Aortic hypertrophy and "waterlogging" in the development of coarctation hypertension.

Abstract

To study the mechanisms and roles of vascular structural changes during the development of hypertension, we coarcted or sham-coarcted the abdominal aorta of rats. At intervals of 3 to 56 days later, we obtained standardized segments of thoracic and abdominal aortas for measurement of dry weight, water content, and amino acid content. Carotid arterial pressure was elevated by day 5 in coarcted rats and remained elevated. Femoral and tail arterial pressures remained normal. Cardiac ventricular weight and dry weight of the thoracic aorta, normalized for body weight, rose rapidly over 3-10 days in coarcted rats, remaining constant at 50-60% above levels in sham-coarcted rats thereafter. In contrast, water content of thoracic aorta in coarcted rats peaked at 123% of control values on day 7 (p<0.001), falling rapidly thereafter to levels about half of peak. Increments in dry weight and water content of the normotenslve abdominal aortic segments were of far lesser magnitude and occurred 1 to 2 weeks later, probably reflecting the effects of initial hypotension of the hindquarters. Percent hydroxyproline of intima-media segments of the thoracic aorta remained normal during the 8-week period, indicating that increases in aortic dry weight did not represent disproportional fibrosis and thus are attributable to muscular hypertrophy. These results provide support for the hypothesis that arterial wall "waterlogging" is primarily an early manifestation of the hypertensive process. The greatest magnitude of waterlogging coincides with the rapid early increase in aortic dry weight, representing hypertrophy, which suggests common mechanisms, such as activation of Na + -H + antiport. (Hypertension 1989;14:316-321)

Relationship of Cardiac Hemodynamic and Biochemical Adaptations to Mortality during Long-Term Aortic Constriction

“…In fact, many authors using this model do not routinely monitor mortality (2,13,24), while in reports concerning other methods of surgical intervention producing heart failure, long-term studies are difficult to perform because of the prohibitively high mortality rate approaching 75% of total (25). Animal models are necessarily required for investigating the disease, and the large number of studies using hypertension as a stimulus for the induction of heart failure have provided an important data base for future experimentation.…”