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Exercise training activates large-conductance calcium-activated K(+) channels and enhances nitric oxide production in rat mesenteric artery and thoracic aorta.

Exercise training has reversible beneficial effects on cardiovascular diseases, e.g. hypertension, which may result from a decrease in systemic vascular resistance. The purpose of this study was to investigate possible mechanisms associated with the changes in vascular reactivity in large and small arteries with vasoconstrictors and vasodilators in rats after exercise. Wistar-Kyoto rats were trained for 8 weeks (Ex group) on a treadmill and compared with sedentary counterparts (Sed group). After the measurement of blood pressure and heart rate at 8 weeks, rat mesenteric arteries and thoracic aortas were excised and prepared as rings for this study. In addition, special care was taken not to damage the endothelium of the preparations. Our results showed that exercise training for 8 weeks (1) not only prevented an increase in blood pressure but also caused a fall in heart rate, (2) attenuated the contractions induced by both prostaglandin F(2alpha) (PGF(2alpha)) and high K(+) in the mesenteric artery, but reduced the PGF(2alpha)-induced contraction in the aorta only, (3) enhanced the relaxation elicited by acetylcholine (ACh) in both mesenteric arteries and aortas, and (4) increased nitrate [an indicator of nitric oxide (NO) formation] in plasma. The enhancement of ACh-induced relaxation in the mesenteric arteries in the Ex group was suppressed by pretreatment with N(omega) -nitro-L-arginine methyl ester (L-NAME), tetraethylammonium (TEA; a nonselective inhibitor of K(+) channels) or charybdotoxin [CTX; a selective inhibitor of large-conductance calcium-activated K(+) (BK(Ca)) channels], whereas in the aorta that response was attenuated by TEA or CTX and almost completely abolished by L-NAME. However, with a combination of L-NAME plus CTX in the mesenteric artery, ACh-induced relaxation was completely abolished in the Sed group, but not in the Ex group. These results suggest that in addition to NO, activation of BK(Ca) channels in the vascular beds, at least in part, also contributes to vasodilatation in animals with exercise training.

Acetylcholine↗
PubMed2006

Efalizumab, a reversible T-cell modulator for psoriasis.

The humanized monoclonal antibody (MAb) efalizumab (Raptiva) was developed to meet a longstanding need for specific, safe, and effective anti-psoriatic treatments. Efalizumab, which is directed at the lymphocyte surface protein LFA-1, prevents multiple interactions between T cells and other cell types. Here, we review the inflammatory pathway that drives the development of psoriasis, and we discuss several mechanisms by which efalizumab suppresses skin inflammation in psoriasis. Efalizumab reversibly increases circulating T-cell counts, as T cells--including pathogenic CD8 memory T cells that are prominent in psoriatic lesions-- are specifically restrained from leaving the bloodstream and entering the skin. Within two weeks of the onset of efalizumab treatment, cell surface and intracellular LFA-1 pools are substantially cleared by lysosomal degradation. Residual surface LFA-1 molecules remain saturated with bound efalizumab for some weeks following cessation of treatment. Efalizumab's pharmacodynamic properties are consistent with its profound and reversible beneficial effects on the histopathology of psoriatic skin.

Antibodies, Monoclonal↗
PubMed2000

Exogenous apotransferrin and exchange transfusions in hereditary iron overload disease.

OBJECTIVE: To investigate whether apotransferrin administration and exchange transfusion can improve outcome in patients with the recently described recessive congenital iron overload disease, presenting with intrauterine growth retardation, severe lactic acidosis, aminoaciduria, and hemosiderosis of the liver that so far has been treatment-resistant and lethal. METHODOLOGY: Because the patients have hypotransferrinemia, hyperferritinemia, increased transferrin saturation, and bleomycin detectable iron in plasma, we designed a treatment regime aiming at decreasing free iron and iron overload. The serum transferrrin concentration was increased to adult level (2-5 g/L) by intravenous apotransferrin administrations and thereafter exchange transfusion was performed. RESULTS: Two patients were treated. In patient 1, the transferrin saturation decreased from a baseline value of 100% and remained normal after the third exchange transfusion, and in patient 2, a reversible beneficial effect was seen on transferrin saturation and bleomycin-detectable iron. However, both infants died later of the disease, at 10 and 8 weeks of age, respectively. CONCLUSIONS: Exogenous apotransferrin administration proved to be safe and might deserve evaluation in other neonatal diseases with presence of free iron in plasma.

Apoproteins↗