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Scientists Might Have Found a New Cause of High Blood Pressure, And a Way to Treat It : ScienceAlert (opens in a new tab)

sciencealert.com · 2026-10-04

Short answerEvidenceSource

Short answer

Mixed

Mixed.

The claims we could check match the study, but some claims were not covered by the evidence reviewed.

  • 3 supported
  • 2 not covered

Checked against the study summary. The full text wasn't available, so some details couldn't be settled either way.

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1
2

NewsLink checks it

Mixed

Every claim we could check holds up. Three of five claims match the study. This overall rating is based only on the claims we could check. Two claims the study doesn't address.

  • 3 supported
  • 2 not covered
Open claim evidence
3
Source paper

Source layer

The 5 papers the story cites

Source study separated from background citations.

The research anchor for the report.

Then inspect each claim

Evidence layer

Claim by claim

Each claim gets a verdict. Expand it to see the evidence directly below.

5 claims in this story

Showing all 5 claimsChoose a verdict to focus the list.

Claim 1 of 5Not coveredThe article says the findings may help explain why sleep apnea is associated with higher blood pressure, because pFL neurons respond to high CO2 or low oxygen levels.View evidenceHide evidence

Why this verdict

The profile supports a chronic intermittent hypoxia rat model of neurogenic hypertension, which is relevant to hypoxia-linked hypertension mechanisms. However, at abstract depth it does not verify the story’s sleep-apnea framing or the specific claim that pFL neurons respond to high CO2 or low oxygen levels. Those details may come from background or full-text discussion, but they are not established in the supplied profile.

1

Study evidence

pFL neurons project to RVLM and A5 presympathetic neurons and excite them during expiration.

“pFL neurons projected to the RVLM and A5 presympathetic neurons and excited them during expiration, but in hypertension, only the pFL-RVLM synaptic transmission was enhanced.”
2

Study evidence

Pharmacogenetic inhibition of pFL neurons eliminated expiratory-related sympatho-excitation and normalized arterial pressure in rats made hypertensive by chronic intermittent hypoxia.

“Using optogenetic and pharmacogenetic modulation, pFL neurons were either excited or inhibited in rats”
Claim 2 of 5Not coveredThe story says the researchers are exploring a strategy to target carotid bodies from outside the brain, and mentions a separate University of Auckland study of pyridoxal 5′ phosphate blocking P2X3 in carotid bodies as supporting evidence for the same target.View evidenceHide evidence

As statedblood pressure dropped by an average of almost 16 mmHg

Why this verdict

The supplied paper profile does not mention carotid bodies, peripheral targeting outside the brain, P2X3 blockade, pyridoxal 5′ phosphate, the University of Auckland study, or a nearly 16 mmHg blood-pressure reduction. Because those points are outside the abstract-level evidence provided for this paper, they cannot be verified here.

Claim 3 of 5SupportedA 2025 study found evidence that a specific brain region, the lateral parafacial (pFL), could be contributing to some cases of high blood pressure and may offer a way to reverse it.View evidenceHide evidence

Why this verdict

The abstract-level profile supports the core hedged claim: pFL activity is implicated in a rat model of neurogenic hypertension, activation raises arterial pressure, and inhibiting/silencing pFL neurons normalizes arterial pressure in hypertensive rats. The support is limited to animal/CIH-model evidence, which the story caveats acknowledge.

1

Study evidence

Optogenetic activation of pFL neurons triggered active expiration.

“pFL neurons were manipulated by viral transfection.”
2

Study evidence

pFL neurons project to RVLM and A5 presympathetic neurons and excite them during expiration.

“pFL neurons projected to the RVLM and A5 presympathetic neurons and excited them during expiration, but in hypertension, only the pFL-RVLM synaptic transmission was enhanced.”
Claim 4 of 5SupportedThe article says the pFL is linked to breathing control and, in rat experiments, it could also tighten blood vessels; the researchers think that combination may drive hypertension in some cases.View evidenceHide evidence

Why this verdict

The profile supports a causal animal-mechanism claim that pFL neurons trigger active expiration, increase expiratory-phase sympathetic activity, excite presympathetic RVLM/A5 neurons, and thereby raise arterial pressure. The wording about tightening blood vessels is a simplified rendering of sympathetic vasomotor drive rather than a directly quoted vascular-constriction measurement in the abstract, but the claimed mechanism is broadly supported and hedged.

1

Study evidence

Optogenetic activation of pFL neurons triggered active expiration.

“pFL neurons were manipulated by viral transfection.”
2

Study evidence

pFL neurons project to RVLM and A5 presympathetic neurons and excite them during expiration.

“pFL neurons projected to the RVLM and A5 presympathetic neurons and excited them during expiration, but in hypertension, only the pFL-RVLM synaptic transmission was enhanced.”
Claim 5 of 5SupportedIn hypertensive rats, activating pFL neurons raised blood pressure, while inactivating the region lowered blood pressure to normal levels, according to the researchers.View evidenceHide evidence

Why this verdict

This is directly supported by the profile: optogenetic activation of pFL neurons increased sympathetic activity and arterial pressure, while pharmacogenetic inhibition eliminated expiratory-related sympatho-excitation and normalized arterial pressure in CIH-induced hypertensive rats.

1

Study evidence

Optogenetic activation of pFL neurons triggered active expiration.

“pFL neurons were manipulated by viral transfection.”
2

Study evidence

Pharmacogenetic inhibition of pFL neurons eliminated expiratory-related sympatho-excitation and normalized arterial pressure in rats made hypertensive by chronic intermittent hypoxia.

