Hypotrophy of conduit artery walls of the offspring of nitric oxide-defective rats

Abstract

The objective of the present study was to investigate the structure of the arterial walls of the offspring stemming from nitric oxide (NO)-defective hypertensive parents. The parents were treated with N Gnitro-L-arginine methyl ester (40 mg kg -1 day -1 ) for 5 weeks. Blood pressure was measured noninvasively in six 30-day-old rats and nine age-matched controls. The cardiovascular system was perfused with glutaraldehyde at 120 mmHg. The thoracic aorta and carotid artery were processed for electron microscopy, and geometry was determined by light microscopy. Endothelial cells, smooth muscle cells (SMC) and extracellular matrix (ECM) were determined by the point counting method in electron micrographs of the carotid artery. The blood pressure of experimental offspring was 150.0 ± 2.3 vs 104.6 ± 2.1 mmHg (P < 0.01) for the controls and their heart/body weight ratio of 3.9 ± 0.1 vs 4.4 ± 0.2 (P < 0.05) for the controls indicated cardiac hypotrophy. The wall thickness (tunica intima and media) of the thoracic aorta and carotid artery of experimental offspring was decreased to 78.9% (P < 0.01) and 83.8% (P < 0.01), respectively, compared to controls, as confirmed by a respective cross-sectional area of 85.3% (P < 0.01) and 84.1% (P < 0.01). The wall thickness/ inner diameter ratio was reduced to 75% (P < 0.01) in the thoracic artery and to 81.5% (P < 0.01) in the carotid artery. No change in endothelial cell volume density or ECM was observed in the tunica intima of the carotid artery, and SMC volume density was lower in the tunica media (37.6 ± 0.9 vs 44.7 ± 1.1% for controls, P < 0.01), indicating compromised SMC development. Interference with arginine metabolism, a decrease in NO, and other factors are possible mechanisms underlying the structural alterations of the cardiovascular system of offspring from NO-defective hypertensive rats.

Long-term effect of prazosin and losartan administration on blood pressure, heart, carotid artery, and acetylcholine induced dilation of cardiovascular system of young Wistar rats and SHR

“…Griffin et al (1991) reported that infusion of subpressor doses of ang II leads to an increase in the thickness of the arterial media and ratio of media to lumen in the resistant arteries. Further, the discrepancy between BP and trophicity of the arterial wall has also been observed in 4-week-old Wistar rats that were progenies of NO-deficient parents, where hypertension was accompanied with hypotrophy of the heart and arterial wall (Kristek and Gerova 2004). In addition, BPindependent decrease in cardiac hypertrophy was observed after long-term administration of exogenous NO donors and/or sildenafil to SHRs (Kristek et al 2007).…”

Age-dependent ultrastructural changes of coronary artery in spontaneously hypertensive rats

“…Similar lower BW was observed in 4week-old rats from dams, which were administrated with L-NAME (Gerova et al 2002). Long-term administration of L-NAME evokes hypertension in offspring and adults (Kristek and Gerova 2004).…”

Downregulation of oxytocin and natriuretic peptides in diabetes: possible implications in cardiomyopathy

“…However, the high variability of transcript measurements in the individual hearts of db/db mice questions the significance of this finding and hampers the conclusion drawn on the dynamics of ANP expression during the progression of cardiac pathology in this model. Alteration in the cardiovascular system, such as atrophy of the arterial walls in the offspring of NO‐defective rats, has been shown (Kristek & Gerova, 2004), suggesting the contribution of NO deficiency in cardiac atrophy. This is in agreement with the lower expression of NOS in db/db mice and indicates that endothelial dysfunction is involved in cardiovascular complications of diabetes (Forstermann & Munzel, 2006).…”