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Thyrotropin-releasing hormone increases plasma norepinephrine in man
Hormone Research
|January 1, 1981
Summary
Thyrotropin-releasing hormone (TRH) increases blood pressure and plasma norepinephrine levels in humans. These TRH-induced blood pressure changes may be linked to norepinephrine release, not the renin-angiotensin-aldosterone system.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
Background:
- Thyrotropin-releasing hormone (TRH) is a key regulator of thyroid-stimulating hormone.
- The cardiovascular and hormonal effects of exogenous TRH in humans are not fully elucidated.
Purpose of the Study:
- To investigate the effects of exogenous TRH administration on blood pressure and key hormonal systems in humans.
- To determine the role of catecholamines, renin-angiotensin-aldosterone system, and prolactin in TRH-mediated physiological responses.
Main Methods:
- Administration of exogenous TRH to human subjects.
- Measurement of mean arterial blood pressure.
- Assay of plasma norepinephrine, epinephrine, renin activity, and aldosterone levels.
Main Results:
- TRH administration significantly increased mean arterial blood pressure at 4 and 8 minutes post-administration.
- Plasma norepinephrine levels increased significantly following TRH administration.
- No significant alterations were observed in plasma epinephrine, renin activity, or aldosterone levels.
Conclusions:
- TRH administration induces an increase in circulating catecholamines, primarily norepinephrine, in humans.
- The observed increases in blood pressure following TRH administration are likely mediated by norepinephrine release.
- Acute elevations in prolactin do not appear to influence the renin-angiotensin-aldosterone system in humans.