Slow developing pressor effect of angiotensin II and vascular structure.

AIM: To summarize and discuss four experiments relating to a possible action of angiotensin (Ang) II as a vascular growth factor and to consider the importance of growth factors in hypertension. EXPERIMENT 1: Rats infused with a low dose of Ang II developed a slow pressor response. After 10 days vascular hypertrophy was evident. Other rats infused with Ang II and given hydralazine to prevent the rise in pressure also developed vascular hypertrophy. EXPERIMENT 2: The results of a second experiment suggested that Ang II caused vascular hypertrophy by a mechanism that involves the proto-oncogene c-fos, an intermediary in growth factor action. EXPERIMENT 3: In this experiment hypophysectomy arrested maturation of resistance vessels in the rat and prevented the structural vascular response to increased arterial pressure. Thyroxine and growth hormone prevented both these effects, presumably acting as growth factors. EXPERIMENT 4: In the fourth experiment, young spontaneously hypertensive rats (SHR) given an angiotensin converting enzyme (ACE) inhibitor for 4 weeks did not fully develop hypertension, even after the ACE inhibition had ceased. This effect was prevented by the infusion of Ang II during the ACE inhibition. These results suggest that the blood pressure rise in SHR has a reversible element related to Ang II.
CONCLUSIONS: Ang II causes vascular hypertrophy by a non-pressor mechanism, possibly as a growth factor. Ang II and other growth factors may be important in the development of a normal vascular system and of abnormal vessels in hypertension.