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.

Cromatografia em camada delgada para o diagnóstico da intoxicação por aldicarb ("chumbinho") em cães e gatos / Thin-layer chromatography for aldicarb poisoning diagnosis in dogs and cats

Avaliou-se a cromatografia em camada delgada (CCD) como método de diagnóstico toxicológico para os casos de intoxicação por aldicarb em cães e gatos, utilizando-se 50 amostras de conteúdo gástrico obtidas durante a necropsia e 50 amostras de alimentos utilizados como iscas para intoxicar criminalmente os animais. Todas as amostras resultaram positivas para o aldicarb, mostrando ser a CCD uma técnica qualitativa eficiente, rápida e de baixo custo, com uso potencial na toxicologia veterinária forense

The present study concerns about the identification of aldicarb residues using thin-layer chromatography (TLC) in 50 samples of gastric content obtained from the necropsy of dogs and cats and 50 samples of foods suspected of being used as baits. All samples resulted positive for aldicarb showing that the TLC is an efficient, fast and not expensive qualitative method for the detection of aldicarb, being useful for this purpose in the forensic veterinary toxicology

Uso de Benzodiazepínicos entre Idosos residentes na comunidade: prevalencia, impacto sobre a funçäo cognitiva e sobre o sono / Benzodiazepine tratment among elderly patients in the comunity: prevalence and impact in the cognitive function and sleep

OBJETIVOS: 1) Determinar a prevalencia do uso diario e continuo de benzoadiazepínicos entre idosos residentes na comunidade.2) Identificar o impacto deste uso sobre os padröes do sono e sobre a funçäo cognitiva.MATERIAL E METODOS: de

Effect of inhibition of nitric oxide synthase on blood pressure and renal sodium handling in renal denervated rats

The role of sympathetic nerve activity in the changes in arterial blood pressure and renal function caused by the chronic administration of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, was examined in sham and bilaterally renal denervated rats. Several studies have demonstrated that sympathetic nerve activity is elevated acutely after L-NAME administration. To evaluate the role of renal nerve activity in L-NAME-induced hypertension, we compared the blood pressure response in four groups (N = 10 each) of male Wistar-Hannover rats weighing 200 to 250 g: 1) sham-operated vehicle-treated, 2) sham-operated L-NAME-treated, 3) denervated vehicle-treated, and 4) denervated L-NAME-treated rats. After renal denervation or sham surgery, one control week was followed by three weeks of oral administration of L-NAME by gavage. Arterial pressure was measured weekly in conscious rats by a tail-cuff method and renal function tests were performed in individual metabolic cages 0, 7, 14 and 21 days after the beginning of L-NAME administration. L-NAME (60 mg kg-1 day-1) progressively increased arterial pressure from 108 + or - 6.0 to 149 + or - 12 mmHg (P<0.05) in the sham-operated group by the third week of treatment which was accompanied by a fall in creatinine clearance from 336 + or - 18 to 222 + or - 59 µl min-1 100 g body weight-1 (P<0.05) and a rise in fractional urinary sodium excretion from 0.2 + or - 0.04 to 1.62 + or - 0.35 per cent (P<0.05) and in sodium post-proximal fractional excretion from 0.54 + or - 0.09 to 4.7 + or - 0.86 per cent (P<0.05). The development of hypertension was significantly delayed and attenuated in denervated L-NAME-treated rats. This was accompanied by a striking additional increase in fractional renal sodium and potassium excretion from 0.2 + or - 0.04 to 4.5 + or - 1.6 per cent and from 0.1 + or - 0.015 to 1.21 + or - 0.37 per cent, respectively, and an enhanced post-proximal sodium excretion compared to the sham-operated group. These differences occurred despite an unchanged creatinine clearance and Na+ filtered load. These results suggest that bilateral renal denervation delayed and attenuated the L-NAME-induced hypertension by promoting an additional decrease in tubule sodium reabsorption in the post-proximal segments of nephrons. Much of the hypertension caused by chronic NO synthesis inhibition is thus dependent on renal nerve activity.