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Cardiovascular system of offsprings of hypertensive rats with defective nitric oxide production
M Gerová1, I Bernátová, J Török
1Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic. gerova@unpf.savba.sk
Insights
Parental nitric oxide synthase (NO synthase) inhibition during pregnancy in rats led to cardiovascular changes in offspring. Offspring exhibited higher blood pressure and altered heart development, indicating lasting effects of NO compromise.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Pharmacology
Background:
- Nitric oxide synthase (NO synthase) plays a crucial role in regulating cardiovascular function.
- Maternal hypertension can impact offspring cardiovascular health.
- The effects of parental NO synthase inhibition on offspring cardiovascular development require further investigation.
Purpose of the Study:
- To investigate the long-term cardiovascular effects on offspring resulting from parental NO synthase inhibition-induced hypertension.
- To assess changes in blood pressure, heart rate, cardiac morphology, NO synthase activity, and vascular reactivity in offspring exposed to parental NO compromise.
Main Methods:
- Two groups of rat offspring were studied: Group I (both parents treated with L-NAME during gestation and lactation) and Group II (dams treated with L-NAME post-delivery).
- Control offspring from untreated parents served as a comparison group.
- Measurements included noninvasive blood pressure and heart rate, body and heart weight, heart/body weight ratio, cardiac NO synthase and ornithine decarboxylase activity, and acetylcholine-induced aortic relaxation.
Main Results:
- Offspring from both L-NAME treated groups exhibited significantly higher blood pressure and a tendency towards decreased heart rate compared to controls.
- Group I offspring showed cardiac hypotrophy (decreased heart and body weight, reduced HW/BW ratio) with decreased NO synthase activity and increased ornithine decarboxylase activity.
- Vascular reactivity to acetylcholine in aortic rings was preserved in offspring from both experimental groups.
Conclusions:
- Parental NO synthase inhibition during critical developmental periods induces significant cardiovascular alterations in offspring, including hypertension and cardiac hypotrophy.
- Despite altered cardiac parameters, vascular endothelial function appears to be maintained.
- These findings highlight the susceptibility of the developing cardiovascular system to parental NO compromise.
Abstract:
The question was addressed of how nitric oxide synthase (NO synthase) inhibition-induced hypertension in rat parents would affect the cardiovascular system in their offsprings. Two experimental groups were set up: Group I -- offsprings of parents who had both been administered NO synthase inhibitor L-nitro-arginine methyl ester (L-NAME 40 mg/kg/day) for 5 weeks, the treatment of dams continued till week 12. Group II -- offsprings fed by dams administered L-NAME after delivery only for a period of 4 weeks. Control age-matched offsprings formed the third group. Blood pressure and heart rate in parents and in 3-week-old offsprings were determined noninvasively. In the offsprings, body and heart weight were measured and the heart/body weight ratio (HW/BW) was calculated. The NO synthase activity, and also ornithine decarboxylase activity as a marker of polyamine production, were determined in the heart. The acetylcholine-induced relaxation of aortic rings was also followed. A marked blood pressure increase with a tendency to a decreased heart rate was found in the offsprings of Group I. A significant decrease in heart weight and body weight with a decreased HW/BW ratio indicated cardiac hypotrophy that contrasted with the decrease in NO synthase activity and increase in ornithine decarboxylase activity in the heart. Noteworthy was also the finding of completely preserved relaxation of the aorta to acetylcholine. Offsprings of Group II were similarly characterized by significantly higher blood pressure, a tendency to decreased heart rate, a decrease in heart weight, but not of the HW/BW ratio. The contrasting findings of heart weight decrease on the one hand and NO synthase activity decrease and ornithine decarboxylase increase on the other, were also found in this group. Full relaxation of the aorta to acetylcholine was preserved. It can be concluded that remarkable alterations in the cardiovascular system were found in offsprings of hypertensive NO compromised parents.
