Clonidine for treating patients with mild hypertension and angina pectoris
An increase in the activity of the adrenergic nervous system is one of the features of mild hypertension and is thought to contribute to the mechanism of the disease (De Quatro and Chan 1972; Champlain et al. 1981). Both hypertension and augmented sympathetic drive help to produce the symptoms of angina pectoris by increasing af-terload and accelerating metabolic rate, respectively. Each of these mechanisms raises the oxygen demand of the heart muscle and is likely to lead to a shortage of oxygen, which is known to trigger coronary pain.
KeywordsAngina Pectoris Mild Hypertension Double Product Chronic Angina Pathetic Nervous System
Unable to display preview. Download preview PDF.
- 1.Ceremuzyński L, Łada J, Maruchin M, Dluzniewski M, Herbaczyńska-Cedro K (1979 a) Suppression of catecholamine excretion by low doses of Clonidine in healthy subjects and feasibility study on Clonidine application in angina pectoris. Drug Res 5:829–835.Google Scholar
- 3.Challoner DR, Steinberg D (1966) Oxidative metabolism of myocardium as influenced by fatty acids and epinephrine. Am J Physiol 211:897–902.Google Scholar
- 6.Finney DJ, Latscha R, Benett BM, Hsu P (1963) Tables for testing significance in a 2x2 contingency table. Cambridge University Press, Cambridge.Google Scholar