The Pharmacological Differences in Antianginal Effects of Long-Lasting Calcium Channel Blockers: Azelnidipine and Amlodipine.

The Pharmacological Differences in Antianginal Effects of Long-lasting Calcium Channel Blockers: Azelnidipine and Amlodipine.

Filed under: Depression Treatment

J Cardiovasc Pharmacol. 2013 Jan; 61(1): 63-9
Fujisawa M, Yorikane R, Matsuoka Y, Koike H, Ueno K

ABSTRACT:: We examined antianginal effects of azelnidipine and amlodipine in an arginine vasopressin-induced rat anginal model. Oral administration of azelnidipine or amlodipine produced long lasting inhibition of arginine vasopressin-induced ST-segment depression in electrocardiogram. The degrees of inhibition with azelnidipine at doses of 1 and 3 mg/kg were comparable to those with amlodipine at 3 and 10 mg/kg. Both drugs lowered mean blood pressure in a dose-related manner, whereas only azelnidipine decreased heart rate. Azelnidipine at 3 mg/kg and amlodipine at 10 mg/kg produced a similar decrease in the rate pressure product, an index for cardiac oxygen consumption. Their inhibitory effects on calcium-induced vascular contraction were compared in isolated porcine coronary arteries. Both drugs produced a slow-developing inhibition of calcium-induced contraction. Although their inhibitory effects were similar, the way the both drugs inhibited calcium-induced contraction differed with each other. After removing the drug from bathing solution, the inhibitory effects of azelnidipine were not blunted but were sustained for a long time, which indicates that azelnidipine has high vascular affinity. On the other hand, those of amlodipine were rapidly blunted. These results suggest that the mechanisms underlying antianginal effects of azelnidipine differ from those of amlodipine. The antianginal effect with azelnidipine may be accounted for by its high affinity to the coronary blood vessels and the heart rate slowing effect, both of which are not shared with amlodipine.
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Gender disparities in health and healthcare: results from the Portuguese National Health Interview Survey.

Filed under: Depression Treatment

Cad Saude Publica. 2012 Dec; 28(12): 2339-48
Perelman J, Fernandes A, Mateus C

Although women experience poorer health conditions during their lives, they live longer than men. The main explanations for this paradox suggest that women’s excess of ill-health is limited to minor illnesses and their different attitudes toward health. The authors test these assumptions by investigating disparities between men and women in health and healthcare in Portugal. Data are used from the Portuguese National Health Interview Survey 2005/2006 (N = 33,662). Multivariate regressions showed that women were more likely to report worse self-rated health, more days with disability, higher prevalence of hypertension, chronic pain, cancer, anxiety and depression, and more medical consultations. Heart disease was significantly more prevalent among men, possibly explaining part of the paradox. Women’s more frequent use of medical consultations may reflect their heightened awareness of health problems, which may protect them against early death. Gender differences in socioeconomic status explain part of the differences in health, but fail to provide a complete understanding.
HubMed – depression


CaMKII-dependent phosphorylation of GluK5 mediates plasticity of kainate receptors.

Filed under: Depression Treatment

EMBO J. 2013 Jan 4;
Carta M, Opazo P, Veran J, Athané A, Choquet D, Coussen F, Mulle C

Calmodulin-dependent kinase II (CaMKII) is key for long-term potentiation of synaptic AMPA receptors. Whether CaMKII is involved in activity-dependent plasticity of other ionotropic glutamate receptors is unknown. We show that repeated pairing of pre- and postsynaptic stimulation at hippocampal mossy fibre synapses induces long-term depression of kainate receptor (KAR)-mediated responses, which depends on Ca(2+) influx, activation of CaMKII, and on the GluK5 subunit of KARs. CaMKII phosphorylation of three residues in the C-terminal domain of GluK5 subunit markedly increases lateral mobility of KARs, possibly by decreasing the binding of GluK5 to PSD-95. CaMKII activation also promotes surface expression of KARs at extrasynaptic sites, but concomitantly decreases its synaptic content. Using a molecular replacement strategy, we demonstrate that the direct phosphorylation of GluK5 by CaMKII is necessary for KAR-LTD. We propose that CaMKII-dependent phosphorylation of GluK5 is responsible for synaptic depression by untrapping of KARs from the PSD and increased diffusion away from synaptic sites.
HubMed – depression



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