Efficacy of Botulinum Toxin Type-A I in the Improvement of Mandibular Motion and Muscle Sensibility in Myofascial Pain TMD Subjects: A Randomized Controlled Trial.

This study assessed the effects of botulinum toxin type A (BoNT-A) in mandibular range of motion and muscle tenderness to palpation in persistent myofascial pain (MFP) patients (ReBEC RBR-2d4vvv). Eighty consecutive female subjects with persistent MFP, were randomly divided into four groups ( = 20): three BoNT-A groups with different doses and a saline solution group (placebo control group). Treatments were injected bilaterally in the masseter and anterior temporalis muscle in a single session.

C-type natriuretic peptide-induced relaxation through cGMP-dependent protein kinase and SERCA activation is impaired in two kidney-one clip rat aorta.

Aims: Hypertension underlies endothelial dysfunction, and activation of vasorelaxation signaling with low dependence on nitric oxide (NO) represents a good alternative for vascular modulation. C-type natriuretic peptide (CNP) causes relaxation by increasing cyclic guanosine 3',5'-monophosphate (cGMP) or Gi-protein activation through its natriuretic peptide receptor-B or -C, respectively. We have hypothesized that CNP could exerts its effects and could overcome endothelial dysfunction in two kidney-one clip (2K-1C) hypertensive rat aorta.

Hypotensive effect and vascular relaxation in different arteries induced by the nitric oxide donor RuBPY.

NO donors are compounds that release NO that can be used when the endogenous NO bioavailability is impaired. The compound cis-[Ru(bpy)(py)(NO)](PF) (RuBPY) is a nitrite-ruthenium, since it has a NO in its molecule. The aim of the present study was to evaluate the effect of RuBPY on arterial pressure, as well as on the vascular relaxation of different vascular arteries in renal hypertensive (2K-1C) and normotensive (2K) rats.

Ruthenium complexes as NO donors for vascular relaxation induction.

Nitric oxide (NO) donors are substances that can release NO. Vascular relaxation induction is among the several functions of NO, and the administration of NO donors is a pharmacological alternative to treat hypertension. This review will focus on the physicochemical description of ruthenium-derived NO donor complexes that release NO via reduction and light stimulation.

Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats.

We investigated the involvement of nitric oxide (NO) and reactive oxygen species (ROS) on autonomic cardiovascular parameters, vascular reactivity, and endothelial cells isolated from aorta of monosodium glutamate (MSG) obese rats. Obesity was induced by administration of 4 mg/g body wt of MSG or equimolar saline [control (CTR)] to newborn rats. At the 60th day, the treatment was started with N(G)-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg) or 0.