Par RESUMEN Fundamento y objetivos: la automonitorización de glucemia capilar en pacientes con diabetes tipo 2 podría indicar el grado de control metabólico. Los objetivos del presente trabajo fueron evaluar en qué momento del día las glucemias capilares mostraban mejor correlación con las cifras de (r=0,44; p=0.0047) and before dinner (r=0.44; p=0.0041
Androgens exert beneficial effects on vascular function by regulating the release and function of NO, prostanoids and reactive oxygen species. Since organ culture induces phenotypic changes in endothelial cells similar to those observed in some cardiovascular diseases, the aim of this study was to analyze the preventive role of male sex hormones on the vascular damage induced by organ culture. We used aortic segments from control and orchidectomized rats incubated for 20 hours at 37ºC in serum free culture medium. In this system we studied: i) the prostanoids and H2O2 production in the culture medium; ii) the hyperpolarizing mechanisms on the responses induced by acetylcholine (Ach) and by the NO donor, sodium nitroprusside (SNP) and iii) the effect of TXA2‐mimetic U‐46619 on vasodilator responses. The results showed that organ culture: i) increased the production of prostanoids and H2O2 in aorta from both groups of rats; ii) decreased the Ach‐induced relaxation in aorta from orchidectomized rats, while increased that induced by SNP and iii) decreased the Ach‐ and SNP‐induced responses after incubation with U‐46619 only in orchidectomized rats. These findings suggest a preventive role of male sex hormones on organ culture‐induced vascular damage. Grant Funding Source: Supported by grants (to M. F.) from the Fondo de Investigaciones Sanitarias (PI0011406) and (to F. R. B.) from the Sociedad Española de Urología (2013‐14).
Sex hormones regulate vascular function through nitric oxide (NO), thromboxane A2 (TXA2), and prostaglandin E2 (PGE2) among other factors. Since NO, TXA2 and PGE2 are known to regulate the epidermal growth factor receptor (EGFR) and downstream signaling pathways, the purpose of this study was to investigate whether the loss of ovarian function alters the production of these effectors regulating the activity of the mitogen‐activated protein kinase/extracellular‐regulated kinases 1 and 2 (MAPK‐ERK1/2), an EGFR downstream pathway. For this purpose, mesenteric arteries from control and ovariectomized Sprague‐Dawley rats (6‐months old) were used to analyze: i) the release of NO, TXA2 and PGE2; ii) the vascular reactivity to acetylcholine (Ach), the NO donor sodium nitroprusside, the TXA2‐mimetic compound U‐46619, and exogenous PGE2; and iii) the activation status of MAPK(ERK1/2). Our results show that ovariectomy: i) does not change NO release while decreases its vasodilator action; ii) increases the release and vasoconstrictor action of TXA2 and PGE2; and iii) increases the basal activity of the MAPK(ERK1/2) pathway. We conclude that activation of the EGFR/MAPK axis by these effectors could contribute to increase the proliferation rate of vascular smooth muscle cells, leading to increase peripheral resistance and hypertension. Grant Funding Source: Supported by the Fondo de Investigaciones Sanitarias (PI0011406) to MF.
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