CoChat
Sign Up
Cited by 160Thyroid Disorders and TreatmentsCardiac electrophysiology and arrhythmiasReceptor Mechanisms and Signaling

Catecholamine sensitivity, thyroid hormone and the heart

Open access
Levey, Gerald S.·1971·The American Journal of Medicine
DOI 10.1016/0002-9343(71)90331-7
Open this paper in CoChat — free account

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/0002-9343(71)90331-7

Cites

52 of 52 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Sympatho-adrenal stimulation could contribute to sustain BP levels during acute hypothyroidism as a possible mechanism counteracting the decrease in myocardial inotropism and cardiac output.

    “Sympatho-adrenal stimulation could thus contribute to sustain BP levels during acute hypothyroidism as a possible mechanism counteracting the decrease in myocardial inotropism and cardiac output (4,14,15).”

    From The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans (2002) · cites this paper as [14]

    The Physiologic and Pharmacologic Studies section (page unavailable) reports reduced intrinsic contractility in hypothyroid cat heart muscle but unaltered responsiveness to catecholamines and sympathetic nerve stimulation. This supports the possibility of an adrenergic response despite reduced contractility, but the paper does not say that sympatho-adrenal stimulation sustains blood pressure or offsets reduced cardiac output during acute hypothyroidism. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • In the hyperthyroid state, an increase in renin release secondary to the hormone-dependent decrease in systemic vascular resistance may stimulate the angiotensin-aldosterone axis and sodium reabsorption.

    “in the hyperthyroid state the increase in renin release secondary to the hormone-dependent decrease in systemic vascular resistance may stimulate the angiotensin-aldosterone axis and consequently sodium reabsorption (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23).”

    From The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans (2002) · cites this paper as [14]

    The Physiologic and Pharmacologic Studies section describes hyperthyroidism’s hyperdynamic circulation and thyroid hormone’s effects on the heart, but does not address the proposed renal mechanism. Searches for renin release, systemic vascular resistance, aldosterone, and sodium reabsorption found no passage supporting that chain; page numbers were unavailable in our copy. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

3 of the 55 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Related

Authors
Levey, G. S.
Affiliations
University of Miami (US)
Corresponding author
Levey, Gerald S.
Venue
The American Journal of Medicine
Publisher
Elsevier BV
Published
1971-04
Volume
50
Issue
4
Pages
413-420
ISSN
0002-9343 (ISSN-L)
DOI
10.1016/0002-9343(71)90331-7
OpenAlex
W2070055155
Cited by
160
References
55
Citations by year
2024: 2 · 2020: 2 · 2018: 1 · 2016: 1 · 2015: 2 · 2012: 1
FWCI
12.81
Type
journal article
Language
en
Open access
Licence
Locations
The American Journal of Medicine (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
catecholamine sensitivity, thyroid hormones, hyperthyroidism, hypothyroidism, inotropic effect, chronotropic effect, adenylate cyclase, hyperdynamic circulation, propranolol, heart rate, cardiac contractility

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review