Effects of high sugar diets on renal fluid, electrolyte and mineral handling in rats: relationship to blood pressure.

OBJECTIVE: We examined whether sugar-induced systolic blood pressure (SBP) elevations in rats may develop, in part, through a mechanism common to salt-induced hypertension, i.e., renal retention of water and salt. DESIGN: Spontaneously hypertensive rats (SHR) ate four diets: two high (> 50% of calories) and two low (< 12% of calories) in sugar (sucrose). SBP, various urinary parameters, and the renal angiotensin and prostaglandin systems were assessed. RESULTS: SHR consuming diets high in sugar showed significantly decreased urinary volume and excretion of electrolytes, which coincided with increasing SBP. When low sugar diets replaced high sugar diets, SBP and urinary parameters rapidly returned to baseline. SHR received captopril while consuming high sugar diets, and both SBP and urinary parameters assumed baseline values, comparable to ones seen in SHR consuming low sugar diets. A direct angiotensin II receptor antagonist (DuPont 753) did not influence SBP. However, we found decreased PGE2 excretion in SHR consuming excess sugar. CONCLUSIONS: Salt and water retention occur early during sugar-induced hypertension due to reduced renal excretion, consistent with some part in the pathogenesis. The effects of high sugar diets on SBP were not due to angiotensin II inhibition, however, decreased availability of vasodilatory prostaglandins may play a role in the renal events and sugar-induced hypertension in SHR.

Rabbit and human renotropin are not epidermal growth factor.

Sera obtained from rabbits and humans after unilateral nephrectomy (uni sera) compared with sera obtained preoperatively (control sera) significantly stimulate 3H-thymidine incorporation into the DNA of cultured renal tissue from the respective species. In contrast, rabbit liver cells in culture are not stimulated by the uni sera compared with control sera obtained from rabbits. Mouse epidermal growth factor (EGF) added to tissue cultures significantly stimulates both kidney and liver cells of rabbits and kidney cells of humans. Antiserum against EGF overcomes, at least to some extent, the enhancing effect of EGF under all circumstances, but does not influence the stimulatory ability of uni serum obtained from rabbit and human kidney cells from the respective species. In addition, the activity of EGF was not different in the presence of uni and control sera. This study corroborates the presence of renotropic activity in the sera of rabbits and humans after removal of functioning renal mass and shows that this activity is not derived from EGF, nor does it work by potentiating some aspect of the EGF system.