THE VASOCONSTRICTOR EFFECTS OF L-NAME, A NITRIC-OXIDE SYNTHASE INHIBITOR, IN PREGNANT RABBITS

1 We have used anaesthetized, acutely instrumented non-pregnant (NP) a nd late pregnant (P) New Zealand white rabbits to examine the possible role of nitric oxide (NO) in the pregnancy-induced fall of vascular t one and arterial pressure. Systemic, renal and pulmonary vascular resi stance, as well as plasma concentrations of cyclic GMP (PcGMP) were co mpared before and after the inhibition of NO synthesis by N-G-nitro-L- arginine methyl ester (L-NAME). 2 P rabbits had lower baseline total p eripheral resistance (TPR), mean arterial pressure (MAP) and higher Pc GMP than NP controls (all P<0.05 or less). L-NAME (1, 10, 50 mg kg(-1) , i.v.) resulted in dose-dependent elevation of TPR in both groups. Ho wever, the absolute, as well as percentage increases in TPR were great er (P<0.05) in NP than in P rabbits. 3 Cardiac output (GO) was reduced more (P<0.01) by NO inhibition in NP than P rabbits. Therefore, despi te the smaller increase in TPR, the elevation of MAP was greater (P<0. 001) in P than NP rabbits. After L-NAME, NP rabbits developed more sev ere bradycardia and a greater increase of pulmonary vascular resistanc e which might have contributed to the more pronounced reduction of CO. 4 PcGMP increased in both groups following L-NAME, but more (P<0.01) in NP than P rabbits. 5 Infusion of acetylcholine (ACh, 0.02 mu mol l( -1) kg(-1)) reduced MAP and TPR more (both P<0.05) in NP than P rabbit s and L-NAME reduced the ACh-induced depressor response only in NP rab bits. 6 These results suggest that the low vascular lone and arterial pressure in pregnant rabbits is not mediated by NO.