Arterial Hypertension: Pathogenesis, Diagnosis, and Therapy by W. M. Manger, I. H. Page (auth.), Julian Rosenthal M.D.

By W. M. Manger, I. H. Page (auth.), Julian Rosenthal M.D. (eds.)

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Additional info for Arterial Hypertension: Pathogenesis, Diagnosis, and Therapy

Sample text

M. Manger, I. H. Page pertension. 3 In: Genest J, Koiw E, Kuchel 96. Fitzsimons JT, Simons BJ (1969) The effect on drinking in the rat of intravenous infusion of angioo (eds) Hypertension. McGraw-Hill, New York, pp 559-566 tensin, given alone or in combination with other stimuli of thirst. J Physiol 203:45-57 114. Genest J, Boucher R, Kuchel 0, Nowaczynski W 97. Folkow B (1971) The haemodynamic consequences (1973) Renin in hypertension: how important as a of adaptive structural changes of the resistance of risk factor?

H. Page dence has accumulated indicating that low- and normal-renin patients are equally susceptible to heart attacks and strokes. On the other hand, all agree that high-renin patients have more severe hypertension (as also occurred in the study by Brunner and associates 33-see Table 4), and a higher incidence of vascular damage and complications. The degree of hypertension, and not the level of plasma renin or angiotensin, seems to be the critical determinant of vascular damage. Kaplan appropriately concluded that "renin profiling remains an interesting investigational tool and offers little help to the patient or his physician.

In the great majority, cardiac output is normal; however, an increased output occurs in some borderline hypertensives during the early development of hypertension. The reasons for these hemodynamic abnormalities remain undetermined. Some believe that hemodynamic and biochemical abnormalities in borderline hypertension result from neurogenic alterations in cardiovascular function; yet this remains circumstantial. A number of investigators have quantitated plasma catecholamines in an effort to assess the activity of the adrenergic system and its role in the causation of hypertension.

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