Abstract

This review is concerned with the structure and function of resistance arteries in hypertension. By use of a variety of techniques, results indicate that raised blood pressure, in patients with essential hypertension and in animal models of hypertension, is associated with abnormalities in the structure of small arteries, expressed as an increased media: lumen ratio and reduced lumen. Functional changes, expressed as an increased sensitivity of resistance arteries to various agonists, have been seen in the spontaneously hypertensive rat, but there is no evidence for such increased sensitivity of resistance arteries in patients with essential hypertension. The role of resistance artery structural abnormalities in the long term control of peripheral resistance is not clear. On the one hand, resistance artery structure appears to be determined by the factors which produce the hypertension, both directly through neurohumoral influences and indirectly through the resulting raised intravascular pressure. On the other hand, the limited experimental evidence available suggests that small artery structure does not have a dominating effect on blood pressure and thus on the control of peripheral resistance. Furthermore, once produced, it is difficult to obtain regression of an abnormal structure. These results suggest that small artery structure is determined primarily by the prevailing intravascular pressure and the mechanisms which produce it. It is still not clear if small artery structure in itself is a major controller of peripheral resistance, but it appears that the effects of altered small artery structure may be overridden by extravascular factors.

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