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Moreover, NO deficiency may negatively affect the anticancer process itself.
Clinical trials with L-arginine supplementation appear to correct the NO deficiency and ameliorate pulmonary hypertension.
Prostacyclins and endothelin receptor antagonists also are able to reduce the NO deficiency state in patients with PAH [ 49].
The authors also demonstrated that a NO deficiency contributes to allergen-induced airway hyperresponsiveness after the early airway responsiveness.
In the presence of impaired NO bioavailability, the endothelium implements various physiological pathways in the attempt to compensate for NO deficiency.
The first represents direct inhibition of NO production leading to reduced vasodilatation, and the second consists in the increased proliferation of vascular medial cells mediated by NO deficiency and resulting in fixation of hypertension.
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Why is this TP-receptor mediated mechanism enhanced in NO-deficiency?
Our results indicate that activation of TP-receptors increases cerebral vasomotion and CBF oscillations in NO-deficiency.
Pharmacological inhibition of this enhanced reactivity may be beneficial to prevent vasospasm in cerebrovascular disorders associated with NO-deficiency.
The above described results indicated that weak pharmacological stimulation of TP-receptors, which induced negligible effects under physiological conditions, evoked vasomotion and CoBF oscillations in NO-deficiency.
Since NO suppresses platelet aggregation as well as vascular release of TXA2, NO-deficiency is often associated with activation of TP-receptors.
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