Increase by N^G‐nitro‐L‐arginine methyl ester (L‐NAME) of resistance to venous return in rats

Abstract

1 The effects of the nitric oxide (NO) synthase inhibitor, N0-nitro-L-arginine methyl ester (L-NAME), on mean circulatory filling pressure (MCFP), total peripheral resistance (TPR), cardiac output (CO) and resistance to venous return (Rv) were studied in rats.2 In conscious, unrestrained rats, L-NAME (0.5-16mgkg-') dose-dependently increased mean arterial pressure (MAP) but not MCFP, an inverse index of venous compliance, either in the absence or presence of the ganglionic blocker mecamylamine (10mgkg-'). 3 In pentobarbitone-anaesthetized rats, L-NAME (2, 4, 8 mg kg-') increased MAP and reduced CO in a dose-related manner but did not change MCFP. TPR (+ 84, + 140 and + 192%) as well as R, (+ 62, +72, +110%) were dose-dependently increased by L-NAME. 4 Our results show that L-NAME reduces CO by increasing arterial as well as venous resistances. L-NAME does not affect MCFP.

Inhibition of neuronal nitric oxide reduces anxiety-like responses to pair housing

“…In contrast to these results, administration of L-NAME, L-NOARG, or 7-nitroinazole (7-NI) decreases anxiety-like responses in the elevated plus-maze [9][10][11]15,35,45]. The nonselective properties of L-NAME and L-NOARG may be an important contributing factor in the disparate results that have been reported across studies, as these drugs influence both neuronal and endothelial NOS [47]. Furthermore, these drugs may increase anxiety-like responses through nonspecific changes such as vasoconstriction or reduced locomotor activity [7,35].…”

“…Although substantial variability exists in reports of the effects of NOS inhibitors on anxietylike responses, the type of NOS inhibitor may explain much of the variability in the effects of NOS inhibition on anxiety-like responses. Both L-NAME and L-NOARG may alter anxietylike behaviours though vasoconstriction or hypertension by affecting eNOS [47], whereas NOS inhibitors selective for the neuronal isoform only affect NO signaling through nNOS [3,27].…”

Services to Operate and Maintain the Microwave Research Facility at Brooks Air Force Base, San Antonio, Texas

“…L-NAME inhibits both neuronal NOS and endothelial NOS. Smaller amounts of nitric oxide, an endogenous vasodilator, resulting from inhibition of endothelial NOS causes smaller vessel diameter that leads to decreased local blood flow and increased blood pressure [Moore et al, 1991;Wang et al, 1995;Handy et al, 1996;Hu et al, 1997;Yamamoto et al, 1998]. However, the effects of L-NAME on nociception and locomotor activity seen here are most likely due to actions in the central nervous system (CNS).…”

Augmented Pulmonary Vascular and Venous Constrictions to N^G-Nitro-<i>L</i>-Arginine Methyl Ester in Rats with Monocrotaline-Induced Pulmonary Hypertension

“…L-NAME has also been shown to increase both systemic vascular resistance and venous resistance [4,5]. These results show that endogenous NO has tonic dilator influence on arterial and venous resistance vessels.…”

“…The steady-state mean arterial pressure and CVP readings, denoted as final arterial pressure (FAP) and venous plateau pressure (VPP), respectively, were used to calculate mean circulatory filling pressure (MCFP) as follows: MCFP = VPP + 1/60 (FAP -VPP), where 1/60 represents the ratio of arterial to venous compliance [5].…”