Structure and function of peripheral vascular smooth muscle in hypertension

This paper reviews previous work from our laboratory concerning the role of resistance vessel abnormalities in the pathogenesis of high blood pressure both in humans and in the spontaneously hypertensive rat. In both humans and rat, a number of resistance vessel characteristics differ between those from hypertensive individuals and those from normotensive controls, including vascular structure (expressed as media:lumen ratio in rat vessels and media cross-sectional area in human vessels) and the sensitivity of the norepinephrine concentration-response curve to cocaine (expressed as a "cocaine shift," and possibly being a marker for amount of sympathetic innervation). Moreover, in F2-generation hypertensive/normotensive rats at least, there was a weak (p = 0.06) correlation between vascular structure and cocaine shift. These results suggest that vascular structure is altered in hypertension, and we have been interested in whether treatment causes regression of these abnormalities. In essential hypertensive patients who had been treated for about 1 year, or in rats that were treated from age 4 to 24 weeks, neither vascular structure nor "cocaine shift" was fully normalized. It is suggested that this failure to obtain full regression may be due to the cellular basis for the altered vascular structure, which in the rats is due to hyperplasia. Failure to obtain full regression of vascular structure could have important consequences concerning the hemodynamics of treated hypertensive individuals.