Increased calcium influx mediates increased cardiac stiffness in hyperthyroid rats

Area of Science:

• Cardiovascular Physiology
• Endocrinology

Background:

• Hypertension models like SHR and DOCA-salt rats exhibit cardiac hypertrophy, fibrosis, and increased left ventricular diastolic stiffness.
• Hyperthyroidism also causes cardiac hypertrophy and hypertension, but without significant collagen changes, yet diastolic stiffness increases.

Purpose of the Study:

• To investigate the role of increased calcium influx in the development of diastolic stiffness in hyperthyroidism.
• To determine if verapamil, a calcium channel blocker, can mitigate hyperthyroidism-induced cardiac stiffness.

Main Methods:

• Rats were administered triiodothyronine (T3) to induce hyperthyroidism, with or without verapamil treatment.
• Measurements included body temperature, left ventricular weight, systolic blood pressure, and left ventricular diastolic stiffness.
• Thoracic aortic rings were used to assess contractile responses to noradrenaline and relaxation responses to acetylcholine and sodium nitroprusside.

Main Results:

• T3 administration significantly increased body temperature, left ventricular weight, systolic blood pressure, and diastolic stiffness, while collagen content remained unchanged.
• Verapamil treatment in hyperthyroid rats completely prevented increased diastolic stiffness and systolic blood pressure, and attenuated increases in body temperature and left ventricular weight.
• Verapamil restored acetylcholine-induced relaxation in thoracic aortic rings.

Conclusions:

• Increased calcium influx is a potential mediator of increased diastolic stiffness in hyperthyroidism, independent of collagen deposition.
• Verapamil effectively counteracts hyperthyroidism-induced diastolic stiffness and hypertension in rats.