A pecuária de corte no Paraná – desenvolvimento, caracterização e o papel das pastagens

Esta revisão procura analisar, para o caso do estado do Paraná, Brasil, o desenvolvimento  e as características da pecuária de corte, bem como a distribuição, o papel e o potencial produtivo das pastagens. As alterações nas áreas de pastagens são discutidas. A pecuária de corte no Paraná está baseada quase que no uso  exclusivo de pastagens utilizadas sob pastejo. O clima no estado é o determinante para a ampla adaptação e a maior utilização de gramíneas que crescem nas estações da primavera e verão. As gramíneas forrageiras, além de prover alimento (pasto, feno, silagem) para a indústria bovina,  apresentam importante papel paisagístico, na manutenção da flora campestre e na conservação do solo e da vida selvagem. O potencial de produção animal de forrageiras de verão e de inverno utilizadas de modo intensivo é alto. Muitas pesquisas com pastagens devem ainda ser realizadas. O reconhecimento do papel e do potencial das pastagens é de suma importância para o desenvolvimento da pecuária de corte desse estado do Brasil

Protective effects of BAY 41-2272 (sGC stimulator) on hypertension, heart, and cardiomyocyte hypertrophy induced by chronic L-NAME treatment in rats

This Study evaluated the effects of BAY 41-2272 (BAY), a specific activator of sGC NO-independent action on changes of mean arterial blood pressure, heart and left ventricle weight indexes, cardiomyocyte hypertrophy (Vv) and fibrosis area induced by chronic N-nitro-L-arginine methyl ester (L-NAME) treatment in rats. The animals were divided into (a) control group, (b) L-NAME group, (c) L-NAME+BAY group, and (d) BAY group. Eight weeks of L-NAME treatment caused a significant increase in mean arterial blood pressure when compared with untreated rats (173 +/- 11.1 and 109 +/- 5.0 mm Hg, respectively; P < 0.01). L-NAME+BAY cotreatment abolished the L-NAME-induced hypertension (112 +/- 5.1 mm Hg; P < 0.01). Significant increases in heart and left ventricle weight indexes and in Vv were observed in the L-NAME-treated animals compared with control group, and concomitant treatment with BAY significantly attenuated this hypertrophic effect. Treatment with L-NAME presented several areas of repairing fibrosis in left ventricles, and this effect was also abolished by BAY cotreatment. Our results demonstrate that BAY 41-2272 inhibits hypertension and prevents heart abnormalities (cardiac hypertrophy and increased fibrosis areas) induced by NO synthase inhibition47339139

Pharmacokinetic profile of atenolol aspirinate

We report microwave-assisted synthetic routes, the pharmacokinetic profile along with results from ulcerogenicity and mutagenicity studies of atenolol aspirinate, and an already described derivative, in which acetyl salicylic acid (aspirin) was connected to atenolol by an ester linkage. Atenolol aspirinate was stable towards aqueous hydrolysis but rapidly hydrolyzed in plasma (t(1/2) = 7.6 min). The results showed that the rapid and complete hydrolysis generates atenolol salicylate, which assumes a conformation stabilized by two intramolecular H-bonds, avoiding its further hydrolysis to salicylic acid and atenolol

Pathophysiology of Hypertension in the Absence of Nitric Oxide/Cyclic GMP Signaling

The nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling system is a well-characterized modulator of cardiovascular function, in general, and blood pressure, in particular. The availability of mice mutant for key enzymes in the NO-cGMP signaling system facilitated the identification of interactions with other blood pressure modifying pathways (e.g. the renin-angiotensin-aldosterone system) and of gender-specific effects of impaired NO-cGMP signaling. In addition, recent genome-wide association studies identified blood pressure-modifying genetic variants in genes that modulate NO and cGMP levels. Together, these findings have advanced our understanding of how NO-cGMP signaling modulates blood pressure. In this review, we will summarize the results obtained with mice with disrupted NO-cGMP signaling and highlight the relevance of this pathway as a potential therapeutic target for the treatment of hypertension