ENDOTHELIUM INCREASES MEDIAL HYDRAULIC CONDUCTANCE OF AORTA, POSSIBLY BY RELEASE OF EDRF

In eight anesthetized New Zealand White rabbits, the aorta was cannulated in situ for measurement of hydraulic conductance (L(p)) at different pressures with and without endothelium. De-endothelialization increased L(p) at greater-than-or-equal-to 75 mmHg but not at 50 mmHg. Because endothelium resists transmural water flow, the endothelium must also increase medial L(p) at 50 mmHg. To determine whether this effect results from secretion of endothelial-derived relaxing factor (EDRF), L(p) was measured in eight rabbits in the presence and absence of N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of EDRF synthesis. At 50 mmHg L-NAME reduced L(p) from 6.79 +/- 2.19 to 2.59 +/- 1.41 (SD) x 10(-8) (P < 0.05, paired Student's t test). After L-NAME was removed, L(p) returned to its control value. At 125 mmHg L-NAME did not significantly change L(p), although endothelial permeability seemed to increase. L-NAME did not affect L(p) of nine de-endothelialized vessels at either pressure. An additional five experiments showed that the effect of L-NAME at 50 mmHg was reversed by L-arginine. Eleven additional experiments demonstrated that N(G)-nitro-D-arginine methyl ester does not affect L(p) at 50 mmHg. These results indicate that EDRF increases L(p) of the rabbit aorta at low pressures.