Intrinsic relaxation factors and length-dependent sensitivity in the rat aorta

Possible mechanisms for length-dependent sensitivity may involve intrinsic relaxation factors of the arterial wall. The role of the endothelium, beta-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 (Lmax) than at 80% Lmax 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% Lmax, but not at Lmax. Relaxation sensitivity to atrial natriuretic factor was the same at Lmax and at 80% Lmax 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 beta-receptor activity, however, (ii) basal levels of endothelium-derived relaxing factor and beta-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.