By Alan B. Weder (auth.), Norman K. Hollenberg MD, PhD (eds.)
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Additional resources for Atlas of Heart Diseases: Hypertension: Mechanisms and Therapy
45. : The association of borderline hypertension with target organ changes and higher coronary risk: Tecumseh Blood Pressure Study. JAMA 1990, 264:354-358. 46. : Familial dyslipidemic hypertension: evidence from 58 Utah families for a syndrome present in approximately 12% of patients with essential hypertension. JAMA 1988,259:3579-3586. 47. : Population-based frequency of dyslipidemic syndromes in coronary-prone families in Utah. Arch Intern Med 1990, 150:582-588. 48. Wallin G, Kunimoto MM, Sellgren J: Possible genetic influence on the strength of human muscle nerve sympathetic activity at rest.
23. Liddle GW, Bledsoe T, Coppage WS: Aldosteronism but with negligible aldosterone secretion. Trans Am Assoc Physiol1963, 76:199-213. 24. Botero-Velez M, Curtis JJ, Warnock DG: Brief report: Liddle's syndrome revisited: a disorder of sodium resorption in the distal tubule. N Engl J Med 1994, 330:178-181. 25. : Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel. Cell 1994, 79:407-414. 26. : Hypertension caused by a truncated epithelial sodium channel gamma subunit: genetic heterogeneity of Liddle syndrome.
Close to 40% of all unselected patients wit h hyper tension show such a hyperkinetic circu lation. There is good biochemical, pharmacologic, and physiologic evidence for increased sympathetic and decreased parasympathetic tone in these patients, which is reviewed later in the chapter. able later in the course of hypertension. A large proportion of previously hyperkinetic patients later of altered organ characteristics, in which cardiac responses are decreased and vascular reactivity is enhanced, also provides a basis for understanding why the sympathetic tone appears to become reset toward "normal" values during the development of established hypertension.