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Cardiac and renal hyperplasia in newborn spontaneously hypertensive rats
Insights
Neonatal cardiac hyperplasia in spontaneously hypertensive rats (SHR) is a generalized phenomenon affecting the heart and kidneys. This study found increased DNA content, indicating hyperplasia, not hypertrophy, in these organs of SHR.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Hypertension Research
Background:
- Cardiac hyperplasia is a known condition in newborn spontaneously hypertensive rats (SHR).
- Previous research has noted this phenomenon, but its scope within the SHR model was unclear.
Purpose of the Study:
- To determine if neonatal cardiac hyperplasia in SHR is an isolated cardiac event or a generalized systemic issue.
- To investigate the cellular mechanisms (hyperplasia vs. hypertrophy) driving organ enlargement in SHR.
Main Methods:
- Analysis of protein and DNA content in the ventricles, kidneys, and liver of newborn SHR, Wistar, and Wistar-Kyoto (WKY) rats.
- Measurement of total organ weight and organ-to-body weight ratios.
Main Results:
- SHR exhibited significantly greater heart and kidney weights, and organ/body weight ratios compared to controls, independent of total body weight.
- Elevated relative DNA content in the heart and kidneys of SHR indicated hyperplasia as the primary cause of organ enlargement.
- The liver did not show significant differences in weight or organ/body weight ratio between SHR and controls.
Conclusions:
- Neonatal cardiac hyperplasia in SHR is not confined to the heart but is a generalized phenomenon affecting the kidneys as well.
- The observed organ enlargement is primarily due to hyperplasia (increased cell number) rather than hypertrophy (increased cell size).
- The underlying cause for this selective hyperplasia in the heart and kidneys of SHR remains undetermined, with potential factors including hemodynamic stimuli, genetic abnormalities, growth factors, or innervation.
Abstract:
Cardiac hyperplasia in newborn spontaneously hypertensive rats (SHR) has been noted by our group as well as by other investigators. The present study was designed to establish whether early (neonatal) hyperplasia is confined to the heart or is a generalized phenomenon in this hypertensive model. The ventricles, kidney and liver of newborn SHR, Wistar and Wistar-Kyoto (WKY) rats were analysed for their protein and DNA content. Total organ weight and the organ/body weight ratio of the heart and kidney but not of the liver were significantly greater in the SHR than in the control rats, irrespective of total body weight. The higher relative DNA content (per 100 mg of tissue or 100 g body weight) indicated that hyperplasia rather than hypertrophy was responsible for the enlarged heart as well as the kidney of newborn SHR. The cause of this selective cardiac and renal hyperplasia is not yet known: it may be due to putative 'haemodynamic growth stimuli', an intrinsic genetic abnormality of cells in the heart and kidney, circulating growth-promoting factors, or innervation.