“Using optogenetic and pharmacogenetic modulation, pFL neurons were either excited or inhibited in rats”
Then look for missing context

Context layer

What the story left out

Important study details the story did not include.

  • In CIH-induced neurogenic hypertension, pFL neurons project to RVLM and A5 presympathetic neurons, with selectively enhanced pFL→RVLM synaptic transmission.

    The story conveys a broad breathing/sympathetic blood-pressure pathway but does not reflect the specific circuit result that pFL→RVLM transmission, not pFL→A5 transmission, is selectively enhanced in the hypertensive model.

    From In vivo/in situ/in vitro circuit physiology in rats (CIH model)

  • The abstract does not provide quantitative effect sizes, sample sizes, statistical details, stimulation parameters, or duration of blood-pressure normalization.

    The story does not acknowledge these abstract-level limitations for the pFL experiments. Its numerical blood-pressure magnitude appears tied to a separate carotid-body/P2X3 study rather than to the profiled pFL paper.

    From Viral transfection + optogenetic excitation with multisite electrophysiological and physiological recordings in rat prep

4 things the story did carry across
  • pFL activation in rats evokes active expiration, increases expiratory-phase sympathetic activity, and raises arterial pressure.
  • Pharmacogenetic inhibition or silencing of pFL neurons eliminates expiratory-related sympatho-excitation and normalizes arterial pressure in hypertensive rats.
  • The evidence is from rat experiments, including a chronic intermittent hypoxia model; translational relevance to humans is not established in the abstract.
  • The paper proposes suppressing pFL neurons as a potential therapeutic approach for neurogenic hypertension, but testing of drug strategies in humans is not shown in the abstract.
Then read the study layer

Study layer

Study at a glance

Scan the study first. Expand only the parts you want to inspect.

Pieces of work

3

Evidence read

study summary

Lead result

in vivo animal

1Lead resultin vivo animalSilencing/inhibiting pFL neurons is antihypertensive in hypertensive rats by eliminating expiratory-related sympatho-excitation and normalizing arterial pressure.Pharmacogenetic inhibition of pFL neurons in CIH-induced hypertensive rats (in vivo)Expand

In plain English

Pharmacogenetic inhibition (silencing) of lateral parafacial (pFL) neurons in rats rendered hypertensive by chronic intermittent hypoxia eliminated expiratory-related sympatho-excitation and normalized arterial pressure.

Key findings

  • Pharmacogenetic inhibition of pFL neurons eliminated expiratory-related sympatho-excitation and normalized arterial pressure in rats made hypertensive by chronic intermittent hypoxia.
“Using optogenetic and pharmacogenetic modulation, pFL neurons were either excited or inhibited in rats”
What this piece can’t prove
  • The abstract does not provide sample sizes, statistical analyses, effect magnitudes, or duration of blood pressure normalization after inhibition.

3 further details could not be confirmed from the summary.

2in vivo animalpFL (lateral parafacial) expiratory oscillatory neurons can drive active expiration and expiratory-phase sympatho-excitation, increasing arterial pressure when activated.Viral transfection + optogenetic excitation with multisite electrophysiological and physiological recordings in rat preparationsExpand

In plain English

In rats, optogenetic excitation of lateral parafacial (pFL) expiratory neurons evoked active expiration, increased expiratory-phase sympathetic activity, and raised arterial pressure; these neurons project to and excite RVLM and A5 presympathetic neurons, and in a chronic intermittent hypoxia (neurogenic hypertension) model the pFL→RVLM synaptic transmission was selectively enhanced.

Key findings

  • Optogenetic activation of pFL neurons triggered active expiration.
  • pFL activation increased expiratory-phase sympathetic activity and caused arterial blood pressure to rise.
“pFL neurons were manipulated by viral transfection.”
What this piece can’t prove
  • Abstract does not provide quantitative effect sizes, stimulation parameters, sample sizes, or statistical details.
  • Summary based on abstract text only; methodological and result details that may be in the full paper are not available here.

1 further detail could not be confirmed from the summary.

3in vivo animalIn neurogenic hypertension induced by chronic intermittent hypoxia, expiratory-related sympathetic drive is enhanced via strengthened pFL synaptic drive to RVLM (and projections to A5), linking pFL oscillations to hypertension mechanisms.In vivo/in situ/in vitro circuit physiology in rats (CIH model)Expand

In plain English

In a rat model of neurogenic hypertension produced by chronic intermittent hypoxia (CIH), lateral parafacial (pFL) neurons project to presympathetic RVLM and A5 neurons and drive expiratory-phase excitation; in CIH hypertension the synaptic transmission from pFL to RVLM (but not to A5) is selectively enhanced, linking emergent pFL expiratory oscillations to heightened sympathetic vasomotor drive.

Key findings

  • pFL neurons project to RVLM and A5 presympathetic neurons and excite them during expiration.
  • In CIH-induced hypertension, synaptic transmission from pFL to RVLM is selectively enhanced while pFL→A5 transmission is not.
“pFL neurons projected to the RVLM and A5 presympathetic neurons and excited them during expiration, but in hypertension, only the pFL-RVLM synaptic transmission was enhanced.”
What this piece can’t prove
  • Findings derive from a rat CIH model of neurogenic hypertension; translational relevance to human hypertension requires further evidence.

2 further details could not be confirmed from the summary.

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Papers considered

The selected paper, plus nearby candidates.

PubMed, Crossref, Europe PMC · 19 candidate papers

And 13 more candidates considered.