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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, NG‐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 μl/kg/min. Vascular tone was step‐wise increased with 3, 10 and 30 μg/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 ≤ 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.