Low-dose l -arginine administration increases microperfusion of hindlimb muscle without affecting blood pressure in rats

Abstract

The objective of this work was to evaluate the influence of exogenous L-arginine on the capillary blood flow of peripheral tissues of normotensive subjects. Rats were anesthetized with sodium pentobarbital, and the blood flow of femoral, dorsal, and ventral skin and gastrocnemius and soleus muscle was measured by laser Doppler flow and microsphere methods to compare the blood flow before and after the L-arginine infusion. L-Arginine lowered the mean blood pressure in a dose-dependent manner, but a statistically significant reduction in mean blood pressure was detected only at a high dose of 500 mg/kg of body weight. The significant blood flow increment was detected after the L-arginine infusion at doses of 50 and 150 mg/kg without causing hypotension. Nicardipine, a calcium channel blocker, also increased the skin blood flow, but the blood flow increment and blood pressure fall were comparable. A significant increment in microperfusion was detected in gastrocnemius, soleus muscle, and ventral skin compared with control group by the microsphere method. No adverse effects were observed during L-arginine and microsphere infusion. The present work indicates that L-arginine infusion increases muscle capillary blood flow in rats that are not performing exercise. Supplementation with L-arginine might provide additional blood flow at rest and during exercise and result in the improvement of muscle performance and exercise capacity.exercise ͉ nitric oxide N itric oxide (NO) is a widespread signaling molecule that is involved in mammalian physiological processes including the relaxation of blood vessels (1-3), immune function (4), inhibition of platelet aggregation (5, 6), and neurotransmission (7). The amino acid L-arginine is the natural precursor for the formation of NO (8), and exogenous L-arginine administration causes the relaxation of blood vessels through the action of NO (9, 10). Although NO synthase, the enzyme that produces NO from L-arginine, is theoretically saturated with its natural substrate, exogenous L-arginine administration leads to increased NO production, and this phenomenon is known as the arginine paradox (9, 10). Therefore, many investigators have been interested in the effects of supplementation with L-arginine to produce increased beneficial effects of NO, including prevention of the progression of atherosclerosis (11, 12), prevention of pulmonary artery endothelial dysfunction (13, 14), enhancement of cellular immune response of T lymphocytes (4), and amelioration of hypertension (15,16). Other studies indicate that oral supplementation of L-arginine also corrects endothelial dysfunction of chronic heart failure (17), and it increases exercise capacity in patients with precapillary pulmonary hypertension by increasing peak oxygen consumption and decreasing pulmonary arterial pressure and pulmonary vascular resistance thorough the action of NO (18).Because oxygen and carbon dioxide exchange takes place only in the capillary bed, the peripheral blood flow correlates with the rate of oxygen uptake...

The mechanism of opiorphin-induced experimental priapism in rats involves activation of the polyamine synthetic pathway

“…However, it is important to explore and evaluate new management strategies for the disorder. Arginine supplementation has been identified as improving microvascular function that is associated with several pathologies (14,17,18,24,26,34). The identification that inhibiting arginine catabolism through the use of ODC inhibitors can prevent the development of a priapic-like condition in at least one animal model identifies a new potential treatment paradigm that could be applied to patients with priapism.…”

Antioxidative defence alterations in skeletal muscle during prolonged acclimation to cold: role ofl-arginine/NO-producing pathway

“…In contrast, L-NAME, the non-selective NOSs inhibitor, postponed the cold-induced increase in MnSOD activity seen in the untreated group in the early phase to day 21 of late cold exposure and decreased CuZnSOD activity during the acclimation to cold. It was found that L-arginine enhanced exercise-induced NOSs activation and NO production, which improves aerobic capacity (Maxwell et al, 2001), mechanical and metabolic muscle capability (Maréchal and Gailly, 1999;Ohta et al, 2007) and increases glucose oxidation (Fu et al, 2005). In contrast, L-NAME, through inhibition of NOSs and a decrease in V. Petrovic and others NO availability, diminished skeletal muscle contractions, as well as glucose uptake and oxidation (Robberts et al, 1997).…”

A Slow- Compared with a Fast-Release Form of Oral Arginine Increases Its Utilization for Nitric Oxide Synthesis in Overweight Adults with Cardiometabolic Risk Factors in a Randomized Controlled Study

“…Such a hypothesis is also supported by our finding of a delayed difference in the excretion of labeled nitrate with SR compared with IR. A slow absorption rate may also limit activation of the metabolic disposal of arginine, thereby favoring its utilization in other pathways, including that of NO synthesis (6)(7)(8)(9)(10)(11).…”

“…Endothelial dysfunction that results from impaired NO synthesis and/or bioavailability is considered to be a central feature in the initiation of metabolic syndrome and atherosclerosis (1)(2)(3)(4)(5). Oral L-arginine, taken as an oral dietary supplement, is used for NO synthesis, and such supplementation can modulate NO-related physiologic functions (6)(7)(8)(9)(10)(11).…”