High blood pressure. Causes, symptoms, treatments

Sulfate transport in human placental brush-border membrane vesicles.


Sildenafil alleviated pulmonary hypertension after reoxygenation with cardiopulmonary bypass. Despite increased ET-1 levels, pulmonary vascular resistance was lower with sildenafil treatment, suggesting sildenafil's effect on the pulmonary vasculature is capable of countering vasoconstriction by ET-1. Further study into the role of sildenafil in perioperative therapy and its interactions with ET-1 are warranted.

The purpose of this study was to evaluate the effects of oral Sildenafil for treatment of pulmonary hypertension secondary to congenital heart diseases.

We have recently shown that, in men with erectile dysfunction (ED), free testosterone (FT) directly correlates with penile arterial inflow. This led us to further investigate the effect(s) of androgen administration on cavernous arteries in patients failing sildenafil treatment.

We tested the hypothesis that sildenafil increases myocardial dilator reserve in humans with ischemic heart disease.

Erectile dysfunction affects more than 30 million men in The United States. Since the FDA approved the use of Sildenafil, prescription of this medication has been raising. Adverse events of Sildenafil includes: fatigue, dyspnea, and hypotension. Reported adverse cardiac events associated with the medication use include myocardial infarction, ventricular tachycardia, angina and death, raising concerns about the safety of this agent in patients with coronary artery disease. Published guidelines regarding the management of cardiac patients with erectile dysfunction suggest that Sildenafil may be hazardous in patients with ischemic heart disease. In patients using Sildenafil, myocardial infarctions have been reported to the Food and Drug Administration. Now, we report a patient with myocardial infarction after taking 100 mg of Sildenafil without sexual activity.

Myometrial and omental biopsies were taken from women participating in a randomized placebo-controlled trial using sildenafil citrate in women with preeclampsia. Vasoconstriction and endothelial-dependent relaxation of small arteries was measured utilizing wire myography.

Mean age of patients was 59.64 ± 3.84 years in group A and 60.56 ± 4.12 years in group B (p value = 0.92). Mean prostate volume and mean residual urine were comparable between both groups (p value = 0.74 and 0.42, respectively). Fifteen patients in group A (success rate: 70%) and nineteen patients in group B (success rate: 62.7%) had failed trial without catheter (TWOC) at 7th day following AUR (p value = 0.3). No significant difference was noted between both groups regarding the rate of repeated AUR at one month and three month follow-up period (p = 0.07 and p = 0.45, respectively).

To assess the effects of sildenafil on blue-on-yellow (B/Y) and white-on-white (W/W) Humphrey perimetry in a group of men with erectile dysfunction in 3 months regular use.

Experiments were performed in the rat CUMS model. CUMS rats were treated with Wuling mycelia powder (0.5, 1.0 or 2.0 g/kg, i.g.) to test behavioral changes including the sucrose preference, the crossing number and food consumption. Further, L-arginine (substrate for nitric oxide) (750 mg/kg), 7-nitroindazole (a specific neuronal nitric oxide synthase inhibitor) (25 mg/kg), sildenafil (phosphodiesterase 5 inhibitor) (5 mg/kg) and methylene blue (direct inhibitor of both nitric oxide synthase and soluble guanylate cyclase) (10 mg/kg) were treated for 60 min before each test to detect the possible mechanism of antidepressant-like effect of Wuling mycelia powder.

BOO mice had a significantly greater BC than control mice, with a mean (SD) of 153 (66) vs 58 (13) microL (P = 0.004). Treatment with sildenafil did not significantly alter BC. BOO caused an increase in Pdet compared to controls, with a mean (SD) of 25 (7) vs 12 (5) cm H2O. P(det) was not significantly different after treatment with sildenafil. The median V(DO1) as a percentage of BC was significantly lower in BOO than in control mice (20% vs 53%, P > 0.03) and increased significantly after sildenafil treatment (20% vs 44%, P = 0.04). BOO was associated with a greater bladder weight than in control mice, with a mean (SD) of 89 (32) vs 27 (6) mg (P = 0.001), which was decreased with sildenafil treatment, to 40 (14) vs 89 (32) mg (P = 0.013). BOO caused an increase in detrusor muscular hypertrophy vs control mice, with a median H&E score of 3 vs 2 (P = 0.01) and an increase in fibrosis vs control mice, with a median trichrome score of 3 vs 2 (P = 0.01). BOO + V mice had reduced muscular hypertrophy and fibrosis, with a median H&E score of 3 vs 2 (P = 0.01) and a median trichrome score of 3 vs 1 (P = 0.01).

The method was found to be linear (10-900ng/mL for SLD and NRD while 1-30μg/mL for ARG), accurate and precise (99.35±1.58, 99.62±1.13, and 100.04±1.22% for SLD, NRD and ARG; respectively) and met all other validation requirements.

Pulmonary arterial hypertension, both primary and secondary, continues to pose a therapeutic problem. In this study, we evaluate the efficacy and safety of a low-dose of oral sildenafil in 10 patients with pulmonary arterial hypertension.