l citrulline/hypoxia

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Prolonged hypoxia augments L-citrulline transport by system A in the newborn piglet pulmonary circulation.

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OBJECTIVE Pulmonary arterial endothelial cells (PAECs) express the enzymes needed for generation of l-arginine from intracellular l-citrulline but do not express the enzymes needed for de novo l-citrulline synthesis. Hence, l-citrulline levels in PAECs are dependent on l-citrulline transport. Once

L-Citrulline ameliorates chronic hypoxia-induced pulmonary hypertension in newborn piglets.

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Newborn piglets develop pulmonary hypertension and have diminished pulmonary vascular nitric oxide (NO) production when exposed to chronic hypoxia. NO is produced by endothelial NO synthase (eNOS) in the pulmonary vascular endothelium using l-arginine as a substrate and producing l-citrulline as a

Combined L-citrulline and tetrahydrobiopterin therapy improves NO signaling and ameliorates chronic hypoxia-induced pulmonary hypertension in newborn pigs.

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Newborn pigs with chronic hypoxia-induced pulmonary hypertension (PH) have evidence of eNOS uncoupling. In this model, we showed that therapies that promote eNOS coupling, either tetrahydrobiopterin (BH₄), a NOS co-factor, or L-citrulline, a NO-L-arginine precursor, inhibit PH. We wanted

Rescue Treatment with L-Citrulline Inhibits Hypoxia-Induced Pulmonary Hypertension in Newborn Pigs.

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Infants with cardiopulmonary disorders associated with hypoxia develop pulmonary hypertension. We previously showed that initiation of oral L-citrulline before and continued throughout hypoxic exposure improves nitric oxide (NO) production and ameliorates pulmonary hypertension in newborn piglets.

Hypoxia inhibits L-arginine synthesis from L-citrulline in porcine pulmonary artery endothelial cells.

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Both non-arginine-depleted and arginine-depleted pulmonary artery endothelial cells (PAEC) actively convert citrulline into arginine. Exposure to hypoxia for 4-24 h inhibited arginine synthesis from citrulline in intact cells and in cell homogenates. The conversion of L-citrulline to

L-Citrulline, but not L-arginine, prevents diabetes mellitus-induced glomerular hyperfiltration and proteinuria in rat.

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Diabetes mellitus–induced oxidative stress causes increased renal oxygen consumption and intrarenal tissue hypoxia. Nitric oxide is an important determinant of renal oxygen consumption and electrolyte transport efficiency. The present study investigates whether l-arginine or l-citrulline to promote

Chronic hypoxia inhibits contraction of fetal arteries by increased endothelium-derived nitric oxide and prostaglandin synthesis.

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OBJECTIVE Chronic hypoxia causes redistribution of fetal cardiac output by mechanisms poorly understood. We tested the hypothesis that chronic hypoxia alters vascular reactivity of arteries from near-term fetal guinea pigs. METHODS Pregnant guinea pigs (50 days, term = 65 days) were exposed to

L-citrulline treatment alters the structure of the pulmonary circulation in hypoxic newborn pigs

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Background: Dysregulated nitric oxide (NO) signaling contributes to chronic hypoxia (CH)-induced pulmonary hypertension (PH). NO signaling is improved and pulmonary vascular resistance (PVR) is reduced in CH piglets treated with the

Regulation of cerebellar nitric oxide production in response to prolonged in vivo hypoxia.

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The aim of this study was to assess the influence of prolonged in vivo hypoxia on cerebellar nitric oxide (NO) production. Conscious rats were exposed to 10% O2 (balanced N2) for 12 or 48 hr (arterial PO2 between 35 and 39 mmHg). The animals were then killed, and the cerebella were quickly frozen.

Nitric oxide as a retrograde messenger in the nucleus tractus solitarii of rats during hypoxia.

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1. We examined the role of nitric oxide (NO) in respiratory regulation in the nucleus tractus solitarii (NTS), where L-glutamate release associated with peripheral chemoreceptor activation modulates the hypoxic ventilatory response. 2. Experiments were performed in unanaesthetized freely moving

Sodium-coupled neutral amino acid transporter 1 (SNAT1) modulates L-citrulline transport and nitric oxide (NO) signaling in piglet pulmonary arterial endothelial cells.

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BACKGROUND There is evidence that impairments in nitric oxide (NO) signaling contribute to chronic hypoxia-induced pulmonary hypertension. The L-arginine-NO precursor, L-citrulline, has been shown to ameliorate pulmonary hypertension. Sodium-coupled neutral amino acid transporters (SNATs) are

Decreased synthesis and vasodilation to nitric oxide in piglets with hypoxia-induced pulmonary hypertension.

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Nitric oxide (NO) is thought to play an important role in the regulation of neonatal pulmonary vasculature. It has been suggested that neonates with pulmonary hypertension have a defective NO pathway. Therefore, we measured in 1-day-old piglets exposed to hypoxia (fraction of inspired O(2) = 0.10)

Hypoxia inhibits the induction of argininosuccinate synthetase by endotoxin in lung endothelial cells.

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Pulmonary artery endothelial cells (PAEC) possess a two-step pathway for synthesizing L-arginine from L-citrulline. The first and rate-limiting step is catalyzed by argininosuccinate synthetase (AS). We have previously shown that hypoxia inhibits synthesis of L-arginine from L-citrulline in PAEC. In

Induction of cardiac nitric oxide synthase 2 in rats exposed to chronic hypoxia.

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Induction of nitric oxide synthase (NOS2, also designated as iNOS) in the heart is known to occur in response to various stimuli. It is not known, however, whether in vivo hypoxia leads to cardiac NOS2 induction. We thus investigated the effects of normobaric hypoxia (10% O(2)for 8, 15 and 21 days)

Post-translational modifications of eNOS augment nitric oxide availability and facilitates hypoxia adaptation in Ladakhi women.

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The lower inhaled oxygen per volume at high altitude poses an intimidating challenge for humans to survive and reproduce. Indigenous populations of the Himalayas reportedly exhibit higher microcirculatory blood flow accompanied by higher orders of magnitude of nitric oxide (NO) products in lung,

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