One such strategy involves the development of combined (partial) 5-HT1A agonists and D-2 receptor (partial) selleck compound antagonists such as bifeprunox, SLV313, F15063 and SSR-181507 in an attempt to increase therapeutic efficacy of all symptom domains whilst alleviating adverse side effects. Other novel drugs including SLV310 and SLV314 combine selective serotonin reuptake inhibition (SSRI) functionality with D-2 receptor antagonism in an attempt to not only improve schizophrenic
symptoms, but to also relieve other affective disorders intricately linked with the disorder. The main scope of this review will evaluate the major preclinical and clinical pharmacological findings concerning the aforementioned strategies and pharmacological agents, and compare their therapeutic potential with currently available antipsychotics; however, recent developments at other emerging serotonergic targets such as 5-HT2C, 5-HT6, and 5-HT7 receptors will also be considered. (C) 2008 Elsevier Ltd. All rights reserved”
“Resistance
to the anabolic action of growth hormone may contribute to the loss of strength and click here muscle mass in adult patients with chronic kidney disease. We tested this hypothesis by infusing growth hormone in patients to levels necessary to saturate hormone receptors. This led to a significant decrease of plasma potassium and amino acid levels in control and hyperkalemic patients with chronic kidney disease. These effects were completely or partially blunted in patients with elevated C-reactive protein levels. In forearm perfusion studies, growth hormone caused a further decrease in the negative potassium and protein balance of hemodialysis patients without inflammation but no effect was seen in patients with inflammation. Only IL-6 levels and age were found to be independent correlates in these growth hormone-induced variations
in plasma potassium and blood amino acids. This shows that although a resistance to pharmacologic doses of growth hormone is not a general feature of patients with chronic kidney disease, there is a subgroup characterized by blunted growth hormone action. Our results support the hypothesis that uremia with inflammation, but not uremia per se, MDV3100 inhibits downstream growth hormone signaling contributing to muscle atrophy.”
“Previously, cardioexcitation by serotonin (5-hydroxytryptamine, 5-HT) was believed to be confined to atria in mammals including man, and mediated through 5-HT(4) receptors in pig and man, but 5-HT(2A) receptors in rat. Recent studies, reviewed here, demonstrate that functional 5-HT(4) receptors can be revealed in porcine and human ventricular myocardium during phosphodiesterase inhibition, and that 5-HT(4) receptor mRNA is increased in human heart failure.