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Abstract

We studied the effects of intracerebroventricular and intraperitoneal injection and the in vitro effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, on the nitric oxide synthase activities of the cerebellum, brainstem, hypothalamus, hippocampus, and the remainder of the brain after dissections. Male rats were chronically implanted with lateral icv guide cannula. L-NAME was injected in doses of 0.2, 1, and 5 mg intracerebroventricularly, and 50 mg/kg intraperitoneally. L-NAME induced dose-dependent suppression of NOS activities in each brain region. The threshold dose was 0.2 mg; 1 mg L-NAME completely abolished brain nitric oxide synthase activity 90 min after the injection. Brain NOS activities returned to baseline level 48 h after the injection of 5 mg L-NAME. There were significant differences between the sensitivity of various regions to L-NAME after in vivo but not in vitro administration of the enzyme inhibitor. These findings indicate that intracerebroventricular injection of L-NAME is a useful tool for inhibiting brain nitric oxide synthase activities in vivo. The differences between the sensitivity of different brain regions to L-NAME as well as the relative fast recovery of nitric oxide synthase activities must be taken into account when L-NAME is administered intracerebroventricularly to rats.

Disparate Roles of Oxidative Stress in Rostral Ventrolateral Medulla in Age-Dependent Susceptibility to Hypertension Induced by Systemic l-NAME Treatment in Rats

“…l -NAME reportedly crosses the BBB to alter NOS expression and inhibit NOS activity in brain [ 22 , 23 , 24 ]. At the end of 14-day i.p.…”

“…As such, one of the major findings of the present study is the identification of the suppressive effects of systemic l -NAME treatment on eNOS protein expression, NOS activity, and tissue NO level in RVLM of both young and adult rats. l -NAME has been reported to cross the BBB to reach brain tissues [ 22 , 23 , 24 ]. All three NOS isoforms are constitutively present in RVLM [ 51 ], and their roles in RVLM on neural control of cardiovascular functions, have been extensively reviewed in the literature [ 26 ].…”

“…l -NAME further aggravates the development of hypertension via antagonization of the anti-inflammatory, anti-platelet aggregatory, and/or anti-proliferative actions of NO [ 20 , 21 ]. In addition to its peripheral actions, l -NAME reportedly crosses the blood–brain barrier (BBB) to decrease NOS expression and inhibit NOS activity in brain [ 22 , 23 , 24 ], leading to brain-initiated hypertension. The neural mechanism(s) that underlies the pathogenesis of this form of hypertension induced by systemic l -NAME treatment is not fully understood.…”

Effect of Exogenous Nitric Oxide and Inhibitors of Nitric Oxide Synthase on the Hypothalamic Pituitary Adrenal Axis Responses to Neural Stimuli

“…The compounds and vehicle (sodium phosphate buffer 0.1  M , pH 7.4) were injected 1 h prior to exposure to photic stress. Within this period of time, NOR-3 [19], L -NAME [14, 20]and IL-1ra [21]exhibit optimal effects. In addition, we also monitored blood pressure following the administration of NOR-3, AG and L -NAME.…”

Double Paddle‐Wheel Enhanced Sodium Ion Conduction in an Antiperovskite Solid Electrolyte

“…The performance of many electrochemical systems including batteries, [1] hydrogen and solid oxide fuel cells, [2,3] and electrolytic reactors for the production of raw materials such as aluminum and chlorine [4,5] depends on the transport of specific working ions through an electrolyte. The nature of the electrolytes to be used in the electrochemical systems that will enable the burgeoning clean energy transition remains an important open question.…”