Chronic high-sodium diet intake after weaning lead to neurogenic hypertension in adult Wistar rats.

In this study, we investigated some mechanisms involved in sodium-dependent hypertension of rats exposed to chronic salt (NaCl) intake from weaning until adult age. Weaned male Wistar rats were placed under high (0.90% w/w, HS) or regular (0.27% w/w, Cont) sodium diets for 12 weeks. Water consumption, urine output and sodium excretion were higher in HS rats compared to control. Blood pressure (BP) was directly measured by the arterial catheter and found 13.8% higher in HS vs Cont rats. Ganglionic blockade with hexamethonium caused greater fall in the BP of HS rats (33%), and central antagonism of AT1 receptors (losartan) microinjected into the lateral ventricle reduced BP level of HS, but not of Cont group. Heart rate variability analysis revealed sympathetic prevalence on modulation of the systolic interval. HS diet did not affect creatinine clearance. Kidney histological analysis revealed no significant change in renal corpuscle structure. Sodium and potassium concentrations in CSF were found higher in HS rats despite no change in plasma concentration of these ions. Taken together, data suggest that animals exposed to chronic salt intake to a level close to that reported for human' diet since weaning lead to hypertension, which appears to rely on sodium-driven neurogenic mechanisms.

[Prognostic value of potassium and sodium levels in cerebrospinal fluid and blood in patients with coma. Study of 55 cases]. / Valor prognóstico dos teores de potássio e sódio no líquido cefalorraquiano e no sangue de doentes em coma. Estudo de 55 casos.

This is a prospective study, with 55 patients in coma, in which wasn't chosen sex, age, intensity of coma or etiology. It was measured the concentration of the potassium and the sodium in cerebrospinal fluid, (CSF) and in the serum, to find an auxiliary way to value the prognostic. It is known that the potassium in the CSF is extremely stable, and it maintains the tax without alterations, even when the potassium in CSF is rapid and intensity raised after death. Experimental studies show the potassium raised in CSF in serious damaged brain. Our results show, in patients who recovered consciousness, normal values (means 2,61 mEq/1) of potassium in CSF. The mean of values of potassium in CSF in the group of patients who had bad evolution (they died) show index estatisticaly up of normal values (2,97 mEq/1) and this shows a serious damaged brain and/or irreversible, able to affect the stability of CSF potassium. These index are present in some kind of coma or etiology, showing that raised potassium in CSF, indicates bad prognostic, in some kind of coma. With the sodium, the results show that this ion doesn't serve to this finality, because its concentrations isn't stable in CSF, and change with the blood alterations of natremia.