Cardiac function as related to adrenergic activity in hypertensive left ventricular hypertrophy.
Studies in experimental animals and in hypertensive patients have shown that changes in cardiac anatomy and function are not just a simple consequence of the increased pressure load. The activity of the sympathetic nervous system is one of the factors that may influence cardiac performance and also, possibly, the cardiac anatomy of hypertensive patients. Animal studies have strongly suggested a possible role of adrenergic factors in the development of left ventricular hypertrophy. In man, plasma catecholamines are usually higher in hypertensive patients with left ventricular hypertrophy, and a correlation between left ventricular mass and plasma noradrenaline has also been observed. The decrease of cardiac performance after acute beta blockade has been found to be directly related to basal plasma noradrenaline concentration. An impaired response to beta-adrenergic stimulation has been reported in hypertensive animals and has been confirmed in hypertensive patients with left ventricular hypertrophy.
D000328:Adult; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D004837:Epinephrine / Q000502:physiology; D006321:Heart / Q000294:innervation / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged; D009638:Norepinephrine / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
D011943:Receptors, Adrenergic, beta; D009638:Norepinephrine; D004837:Epinephrine