Proliferative response of the arterial wall in arterial hypertension: hyperplasia versus polyploidy
Carlier, P.; Radelet, M.; Montrieux, C.; Greimers, R.; Rorive, G.
Archives des Maladies du Coeur et des Vaisseaux 78(11): 1710-1715
1985
ISSN/ISBN: 0003-9683 PMID: 3938245 Document Number: 243367
Proliferation changes are along with cell hypertrophy and extracellular deposit the major components of the hypertensive structural changes in large arteries. There is still some doubt about the nature of the proliferative changes: hyperplasia or polyploidization. The aorta and the tail artery of SHR and Goldblatt one-kidney, one clip hypertensive rats (RVHR) were studied at different ages and hypertensive stages. After enzymatic dispersion, cell relative DNA content was assayed by flow cytofluorimetry and by Feulgen microdensitometry. Tissue total DNA content was assayed by fluorimetry. The increase in diploid and tetraploid cells within the hypertensive arteries was further calculated. In the RVHR, hypertension is of very rapid onset and reaches a plateau within 20 days (compared to the normotensive Wistar, systolic BP is 32 mmHg at 15 days, 52 mmHg at 40 days, 45 mmHg at 90 days). An increase in total aortic DNA content (DNA: 32 micrograms at 15 days, 31 micrograms at 40 days, 40 micrograms at 90 days) is found before the development of a significant polyploidy (polyploidy in per cent: 2.3 p. 100 at 15 and 40 days; 12.0 p. 100 at 90 days). Proliferation changes in this model appears to be hyperplasia at the acute phase and polyploidy at the chronic phase. The course of hypertension is slower and less severe in the SHR (compared to the WKY, systolic BP: 0 mmHg in 4 weeks, 17 mmHg in 8 weeks old and 33 mmHg in 35 weeks old rats).