Intrinsic Relaxation Factors and Length-Dependent Sensitivity in the Rat Aorta

Abstract

Abstract

Possible mechanisms for length-dependent sensitivity may involve intrinsic relaxation factors of the arterial wall. The role of the endothelium, β-receptor activity, and atrial natriuretic factor were tested. ED₅₀ and ED₁₀ (concentrations for 50% and 10% maximum response, respectively) were significantly lower at the length of maximum force (L _max) than at 80% L _max for phenylephrine stimulated WKY rat aorta rings. The same result was found for norepinephrine (NE)-stimulated rings before and after endothelium removal, and for NE stimulation in the presence of propranolol. The ED₁₀ for NE, but not its ED₅₀, was significantly decreased by endothelium removal at both lengths. The addition of propranolol decreased the ED₅₀ of NE at 80% L _max, but not at L _max. Relaxation sensitivity to atrial natriuretic factor was the same at L _max and at 80% L _max in phenylephrine-contracted WKY rings. For the rat aorta, it may be concluded that: (i) the mechanism for length-dependent sensitivity does not depend upon the endothelium or β-receptor activity, however, (ii) basal levels of endothelium-derived relaxing factor and β-receptor activity appear to modulate length-dependent sensitivity at low levels of activation, and (iii) sensitivity to atrial natriuretic factor relaxation does not depend upon length.