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A GUIDE TO THE THEORY OF ARTERIAL HYPERTENSION IRVINE H. PAGE, M.D.; J. W. McCUBBIN, M.D.; AND A. C. CORCORAN, M.D.* Somewhat more than twenty-five years ago, study ofarterial hypertension slowly began to assume an importance quite unknown in the centuries before. This was due to both people and specific discoveries. Fortunately , it is unnecessary to choose which was the most important. Thus the past quarter-century has seen great growth in knowledge of the mechanisms of hypertension. As so often happens at the beginning, the problems seem relatively simple. But, as more and more is known, the complexity and beauty of nature's processes become evident, and, with this realization, humility replaces overconfidence. Most investigators now know that the end is not yet; hypertension will not yield its secrets easily. Yet there are many bright vistas along which we may look, andthese may well form the pattern ofdiscovery which will lead to understanding ofhow blood pressure is controlled. Our purpose in this article is to describe where we stand in 1958. I. Mechanisms ofHypertension A. ARTERIOLAR TONE AND REACTIVITY To provide a perspective ofhypertension, it seems appropriate to start by examining the mechanisms that determine arteriolar size, since increased arteriolar resistance to blood flow is largely accountable for most forms of hypertension. Some of these mechanisms are distant from the arteriole and are mediated by nerve impulses or circulating vasoactive agents. Several factors are local; others can be labeled as "intrinsic," and it is these that are perhaps the least understood, least studied, and most unappreciated . The main function of arterioles is to regulate blood flow * Research Division of the Cleveland Clinic Foundation and the Frank E. Bunts Educational Institute, Cleveland, Ohio. 307 through capillaries, and it is highly improbable that the regulatory function is not correlated with the proper need oftissues for blood. It is well known, for instance, that ischemia or exercise, which causes local accumulation of metabolites, causes extreme vasodilation. While these are dramatic examples of the ability of tissues to let their needs be known, there must be similar and continuous effects during more normal states, and it is not unreasonable to expect these influences to modify the intrinsic properties of smooth muscle as well as directly to affect arteriolar size. Arteriolar smooth muscle shows a degree ofinherent tension, or resistance to stretch, even when isolated from all known neurogenic or humoral stimuli. This intrinsic property ofsmooth muscle and the factors that influence it are little understood and should be chief targets for future research . We emphasize the important fact that a change in resting or basal tone causing only a small decrease in arteriolar diameter would result in a disproportionately large rise in resistance to blood flow. Closely associated with tone ofarteriolar muscle is automaticity, a property common to most smooth muscle. Some evidence indicates, for instance , that vascular smooth muscle responds to the stretching effect of blood pressure with active constriction, and other evidence indicates that it undergoes more or less continuous alternating constriction and dilation, even in the absence ofmechanical stimuli. Vasomotion of this sort is difficult to demonstrate clearly and has, therefore, received relatively little study; but it and the factors influencing it can be expected to modify importantly the total peripheral resistance to blood flow. It is logical to search for causes ofhypertension by examining the local mechanisms that influence the arterioles' normal function—-the regulation of blood supply to tissues. These intrinsic properties of arteriolar smooth muscle are very likely influenced significantly by intra- and extra-cellular sodium and potassium concentrations and by movement ofthese ions in and out ofmuscle cells. Sodium and potassium, as well as other ions, are importantly concerned in basic processes of smooth-muscle contraction; on the other hand, a local excess or shortage ofone ion or another, per se, does not seem to be the culprit. Rather, the factors that determine electrolyte metabolism of muscle in turn affect its intrinsic functions. These are numerous and run the gamut from neurogenic impulses through a wide range of humoral 308 /. H. Page,J. W. McCubbin, and A. C. Corcoran ¦ Arterial Hypertension Perspectives in Biology and Medicine · Spring 1958 agents. In this connection...


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