Lack of changes in carotid artery compliance with systemic nitric oxide synthase inhibition

Proximal large elastic arteries (ascending aorta and carotid artery) have an important role in buffering the pulsatile pressure generated from the left ventricle, which forwards continuous peripheral blood flow and protects the brain microcirculation from end-organ damage. Although compliance of distal conduit arteries (extremities' arteries) is attenuated by the nitric oxide synthase (NOS) inhibition, it is yet unknown whether compliance of proximal elastic arteries changes by the systemic NOS inhibition. To address this question, we measured central artery compliance in 17 young adults (26 +/- 1 years) who underwent intravenous infusions of N-G-monomethyl-L-arginine (L-NMMA) or saline (placebo) on separate days. Following the systemic NOS inhibition, the mean arterial pressure (MAP), total peripheral resistance and aortic augmentation index were significantly increased. However, carotid artery compliance was not affected significantly (from 0.10 +/- 0.01 to 0.11 +/- 0.01 mm(2) per mmHg) and the beta-stiffness index (an index of arterial compliance adjusted for the distending pressure) tended to decrease (from 6.63 +/- 0.35 to 6.06 +/- 0.42 a.u., P = 0.07). These parameters were not altered with saline infusion. Changes in the beta-stiffness index tended to correlate negatively with the corresponding changes in MAP (r = -0.31, P = 0.07). These results suggest that carotid artery compliance remains unchanged during the systemic NOS inhibition in spite of systemic vasoconstriction.