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Background and Purpose: Adenosine has been proposed to exert anti-hypertrophic effects. However, the precise regulation and the role of the different adenosine receptor subtypes in the heart and their effects on hypertrophic signalling are largely unknown. We aimed to characterize expression and function of adenosine A1 receptors following hypertrophic stimulation in vitro and in vivo.Experimental Approach: Pro-hypertrophic stimuli and adenosine A1 receptor stimulation of neonatal rat cardiomyocytes and male C57/Bl6 mice, sc. drug administration, real-time PCR, (3) [H]-leucine-incorporation assay, immunostaining, tissue staining, Western blots, gravimetric analyses and echocardiography were applied in this study.Key Results: In neonatal rat cardiomyocyte cultures, phenylephrine, but not angiotensin II or insulin-like growth factor 1 (IGF1), up-regulated adenosine A1 receptors concentration-dependently. The hypertrophic phenotype (cardiomyocyte size, sarcomeric organization, total protein synthesis, c-fos expression) mediated by phenylephrine (10 μM), but not that by angiotensinII (1 μM) or IGF1 (20 ng·mL(-1) ), was counteracted by the selective A1 receptor agonist, N6-cyclopentyladenosine. In C57/BL6 mice, continuous N6-cyclopentyladenosine infusion (2 mg·kg(-1) ·day(-1) ; 21 days) blunted phenylephrine (120 mg·kg(-1) ·day(-1) ; 21 days) induced hypertrophy (heart weight, cardiomyocyte size and fetal genes), fibrosis, MMP 2 up-regulation and generation of oxidative stress - all hallmarks of maladaptive remodelling. Concurrently, phenylephrine administration increased expression of adenosine A1 receptors.Conclusions and Implications: We have presented evidence for a negative feedback mechanism attenuating pathological myocardial hypertrophy following α1 -adrenoceptor stimulation. Our results suggest adenosine A1 receptors as potential targets for therapeutic strategies to prevent transition from compensated myocardial hypertrophy to decompensated heart failure due to chronic cardiac pressure overload. [ABSTRACT FROM AUTHOR]

Copyright of Herz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To ensure penetration results that are comparable under various experimental conditions, cone penetrometers specified by ASABE Standards have been suggested for many years. Elastic-plastic properties are typical of most agricultural materials, so the material being penetrated by a cone penetrometer may contact the penetrometer shaft, and friction on the shaft may affect the penetration force data. Development of a method for quantifying this friction force is expected to improve the accuracy of cone penetrometer data. The objectives of this study were: (1) to evaluate a method for determining friction force on the shaft of a cone penetrometer while penetrating sand and clay soils packed in a specific cylinder, (2) to verify the penetration friction component (PFC) that may significantly influence penetration resistance (PR) measurements for various densities of chopped maize, and (3) to assess the effectiveness of a proposed filter method for adjusting friction on the penetrometer shaft. With these intentions, we embedded strain gauges into an ASABE Standard small cone. The tip was free from the shaft friction, so the output of this sensor was used as a reference in this study. We found the ASABE Standard small cone suitable for a broad range of soil textures, as little PFC was observed from the sand or the clay soil samples. However, considerable friction from penetrating chopped maize was observed at three levels of packed density using the cylinder method. In this situation, with the reference of the sensor output inside the tip, a pair of coefficients (C1 = 2329, C2 = 2120) were optimized to filter the PFC out of the PR measurement. The adjusted data agreed well with those of the reference sensor (R² = 0.968; RAMSE = 6.521 N). Thus, ASABE Standard penetrometers can also be used for silage materials without mechanical modification. [ABSTRACT FROM AUTHOR]

This review article summarizes results of a number of new clinical trials and registries in the field of cardiovascular medicine. Key presentations made at the 74th annual meeting of the German Cardiac Society, held in Mannheim, Germany, in March 2008 are reported. The data were presented by leading experts in the field with relevant positions in the trials and registries. These comprehensive summaries should provide the readers with the most recent data on diagnostic and therapeutic developments in cardiovascular medicine. [ABSTRACT FROM AUTHOR]

Copyright of Der Internist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This article summarizes the results of a number of new clinical trials, registries and metaanalyses in the field of cardiovascular medicine. Key presentations made at the 73rd annual meeting of the German Cardiac Society, held in Mannheim, Germany, in April 2007 are reported. The data were presented by leading experts in the field with relevant positions in the trials, registries or metaanalyses. These comprehensive summaries should provide the readers with the most recent data on diagnostic and therapeutic developments in cardiovascular medicine. [ABSTRACT FROM AUTHOR]

Sympathetic activation is a significant predictor of a poor prognosis in heart failure. Excessive stimulation with norepinephrine produces apoptosis, tachycardia and arrhythmias thereby leading to progression of left ventricular dysfunction and worsening of outcome. β-Blockers reduce morbidity and improve cardiac function. They have been shown to improve survival (MERIT-HF, CIBIS II and US-Carvedilol Trials). A careful uptitration of dosages is achievable with a low rate of side effects. The mechanisms of β-blocker effects in heart failure are cardiac protection from β1-adrenoceptor overstimulation, antiarrhythmic effects, reduction in heart rate and positive energetic effects or a combination thereof. [ABSTRACT FROM AUTHOR]

An abstract of the article "Free Radical Release in Human Failing Myocardium Is Associated With Increased Activity of Rac1-GTPase and Can Be Inhibited by Statin Treatment," by U. Laufs and colleagues is presented.