The Claim
In baboons with thyroid hormone excess, increased beta-adrenergic receptor density does not result in enhanced sensitivity of left ventricular contractility or relaxation to beta-1 or beta-2 adrenergic stimulation, as measured by percent change during dobutamine or terbutaline infusion.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
Even though baboons with too much thyroid hormone have more heart receptors that respond to adrenaline, their hearts don’t beat stronger or relax faster when given drugs that stimulate those receptors.
See the scientific wording
Despite increased beta-adrenergic receptor density, thyroid hormone excess in baboons does not enhance the sensitivity of left ventricular contractility or relaxation to beta-1 or beta-2 adrenergic stimulation when measured as percent change during dobutamine or terbutaline infusion.
What the research says
1 studyStudy: Effects of thyroid hormone on cardiac beta-adrenergic responsiveness in conscious baboons.
Even though the thyroid hormone made the baboon hearts have more receptors that respond to adrenaline-like drugs, the hearts didn’t respond any stronger to those drugs than before — so more receptors didn’t mean more sensitivity.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.