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Growth hormone in cardiac hypertrophy induced by nephrogenous hypertension
Insights
Growth hormone plays a key role in cardiac hypertrophy caused by hypertension. Without growth hormone, even with high blood pressure, rats did not develop cardiac hypertrophy.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
Background:
- The role of growth hormone in cardiac hypertrophy linked to hypertension remains unclear.
- Understanding this relationship is crucial for cardiovascular health research.
Purpose of the Study:
- To investigate the specific role of growth hormone in hypertension-induced cardiac hypertrophy.
- To determine if growth hormone is essential for the development of cardiac hypertrophy under hypertensive conditions.
Main Methods:
- Male rats underwent hypophysectomy or were intact, followed by adrenalectomy and hormone replacement (corticoids, thyroxine, testosterone).
- Systemic hypertension was induced via renal capsule compression.
- Cardiac hypertrophy was assessed in intact and hypophysectomized rats, with and without bovine growth hormone administration.
Main Results:
- Hypertensive rats with intact pituitaries and hypophysectomized rats receiving growth hormone developed cardiac hypertrophy.
- Hypophysectomized rats, despite hypertension and hormone therapy, did not develop cardiac hypertrophy in the absence of growth hormone.
Conclusions:
- Growth hormone is a critical factor in the development of cardiac hypertrophy secondary to systemic hypertension.
- This finding clarifies the ambiguous evidence regarding growth hormone's cardiac effects in hypertension.
Abstract:
Current evidence about the role of growth hormone in cardiac hypertrophy is ambiguous. The purpose of this investigation was to determine whether growth hormone was an important element in the cardiac hypertrophy induced by systemic hypertension. Male rats with either an intact hypophysis or a hypophysectomy were bilaterally adrenalectomized, and corticoids were replaced with exogenous deoxycorticosterone and hydrocortosone. Hypophysectomized rats were further treated with thyroxine, testosterone, and, where appropriate, bovine growth hormone. Selected groups of rats were made hypertensive by means of a surgical compression of the renal capsule which produced systemic hypertension. The magnitude of the hypertension was measured in awake rats by means of a tail plethysmograph and compressing tail-cuff. The hormone replacement program re-established systolic blood pressures in sham-operated, hypophysectomized rats to levels observed in intact-hypophysis, sham-operated rats. Thus, hypertensive, hypophysectomized rats obtained pressures above both hypophysectomized and intact-hypophysis, sham-operated rats. Hypertensive rats with an intact hypophysis and hypophysectomized rats with growth hormone developed cardiac hypertrophy. In spite of the hormone therapy, the above normal systemic blood pressures, and low mortality hopophysectomized rats without growth hormone did not develop cardiac hypertrophy.