Experimental models of hypertension, such as spontaneously hypertensive rats (SHR), show alterations in cellular sodium transport that affects Na(+)-coupled cotransport processes and has been involved in the pathogenesis of this disease. The objective of the present study was to analyze the kinetic properties of the sodium-dependent glucose transport in the jejunum and ileum of SHR and its genetic control, Wistar-Kyoto (WKY) rats, as well as the regulation of the transporter, SGLT1. In hypertensive rats, the increased systolic blood pressure was accompanied by an enhancement of serum aldosterone levels compared with WKY rats, but no alterations were found in their body weight or serum glucose/insulin levels. The values for d-glucose maximal rate of transport (V(max)) were 42 and 60% lower, respectively, in the jejunum and ileum of SHR than those from WKY rats. On the other hand, the values for the Michaelis constant (K(m)) were similar in both animal groups, as was the diffusive component of transport (K(d)). Immunoblotting and Northern blot analysis revealed the existence of a lower abundance of SGLT1 protein and mRNA in SHR. Moreover, hypertensive rats showed a decrease in the molecular mass of SGLT1 that could not be explained in terms of different glycosylation and/or phosphorylation levels or an alternative splicing in the expression of the protein. These findings demonstrate that SGLT1 is regulated at a transcriptional level in the intestine of hypertensive rats, and suggest that this transporter might participate in the dysregulation of sodium transport observed in hypertension.

Abnormalities in carbohydrate metabolism and the insulin resistance status have been associated with hypertension. We have previously described alterations in the sodium-coupled sugar absorption in an experimental model of hypertension; in the present work, we studied the regulation of the sodium-independent, GLUT5-facilitated D-fructose intestinal transport in this pathology. Spontaneously hypertensive rats (SHR) and their normotensive, genetic control Wistar-Kyoto (WKY) rats, were used. Kinetic studies, carried out in ileal brush-border membrane vesicles (BBMVs), revealed a significant reduction (P < 0.05) in the maximal rate of transport (Vmax) for D-fructose in SHR, which, on the other hand, showed unaltered values for the Michaelis constant (Km) and the diffusion constant (Kd). Immunoblotting analysis revealed the existence of lower (P< 0.05) levels of GLUT5 in apical membranes from SHR, this reduction being similar to that of Vmax. Similarly, Northern blot studies on the abundance of GLUT5 mRNA from ileal enterocytes showed a decrease (P< 0.05) in hypertensive rats, following the same pattern mentioned above. Therefore, the impaired D-fructose intestinal absorption is another feature of SHR, and this decrease in D-fructose uptake correlates with a reduction in the abundance of the apical GLUT5 transporter, which is controlled at a transcriptional level.