Key Points

Structured PICO

Main Result

Discussion

Implication

Cite This Study

Also Consider

Also Consider