Cardiovascular effects of ventrolateral periaqueductal gray (vlPAG) AT1 receptors in normotensive and hemorrhagic rats.

Q: What are the key findings of this study?

Angiotensin II microinjection into the vlPAG produced dose-dependent pressor and tachycardic responses in normotensive and hemorrhagic rats, effects that were primarily blocked by Losartan.

Q: What is the clinical evidence from this study?

Population: Normotension and hemorrhage-induced hypotension (n=84). Intervention: Angiotensin II microinjection into the vlPAG vs. Saline. Primary outcome: Maximal and time-course changes in mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) (p=<0.01).

Q: What does this research mean for the field?

Angiotensin II in the ventrolateral periaqueductal gray stimulates cardiovascular activity via AT1 receptors in both normotensive and hemorrhagic rats, primarily through sympathetic nervous system activation. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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

To investigate the central and peripheral cardiovascular effects of Angiotensin II and its AT1 receptors within the ventrolateral periaqueductal gray under normotensive and hemorrhagic conditions.

Esmaeil Hamounpeyma; Reza Mohebbati; Mohammad Naser Shafei

doi:10.22038/ijbms.2026.90860.19601

January 1, 2026Open Access

Cardiovascular effects of ventrolateral periaqueductal gray (vlPAG) AT1 receptors in normotensive and hemorrhagic rats.

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Key result

Angiotensin II in the vlPAG drives dose-dependent pressor responses blocked primarily by losartan.

P<0.01
n=84

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Why the study?

Does Angiotensin II microinjected into the ventrolateral periaqueductal gray alter cardiovascular parameters in normotensive and hemorrhagic rats?

Key Points

To investigate the central and peripheral cardiovascular effects of Angiotensin II and its AT1 receptors within the ventrolateral periaqueductal gray under normotensive and hemorrhagic conditions.
Microinjected saline, Angiotensin II (0.1, 0.2, and 0.3 nmol), and the AT1 receptor antagonist losartan into the vlPAG of normotensive rats and rats subjected to hemorrhage via withdrawal of approximately 15% of blood volume.
Assessed peripheral mechanisms through intravenous administration of hexamethonium (ganglion blocker) or atropine (muscarinic receptor blocker, 1 mg/kg) alone and prior to vlPAG Angiotensin II (0.3 nmol).
Recorded time-course and maximal changes (Δ) in mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) using a PowerLab data acquisition system.
Microinjection of AngII at 0.2 and 0.3 nmol into the vlPAG significantly increased ΔMAP and ΔSBP over time (P<0.05 and P<0.1), with maximal changes peaking at 0.3 nmol (P<0.01 to P<0.001 vs. saline); pretreatment with losartan significantly attenuated these pressor responses (P<0.05 to P<0.01).
During hemorrhage (which reduced baseline MAP by 35-40 mmHg), microinjection of 0.3 nmol AngII significantly attenuated hypotension by increasing ΔSBP and ΔMAP over time (P<0.01 vs. hemorrhage alone), an effect significantly blocked by losartan pretreatment (P<0.05 to P<0.01).
Intravenous hexamethonium significantly attenuated the AngII-induced increases in ΔSBP, ΔMAP, and ΔHR (P<0.01 to P<0.001), whereas atropine significantly potentiated AngII-induced tachycardia (P<0.05).

Structured PICO

Does Angiotensin II microinjected into the ventrolateral periaqueductal gray alter cardiovascular parameters in normotensive and hemorrhagic rats?

P

Population

84 male Wistar rats were evaluated in normotensive and hemorrhagic conditions to assess the cardiovascular effects of ventrolateral periaqueductal gray AT1 receptors.

I

Intervention

Microinjection of Angiotensin II (AngII) (0.1, 0.2, or 0.3 nmol) into the ventrolateral periaqueductal gray (vlPAG), with or without Losartan, hexamethonium, or atropine

C

Comparator

Microinjection of saline into the vlPAG

O

Outcome

Time course and maximal changes (Δ) of mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) over 30 minutessurrogate

Main Result

p-value: p=<0.01

Angiotensin II in the ventrolateral periaqueductal gray stimulates cardiovascular activity via AT1 receptors during both normotensive and hemorrhagic conditions, with peripheral effects mediated largely by sympathetic nervous system activation.

Limitations

Cannot completely rule out contributions from other Angiotensin II receptor subtypes despite Losartan blockade strongly implying AT1R involvement.
The potential role of vasopressin secretion as an alternative pathway for the residual pressor effect after ganglionic blockade was not directly measured.
The neuronal systems, such as adrenergic neurons, that evoked the expression of AT1Rs in the vlPAG were not examined.

Implication

Preclinical only; leaves open whether vlPAG AT1 signaling modulates human hemorrhagic responses.

Abstract

Objectives: The ventrolateral periaqueductal gray (vlPAG) regulates cardiovascular function. Given the presence of Angiotensin II (AngII) and its AT1 receptors (AT1R) in the vlPAG, this study investigated their central and peripheral roles in cardiovascular control during normotensive and hemorrhage (Hem) conditions. Materials and Methods: Saline, three doses of AngII (0.1, 0.2, and 0.3 nmol) were microinjected into the vlPAG. The AT1R blocker Losartan (Losa) was microinjected alone and before AngII in normotensive and Hem conditions. The peripheral mechanisms of AngII were examined by intravenous injection of hexamethonium (Hexa, a ganglion blocker) and atropine (Atro, a muscarinic receptor blocker), alone and before AngII (0.3 nmol), in both normotensive and Hem conditions. Time course and maximal changes (Δ) of mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) were recorded by the PowerLab apparatus and analyzed. Results: <0.01); these responses were augmented by AngII, and Losa blocked this AngII effect. Hexa reduced the cardiovascular improvement induced by AngII during Hem, and Atro enhanced the AngII-induced tachycardia. Conclusion: AngII in the vlPAG stimulates cardiovascular activity via AT1R in both normotensive and Hem conditions. Furthermore, these peripheral effects of AngII are primarily mediated through sympathetic nervous system activation.

Discussion

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Cite This Study

Hamounpeyma et al. (2026) studied Normotension and hemorrhage-induced hypotension (n=84). Angiotensin II microinjection into the vlPAG vs. Saline was evaluated on Maximal and time-course changes in mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) (p=<0.01). Angiotensin II microinjection into the vlPAG produced dose-dependent pressor and tachycardic responses in normotensive and hemorrhagic rats, effects that were primarily blocked by Losartan.

synapsesocial.com/papers/69e8677e6e0dea528ddeb99a https://doi.org/10.22038/ijbms.2026.90860.19601

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Cardiovascular effects of ventrolateral periaqueductal gray (vlPAG) AT1 receptors in normotensive and hemorrhagic rats.

Figures

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Cardiovascular effects of ventrolateral periaqueductal gray (vlPAG) AT1 receptors in normotensive and hemorrhagic rats.

Figures

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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