cAMP acts as a negative regulator of rat aortic SMC proliferation, and SHR-derived cells show resistance to this suppression, suggesting abnormalities in the cAMP system in hypertension.
Implicates cAMP dysregulation in hypertensive vascular pathology; hypothesis-generating for targeted therapies pending human validation.
We investigated the proliferation and the migration of aortic smooth muscle cells (SMC) from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) in culture. The doubling time of SMC was significantly elongated by dibutyrylcAMP (Bt2 CAMP) and cholera toxin (CT) and the migration of SMC was also inhibited by the former. The suppression of the proliferation and the migration of SHR-SMC caused by Bt2 cAMP and CT wasn't so clear comparing with SMC from WKY. These results suggest that CAMP is a negative regulator in the proliferation of rat aortic SMC, and there are some differences between SMC from SHR and WKY in their membrane and/or CAMP second messenger system.
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Nakayama et al. (1987) studied this question.
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