1. Renal hypertension produces a marked and rapidly detectable hypertrophy of the rat aorta, due to smooth muscle cell hyperplasia and connective tissue deposition.
2. As we described previously for collagen synthesis, cell hyperplasia is a very early event which reaches a maximum at a time when the blood pressure is far from its highest level, and thereafter progressively decreases.
3. Reserpine prevents the vascular wall changes on the arterial as well as the venous side of the circulation. On the other hand, captopril although effective in preventing the blood pressure rise does not suppress the hyperplastic response.
4. The arterial hypertensive disease appears to be reversible, when renal ischaemia is corrected. The smooth muscle cell hyperplasia is, however, only partly and slowly reversible.
5. These data suggest that blood pressure is not the only determinant of the vascular wall response, and that the effect of a drug on the blood pressure does not necessarily predict the vascular wall response.