TY - JOUR
T1 - Aortic endothelial cell activity in high renin and normal renin models of hypertension in the rat
AU - Daniel, R. E.
AU - Boitnott, J. K.
AU - Brown, G. D.
AU - Heptinstall, Robert
PY - 1982/12/1
Y1 - 1982/12/1
N2 - To determine whether renin or angiotensin might have an effect on endothelial cell activity, we studied cell replication and cell density in two models of hypertension in the rat. The first was a model in which the plasma renin activity was high during the three time periods studied (1, 2, and 4 weeks after renal artery constriction) and the second, a model with elevated plasma renin activity only during the initial period (1 week). Aortic endothelial cells were labeled with tritiated thymidine prior to killing, and en face endothelial cell monolayers were prepared. The ratio of labeled cells to total cells (thymidine index) and the ratio of total number of cells to number of fields observed (cell density) were calculated for the whole aorta, segments of the aorta, and zones within the segments. In both hypertensive models, an elevation of the thymidine index (indicative of increased endothelial cell replication) was observed at 1 week but not at subsequent times when the levels had returned to those of the controls. Cell density was increased at all time periods studied and like the thymidine index showed no significant differences between the two hypertensive models. Although renin or angiotensin (or other humoral factors) could have been responsible for the increased thymidine index after 1 week, it is considered that hypertension itself is a more likely cause, taking into account the decreased indices at later time periods when one model has high renin levels and the other does not. The increased cell density at all time periods studied in both models is regarded as an adaptive reaction to the increased blood pressure.
AB - To determine whether renin or angiotensin might have an effect on endothelial cell activity, we studied cell replication and cell density in two models of hypertension in the rat. The first was a model in which the plasma renin activity was high during the three time periods studied (1, 2, and 4 weeks after renal artery constriction) and the second, a model with elevated plasma renin activity only during the initial period (1 week). Aortic endothelial cells were labeled with tritiated thymidine prior to killing, and en face endothelial cell monolayers were prepared. The ratio of labeled cells to total cells (thymidine index) and the ratio of total number of cells to number of fields observed (cell density) were calculated for the whole aorta, segments of the aorta, and zones within the segments. In both hypertensive models, an elevation of the thymidine index (indicative of increased endothelial cell replication) was observed at 1 week but not at subsequent times when the levels had returned to those of the controls. Cell density was increased at all time periods studied and like the thymidine index showed no significant differences between the two hypertensive models. Although renin or angiotensin (or other humoral factors) could have been responsible for the increased thymidine index after 1 week, it is considered that hypertension itself is a more likely cause, taking into account the decreased indices at later time periods when one model has high renin levels and the other does not. The increased cell density at all time periods studied in both models is regarded as an adaptive reaction to the increased blood pressure.
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M3 - Article
C2 - 6752572
AN - SCOPUS:0020427488
SN - 0023-6837
VL - 47
SP - 451
EP - 458
JO - Laboratory Investigation
JF - Laboratory Investigation
IS - 5
ER -