The effects of NG-nitro-L-arginine methyl ester on systolic pressure, diastolic pressure and pulse pressure according to the initial level of blood pressure

The objective of this study was to re-examine whether the effect of the nitric oxide synthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on blood pressure depends on peripheral vascular tone. The effects of L-NAME (10 mg/kg, i.v.) on diastolic blood pressure (DBP), systolic blood pressure (SBP), pulse pressure (PP) and heart rate (HR) were studied in pithed rats. Sal-pithed rats received 0.9% NaCl, 10 microl/kg/min. Vascular tone was step-wise increased with 3, 10 and 30 microg/kg/min intravenous phenylephrine infusion (LPhe-pithed, MPhe-pithed and HPhe-pithed rats respectively). L-NAME elicited vasopressor responses in all the animals studied. L-NAME increases in SBP and DBP in Sal-pithed rats were significantly smaller than the ones obtained in phenylephrine infused rats. The increases in DBP elicited by L-NAME were greater in LPhe-pithed rats compared with those of MPhe-pithed and HPhe-pithed rats (i.e. the step-wise rises in DBP obtained with phenylephrine were inversely related to the increases in DBP produced by L-NAME); however, the increases in SBP were similar between these experimental groups. The PP increased during L-NAME-induced pressor responses in phenylephrine-infused rats. l-NAME increases in PP showed the following order: Sal-pithed < LPhe-pithed < MPhe-pithed < or = HPhe-pithed rats. HR was not modified by L-NAME. In conclusion, the vasopressor responses produced by L-NAME in pithed rats are influenced by the pre-existing vasomotor tone in complex form. We did not find a simple positive correlation between the vascular tone or level of arterial pressure, and the magnitude of the diastolic and systolic pressor responses elicited by L-NAME. Interestingly, the increase in PP induced by l-NAME was greater in accordance with the increasing value of baseline arterial pressure. NO synthesis inhibition in the arterial endothelium may possibly explain the increase in PP caused by L-NAME, as resulting from the reduction in proximal conduit artery compliance.