Plasma Volume and Arterial Stiffness in the Cardiac Alterations Associated With Long-Term High Sodium Feeding in Rats

International audienceBACKGROUND: Rats fed an early and long-term high-salt diet (HS, NaCl 8%) developed significant cardiovascular hypertrophy without major changes in blood pressure. The mechanism of this cardiac hypertrophy has not been yet elucidated. METHODS: In the present work, we assessed the influence of volume overload and arterial stiffness on the structural and functional cardiac changes induced by a high salt feeding from weaning to 5 months of age in Sprague-Dawley rats. RESULTS: Cardiac hypertrophy in HS rats was associated with clear augmentation in the size of left ventricular (LV) cardiomyocyte as compared with rats fed regular diet (NS). Echocardiography revealed a marked increase in relative wall thickness. Of note, no alteration of global and regional systolic and diastolic function was detected in HS rats. High sodium consumption was associated with a slight increase in aortic mean and pulse pressure (PP) without effect on pulse wave velocity (PWV) and elastic modulus. Plasma volume and central venous pressure were higher in HS than NS rats. Whereas plasma endothelin level was twofold higher in HS than in NS rats, LV endothelin level was similar in both groups. Treatment by the endothelin receptors blocker bosentan had no detectable effect on the changes induced by HS diet. CONCLUSIONS: High sodium intake was associated with concentric cardiac hypertrophy without change of systolic and diastolic function. Aortic rigidity was not a determinant of cardiac hypertrophy. Beside a likely direct effect of sodium on cardiovascular system the slight increase in arterial pressure and plasma volume play a role

Effects of melatonin on rat pial arteriolar diameter in vivo

1. Based on our finding that melatonin decreased the lower limit of cerebral blood flow autoregulation in rat, we previously suggested that melatonin constricts cerebral arterioles. The goal of this study was to demonstrate this vasoconstrictor action and investigate the mechanisms involved. 2. The effects of cumulative doses of melatonin (10(−10) to 10(−6) M) were examined in cerebral arterioles (30–50 μM) of male Wistar rats using an open skull preparation. Cerebral arterioles were exposed to two doses of melatonin (3×10(−9) and 3×10(−8) M) in the absence and presence of the mt(1) and/or MT(2) receptor antagonist, luzindole (2×10(−6) M) and the Ca(2+)-activated K(+) (BK(Ca)) channel blocker, tetraethylammonium (TEA(+), 10(−4) M). The effect of L-nitro arginine methyl ester (L-NAME, 10(−8) M) was examined on arterioles after TEA(+) superfusion. Cerebral arterioles were also exposed to the BK(Ca) activator, NS1619 (10(−5) M), and to sodium nitroprusside (SNP, 10(−8) M) in the absence and presence of melatonin (3×10(−8) M). 3. Melatonin induced a dose-dependent constriction with an EC(50) of 3.0±0.1 nM and a maximal constriction of −15±1%. Luzindole abolished melatonin-induced vasoconstriction. TEA(+) induced significant vasoconstriction (−10±2%). No additional vasoconstriction was observed when melatonin was added to the aCSF in presence of TEA(+), whereas L-NAME still induced vasoconstriction (−10±1%). NS1619 induced vasodilatation (+11±1%) which was 50% less in presence of melatonin. Vasodilatation induced by SNP (+12±2%) was not diminished by melatonin. 4. Melatonin directly constricts small diameter cerebral arterioles in rats. This vasoconstrictor effect is mediated by inhibition of BK(Ca) channels following activation of mt(1) and/or MT(2) receptors