Some General Considerations on Vascular Reactivity
In Vitro Effects of Vasopressor Agents on the Metabolism of the Vascular Wall
Norepinephrine and epinephrine in pharmacological doses significantly inhibited the synthesis of acid mucopolysaccharides and lipids in incubated dog arterial tissue, whereas angiotensin had no detectable effect on these metabolic functions. Although these findings suggested different metabolic effects of the catecholamines and angiotensin, differences in rates of inactivation of these agents could not be excluded as a cause for their different actions. The inactivation of angiotensin by incubated dog arterial tissue appeared to be over a hundred times more rapid than that of the catecholamines. The differences in the in vitro and the in vivo inactivation of the catecholamines are most likely related to the inability of the denervated tissue to bind, and hence inactivate, the amines. Tissue binding, rather than enzyme degradation of catecholamines, appears to be the major mechanism responsible for the rapid inactivation of the pharmacological activity of the catecholamines. It is suggested that the changes in the reactivity of the blood pressure to cold, norepinephrine, chlorothiazide, and reserpine are related to the binding of catecholamines in the tissues. It is also postulated that one of the basic disturbances in essential hypertension might be an accumulation of pharmacologically active norepinephrine in the arterioles due to insufficient binding of the amine in the tissues.
- © 1964 American Heart Association, Inc.