The understanding of the association between salt intake and precancerous lesions may contribute to clarify the causal relation with gastric cancer. We systematically reviewed 17 articles addressing the association between dietary salt exposure and gastric intestinal metaplasia and conducted meta-analyses for quantitative synthesis (random effects model). Salt exposure was estimated assessing salted/salty food consumption, preference for salted/salty foods, use of table salt, or sodium urinary excretion. Heterogeneity was also large regarding food items evaluated, consumption categories, and data analysis. The combined odds ratio (OR) was 1.68 (95% confidence interval (CI) = 0.98-2.90; I(2) = 55.4%) for the association between salted/salty meat and intestinal metaplasia (4 studies) and the OR was 1.53 (95% CI = 0.72-3.24; I(2) = 76.8%) for salt preference. There was a positive, nonstatistically significant association between intestinal metaplasia and urinary sodium excretion. The heterogeneity of methodological options and results preclude quantitative synthesis or its proper interpretation, even if the available evidence may suggest a positive association between salt and intestinal metaplasia.

In our population of acute HF patients, admission relaxin serum levels were associated with clinical and echocardiographic markers of pulmonary hypertension, RV dysfunction, and overload, suggesting a role for circulating relaxin as a biomarker in this setting.

There is increasing evidence that ACE2/angiotensin 1 - 7/Mas receptor axis has a key role in RAS activity regulation with significant pathophysiological implications in several disease states. A therapeutic intervention at this level may open new doors and change the current approach to RAS targeting.

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As recently demonstrated, angiotensin II (Ang II) induces an increase in myocardial distensibility. Although endothelin-1 and the endocardial endothelium (EE) also modulate myocardial diastolic properties, their interaction with Ang II at this level has not yet been investigated. Increasing concentrations of Ang II (from 10(-8) to 10(-5) M) were studied in rabbit right papillary muscles in the following conditions: (1) baseline; (2) after selective removal of EE with Triton X-100; and (3) with intact EE in presence of a non-selective endothelin receptor antagonist (PD-145065), a selective endothelin type A receptor antagonist (BQ-123), an inhibitor of nitric oxide synthesis (N(G)-nitro-L-arginine (L-NA) or an inhibitor of the NAD(P)H oxidase (apocynin). At baseline, Ang II induced a concentration-dependent positive inotropic effect and an increase in passive muscle length (L) up to 1.020 +/- 0.004 L/L(max). After restoring muscle length to maximal physiological length (L(max)), passive tension decreased by 46.1 +/- 4.0%. When the EE was removed, the effect on myocardial distensibility was abolished. With intact EE in presence of PD-145065, BQ-123 or L-NA, the effects of Ang II on myocardial distensibility were attenuated, with a maximal increase in passive muscle length of 1.0087 +/- 0.0012, 1.0068 +/- 0.0022 and 1.0066 +/- 0.0020 L/L(max) and a decrease in resting tension of 22.6 +/- 3.6, 16.1 +/- 6.0 and 20.4 +/- 5.6%, respectively. In the presence of apocynin, the effect on myocardial distensibility was abolished. In conclusion, the Ang II-dependent acute increase in myocardial distensibility is abolished by the selective removal of the EE and attenuated in the presence of endothelin-1 receptor antagonists, an inhibitor of nitric oxide synthesis or an inhibitor of NAD(P)H oxidase.

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