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Role of adrenals on development of pressure-induced myocardial hypertrophy
Insights
Adrenalectomy significantly reduces pressure-induced myocardial hypertrophy in rats following abdominal aorta coarctation (AC). This effect is attributed to the adrenal cortex, not the adrenal medulla.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Cardiac Remodeling
Background:
- Myocardial hypertrophy is a significant cardiac adaptation to pressure overload.
- The role of adrenal hormones in pressure-induced cardiac remodeling remains incompletely understood.
Purpose of the Study:
- To investigate the impact of adrenalectomy and adrenal medulla removal on the development of myocardial hypertrophy following abdominal aorta coarctation (AC).
Main Methods:
- Male rats underwent sham operation (SO) or AC.
- Three groups were studied: untreated, bilateral adrenalectomy (ADX) prior to AC/SO, and adrenal medulla removal (MDX) prior to AC/SO.
- Carotid blood pressure (CBP), ventricular weight (HW), ventricular RNA concentration, and RNA-to-DNA ratio were assessed 7-10 days post-operation.
Main Results:
- AC induced significant increases in CBP across all groups.
- Ventricular weight and RNA/DNA ratio increased post-AC in untreated and MDX groups, but less so in the ADX group.
- ADX attenuated the development of pressure-induced myocardial hypertrophy, even after normalization for body weight.
Conclusions:
- The adrenal gland, specifically the adrenal cortex, plays a crucial role in mediating pressure-induced myocardial hypertrophy.
- Absence of the adrenal cortex significantly reduces cardiac remodeling in response to hypertension.
- The adrenal medulla does not appear to be essential for this hypertrophic response.
Abstract:
The effect of coarctation of the abdominal aorta (AC) and of sham operation (SO) on the development of myocardial hypertrophy was studied in three groups of male rats, i.e., a group without treatment prior to AC or SO (untreated), a group with bilateral adrenalectomy (ADX) 5-7 days before AC or SO, and a group in which the adrenal medulla was removed (MDX) 5-7 days before AC or SO. MDX resulted in functional elimination of the adrenal medulla without apparent effect on cortical function. The animals were killed 7-10 days after AC or SO. AC produced carotid blood pressure (CBP) increases of 33, 31, and 25 mmHg in the untreated, ADX, and MDX groups, respectively. Ventricular weight (HW), ventricular RNA concentration, and RNA-to-DNA ratio increased significantly after AC only in the untreated and MDX groups. In the ADX group, hypertension was followed by an increase in HW that could be detected only after normalization for body weight. It is concluded that absence of the adrenal gland significantly reduces the development of pressure-induced myocardial hypertrophy. Apparently, this is due to the absence of the adrenal cortex and not absence of the adrenal medulla.