Background: In physical activity (PA) counseling, primary care physicians (PCPs) play a key role because they are in regular contact with large sections of the population and are important contact people in all health-related issues. However, little is known about their attitudes, knowledge, and perceived success, as well as about factors associated with the implementation of PA counseling. Methods: We collected data from 4074 PCPs including information on physician and practice characteristics, attitudes toward cardiovascular disease (CVD) prevention, and measures used during routine practice to prevent CVD. Here, we followed widely the established 5 A's strategy (Assess, Advise, Agree, Assist, Arrange). Results: The majority (87.2%) of PCPs rated their own level of competence in PA counseling as 'high,' while 52.3% rated their own capability to motivate patients to increase PA as 'not good.' Nine of ten PCPs routinely provided at least 1 measure of the modified 5 A's strategy, while 9.5% routinely used all 5 intervention strategies. Conclusions: The positive attitude toward PA counseling among PCPs should be supported by other stakeholders in the field of prevention and health promotion. An example would be the reimbursement of health counseling services by compulsory health insurance, which would enable PCPs to invest more time in individualized health promotion.

Background The cardiac nitric oxide and endothelin-1 (ET-1) systems are closely linked and play a critical role in cardiac physiology. The balance between both systems is often disturbed in cardiovascular diseases. To define the cardiac effect of excessive ET-1 in a status of nitric oxide deficiency, we compared left ventricular function and morphology in wild-type mice, ET-1 transgenic (ET+/+) mice, endothelial nitric oxide synthase knockout (eNOS(-/-)) mice, and ET(+/+)eNOS(-/-) mice. Methods and results eNOS(-/-) and ET(+/+)eNOS(-/-) mice developed high blood pressure compared with wild-type and ET+/+ mice. Left ventricular catheterization showed that eNOS(-/-) mice, but not ET(+/+)eNOS(-/-), developed diastolic dysfunction characterized by increased end-diastolic pressure and relaxation constant tau. To elucidate the causal molecular mechanisms driving the rescue of diastolic function in ET(+/+)eNOS(-/-) mice, the cardiac proteome was analyzed. Two-dimensional gel electrophoresis coupled to mass spectrometry offers an appropriate hypothesis-free approach. ET-1 overexpression on an eNOS(-/-) background led to an elevated abundance and change in posttranslational state of antioxidant enzymes (e. g., peroxiredoxin-6, glutathione S-transferase mu 2, and heat shock protein beta 7). In contrast to ET(+/+)eNOS(-/-) mice, eNOS(-/-) mice showed an elevated abundance of proteins responsible for sarcomere disassembly (e. g., cofilin-1 and cofilin-2). In ET(+/+)eNOS(-/-) mice, glycolysis was favored at the expense of fatty acid oxidation. Conclusion eNOS(-/-) mice developed diastolic dysfunction; this was rescued by ET-1 transgenic overexpression. This study furthermore suggests that cardiac ET-1 overexpression in case of eNOS deficiency causes specifically the regulation of proteins playing a role in oxidative stress, myocytes contractility, and energy metabolism.