What is the clinical evidence from this study?

Study design: Other. Population: Angiotensin II-induced hypertension and anxiety. Intervention: 8-OH-DPAT (5-HT1AR agonist) and chemogenetic inhibition vs. Control/Vehicle. Primary outcome: Anxiety-like behavior.

What question did this study set out to answer?

The research aims to investigate the connection between hypertension and anxiety disorders, focusing on the role of the 5-HT1A receptor in the ventral hippocampus.

May 8, 2026Open Access

Targeting the 5-HT1A receptor in the ventral hippocampus alleviates anxiety-like behavior in mice with angiotensin II-induced hypertension

Q: What does this research mean for the field?

Activating 5-HT1A receptors or inhibiting ventral CA1 neural activity effectively reduces anxiety-related behavior in mice with angiotensin II-induced hypertension. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Key Result

Activating 5-HT1A receptors with the agonist 8-OH-DPAT or chemogenetic inhibition of vCA1 effectively reduced anxiety-related behavior in mice with angiotensin II-induced hypertension.

Key Points

The research aims to investigate the connection between hypertension and anxiety disorders, focusing on the role of the 5-HT1A receptor in the ventral hippocampus.
Mice were subcutaneously administered angiotensin II to induce hypertension and assess resultant anxiety-like behavior.
Electrophysiological analyses and in vivo recordings evaluated neuronal activity in vCA1 neurons under hypertension.
Chemogenetic inhibition was used to observe its effect on anxiety-like behavior in mice.
Ang II administration led to increased systolic blood pressure and heightened anxiety behaviors in mice.
Hippocampal vCA1 neurons exhibited increased responsiveness to anxiety stimuli after Ang II treatment.
Activation of 5-HT1A receptors with 8-OH-DPAT notably decreased anxiety-like behavior, correlating with changes in neuronal excitability.

Structured PICO

Does targeting the 5-HT1A receptor in the ventral hippocampus alleviate anxiety-like behavior in mice with angiotensin II-induced hypertension?

Population

Mice with angiotensin II (Ang II)-induced hypertension

Intervention

Chemogenetic inhibition of neural activity in vCA1 or activation of 5-HT1A receptors with the agonist 8-OH-DPAT

Comparator

null

Outcome

Anxiety-like behavior and neuronal excitability in the ventral CA1 (vCA1)surrogate

This study identifies vCA1 neural activity and 5-HT1AR dysregulation as critical mechanisms in hypertension-associated anxiety, highlighting potential therapeutic targets.

Abstract

Hypertension, a chronic condition, has affected > 1 billion people worldwide and is linked to a heightened risk of anxiety disorders. Despite this association, the exact mechanisms underlying the connections between hypertension and anxiety disorders remain largely elusive. In this research, we observed that systolic blood pressure (SBP) increased in mice subcutaneously administered with angiotensin II (Ang II) alongside signs of heightened anxiety. Furthermore, immunofluorescence and electrophysiological analyses revealed that Ang II enhanced neuronal activity and altered the synaptic activities of ventral CA1 (vCA1) neurons. Meanwhile, in vivo recordings showed that these neurons in Ang II-treated mice were significantly more responsive to anxiety-inducing stimuli. Additionally, chemogenetic inhibition of neural activity in vCA1 effectively alleviated anxiety-like behavior in the treated animal. Moreover, the expression of the serotonin receptor 5-HT1A receptor (5-HT1AR) in vCA1 was suppressed under hypertension. Activating these receptors with the agonist 8-OH-DPAT effectively modified neuronal excitability and reduced anxiety-related behavior in mice. These findings elucidate the critical role of vCA1 neural activity and 5-HT1AR dysregulation in hypertension-associated anxiety, highlighting potential therapeutic targets for managing this condition.

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