The underlying mechanisms for development of hypertension in the metabolic syndrome

High blood pressure is an important constituent of the metabolic syndrome. However, the underlying mechanisms for development of hypertension in the metabolic syndrome are very complicated and remain still obscure. Visceral/central obesity, insulin resistance, sympathetic overactivity, oxidative stress, endothelial dysfunction, activated renin-angiotensin system, increased inflammatory mediators, and obstructive sleep apnea have been suggested to be possible factors to develop hypertension in the metabolic syndrome. Here, we will discuss how these factors influence on development of hypertension in the metabolic syndrome

Faecalibacterium prausnitzii : from microbiology to diagnostics and prognostics

We thank Dr Xavier Aldeguer and MD David Busquets from the Hospital Dr Josep Trueta (Girona, Spain) and M.D Míriam Sabat Mir from the Hospital Santa Caterina (Salt, Spain) for their help and critical discussion concerning clinical aspects. This work was partially funded by the Spanish Ministry of Education and Science through the projects SAF2010-15896 and SAF2013-43284-P, which has been co-financed with FEDER funds. Dr Sylvia H Duncan acknowledges support from the Scottish Government Food, Land and People program.Peer reviewedPostprin

Effects of immunoglobulin G from patients with dilated cardiomyopathy on rat cardiomyocytes

This study was designed to compare the effects of purified antibodies against the β1-adrenoceptor autoantibodies and total immunoglobulin G obtained during immunoadsorption on L-type Ca2+ currents, action potentials and cell shortening, in rat ventricular myocytes. Patients with dilated cardiomyopathy frequently develop autoantibodies against β1-adrenoceptors, which can be removed by immunoadsorption. There is some controversy, however, whether the beneficial effects of this therapeutic option are due to the removal of cardiostimulatory or cardiodepressive antibodies. Therefore we studied the effects of immunoglobulin G on two of the regulators of excitation-contraction coupling and on cell shortening. Immunglobulin G was obtained during immunoadsorption therapy. Dissociated myocytes from rat hearts were electrically stimulated and cell shortening was measured by cell edge detection. Single electrode patch clamp technique in current or voltage clamp mode was used to measure L-type Ca 2+ currents or action potentials, respectively. (-)-Isoprenaline was used for comparative purposes. In comparison to (-)-isoprenaline, immunoglobulin G increased Ca2+ current to a similar extent, but prolonged the plateau duration of action potentials to a lesser extent. Immunoglobulin G and β1-adrenoceptor enhanced cell shortening to a similar degree, however, the effects were smaller than with (-)-isoprenaline. The increase in contraction amplitude was prevented by (-)-bisoprolol. We conclude that both β1-adrenoceptors and immunoglobulin G derived from patients positive for β1-adrenoceptor autoantibodies mediate the cardiostimulatory effects via β1-adrenoceptors