Abstract
Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that ''salt-sensitive'' rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 24-33 |
| Number of pages | 10 |
| Journal | Journal of the American College of Nutrition |
| Volume | 10 |
| Issue number | 1 |
| State | Published - 1991 |
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ASJC Scopus subject areas
- Medicine (miscellaneous)
- Food Science
Cite this
Development of sugar-induced blood pressure elevation after uninephrectomy in a resistant rat strain. / El Zein, M.; Areas, J. L.; Knapka, J.; DiPette, D.; Holland, B.; Al-Karadaghi, P.; Preuss, H. G.
In: Journal of the American College of Nutrition, Vol. 10, No. 1, 1991, p. 24-33.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Development of sugar-induced blood pressure elevation after uninephrectomy in a resistant rat strain
AU - El Zein, M.
AU - Areas, J. L.
AU - Knapka, J.
AU - DiPette, D.
AU - Holland, B.
AU - Al-Karadaghi, P.
AU - Preuss, H. G.
PY - 1991
Y1 - 1991
N2 - Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that ''salt-sensitive'' rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.
AB - Certain rat strains acutely increase blood pressure (BP) when given diets high in NaCl. Prior results showed that ''salt-sensitive'' rat strains, at least the ones studied, also increase BP in response to sugar loading. To examine this relationship further and learn more about the pathogenesis of sucrose-induced BP elevations, we examined the effects of unilateral nephrectomy (uninephrectomy) on sucrose-induced BP changes. The rationale is based upon the findings that renal mass removal sensitizes BP response to salt loading. Over 15 weeks, augmented sugar (sucrose) consumption by Long-Evans (LE) rats did not increase BP markedly compared to rats consuming a diet relatively low in sugar unless uninephrectomy was performed. The differences in BP caused by the high sugar diet in a uninephrectomized rat could not be explained adequately by alterations in catecholamine excretion, plasma renin activity, excesses in blood volume, or the other parameters examined. However, salt-induced hypertension has been attributed to the presence of circulating substances affecting ion transport. Among the dietary groups, there was a significant correlation between the ability of plasma to depress PAH and TEA renal slice uptake and the difference in BP. This is consistent with the presence of a circulating factor affecting cell transport that has its greatest activity in the high sugar-uninephrectomy group of LE rats. We conclude that reducing renal mass potentiates sugar-induced BP elevation similar to salt-induced BP elevation in a normally resistant rat strain, and the rise of BP may be caused by a circulating factor.
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M3 - Article
VL - 10
SP - 24
EP - 33
JO - Journal of the American College of Nutrition
JF - Journal of the American College of Nutrition
SN - 0731-5724
IS - 1
ER -