Endothelial dysfunction in cardiovascular and endocrine-metabolic diseases: an update

The endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. Any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. Reduced endothelium-derived nitric oxide (NO) bioavailability and increased production of thromboxane A2, prostaglandin H2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. In addition, recent studies have demonstrated the role of enhanced overactivation ofβ-adrenergic receptors inducing vascular cytokine production and endothelial NO synthase (eNOS) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. However, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased NO production by eNOS. The present review focuses on the role of NO bioavailability, eNOS uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. These are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations

Role of soil carbon in the landscape functioning of the Alto São Bartolomeu watershed in the Cerrado region, Brazil

El trabajo muestra los resultados del comportamiento térmico de una vivienda social construida masivamente por el Instituto Provincial de la Vivienda (IPV), monitoreada desde el 30 de abril hasta el 05 de junio de 2008. Se localiza en la periferia norte de la capital de Catamarca y su uso es residencial. Esta conformada por porch, cocina-comedor, dormitorios y baño que totalizan una superficie de 43.04 m2. El objetivo principal es conocer el comportamiento térmico en relación a parámetros de confort. En este sentido se monitorearon y analizaron tres periodos representativos: 1) 30/04/08 al 06/05/08, 2) 18 al 24/05/08 y 3) 30/05/08 al 05/06/08. Los resultados han demostrado que cuando las condiciones de las temperaturas exteriores son más rigurosas (altas o bajas) la respuesta del diseño de su envolvente es insuficiente para alcanzar los rangos de confort térmico establecidos y como consecuencia de ello demanda mayor cantidad de energía auxiliar para su acondicionamiento.This study shows the results of the thermal behavior of a house built by the Provincial Housing Institute examined since April 30th until June 5th in the year 2008. The house is placed to the North of the Capital city of Catamarca and it is used as dwelling. It includes a porch, dining room and kitchen, bedrooms and bathroom, all comprising a 43.04m2 covered surface. The main purpose of this work is to know the thermal behavior in ralation to comfort parameters. To this end, three representative periods were observed and analysed: 1) April 30th to May 6th, 2008; 2) May 18th to May 24th, 2008; and 3) May 30th to June 5th, 2008. The results have demonstrated that, when the external weather conditions are more severe (high or low), the answer of the enveloping design is insufficient to reach the established thermal comfort ranges; as a consequence, the design demands more auxiliary power for fitting out.Asociación Argentina de Energías Renovables y Medio Ambiente (ASADES

Cardioprotective effect of ornitho-kinin in an anesthetized, open-chest chicken model of acute coronary occlusion

The generation of bradykinin (BK; Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) in blood and kallidin (Lys-BK) in tissues by the action of the kallikrein-kinin system has received little attention in non-mammalian vertebrates. In mammals, kallidin can be generated by the coronary endothelium and myocytes in response to ischemia, mediating cardioprotective events. The plasma of birds lacks two key components of the kallikrein-kinin system: the low molecular weight kininogen and a prekallikrein activator analogous to mammalian factor XII, but treatment with bovine plasma kallikrein generates ornitho-kinin [Thr6,Leu8]-BK. The possible cardioprotective effect of ornitho-kinin infusion was investigated in an anesthetized, open-chest chicken model of acute coronary occlusion. A branch of the left main coronary artery was reversibly ligated to produce ischemia followed by reperfusion, after which the degree of myocardial necrosis (infarct size as a percent of area at risk) was assessed by tetrazolium staining. The iv injection of a low dose of ornitho-kinin (4 µg/kg) reduced mean arterial pressure from 88 ± 12 to 42 ± 7 mmHg and increased heart rate from 335 ± 38 to 402 ± 45 bpm (N = 5). The size of the infarct was reduced by pretreatment with ornitho-kinin (500 µg/kg infused over a period of 5 min) from 35 ± 3 to 10 ± 2% of the area at risk. These results suggest that the physiological role of the kallikrein-kinin system is preserved in this animal model in spite of the absence of two key components, i.e., low molecular weight kininogen and factor XII