Long-Term Fructose versus Corn Starch Feeding in the Spontaneously Hypertensive Rat

1995 ◽  
Vol 88 (6) ◽  
pp. 719-725 ◽  
Author(s):  
Margriet R. van der Schaaf ◽  
Jaap A. Joles ◽  
Arie van Tol ◽  
Hein A. Koomans

1. Fructose feeding, as opposed to vegetable starch feeding, has been shown to elevate blood pressure and to decrease insulin sensitivity in normotensive rats. The long-term relevance of this is unclear, and data in hypertensive strains are scarce. 2. We studied the effects of 27 weeks of a fructose-versus a corn-starch-enriched (69.5% w/w) diet in the spontaneously hypertensive rat. 3. In both dietary groups, blood pressure increased with ageing, with no apparent difference between the diets. The fructose-fed rats gained less weight. However, even selecting fructose-fed rats that matched the weight gain in the corn starch group, did not reveal a significant elevation of systolic blood pressure over time. 4. Extracellular fluid volume was comparable in fructose-fed and corn-starch-fed rats. No effects on creatinine clearance, proteinuria or renal histology were found. Fasting values of plasma triacylgycerols and cholesterol were increased mildly after 2 weeks on the fructose diet. However, fasting glucose and insulin measured after 2 weeks, and the response to an intraperitoneal glucose load, were no different. After 23 weeks of the diets, fasting values of plasma glucose, insulin, triacylglycerols and cholesterol did not differ. There were small differences in the response of plasma glucose levels to the intraperitoneal glucose load, but the area under the curve was not different. The baseline insulin resistance present in spontaneously hypertensive rats possibly blunts the metabolic response to dietary fructose. 5. After 27 weeks, the diets were switched in crossover design, and measurements were continued until 39 weeks. The fructose diet did not elevate systolic blood pressure in this follow-up experiment. 6. To summarize, long-term fructose versus corn starch feeding did not increase systolic blood pressure in spontaneously hypertensive rats. Metabolic variables were transiently affected and renal function was undisturbed. These findings suggest that long-term fructose feeding, compared with other dietary carbohydrates, is not specifically harmful in the spontaneously hypertensive rat.

Planta Medica ◽  
2020 ◽  
Vol 86 (06) ◽  
pp. 395-404 ◽  
Author(s):  
Fabiana Gomes ◽  
André M. Marques ◽  
Obadia Nathalie ◽  
Marcos Adriano Lessa ◽  
Eduardo Tibiriçá ◽  
...  

Abstract Echinodorus grandiflorus is a semiaquatic plant native to Brazil and belongs to the Alismataceae family. Infusion preparations of the leaves of this plant are often used due to its diuretic, blood pressure lowering, and anti-inflammatory properties. Our aim was to investigate the effects of chronic treatment with the crude hydroalcoholic extract of E. grandiflorus on central and peripheral microvascular changes induced in a model of hypertension and diabetes. The hemodynamic and microvascular effects of E. grandiflorus extract (50, 100, or 200 mg/kg/day for 28 days) or the isolated major diterpene from E. grandiflorus (3 to 10 mg/kg i. v.) were evaluated in spontaneously hypertensive rats using tail plethysmography and intravital fluorescence videomicroscopy, respectively, and were compared to vehicle-treated normotensive Wistar-Kyoto rats. We also investigated the protective effects of chronic treatment with E. grandiflorus (100 mg/kg/day) in brain capillary density and leukocyte-endothelium interactions on the brain vessels of DM-spontaneously (DM: diabetes mellitus) hypertensive rats. Chronically treating spontaneously hypertensive rats with increasing doses of crude hydroalcoholic E. grandiflorus extract resulted in significant dose-dependent reductions in systolic blood pressure and an anti-inflammatory effect on the brain microcirculation of DM-spontaneously hypertensive rat animals. Using laser speckle contrast imaging, we observed that intravenous administration of the major isolated clerodane diterpene metabolite (1 – 10 mg/kg) increased microvascular blood flow by 25% in spontaneously hypertensive rat skeletal muscle. The results of this study show that E. grandiflorus extracts can be useful in the prevention and reduction of microcirculatory damage in arterial hypertension and other diseases that involve microvascular dysfunction.


2000 ◽  
Vol 3 (1) ◽  
pp. 33-38 ◽  
Author(s):  
MICHAEL R. GARRETT ◽  
YASSER SAAD ◽  
HOWARD DENE ◽  
JOHN P. RAPP

Garrett, Michael R., Yasser Saad, Howard Dene, and John P. Rapp. Blood pressure QTL that differentiate Dahl salt-sensitive and spontaneously hypertensive rats. Physiol Genomics 3: 33–38, 2000.—Our purpose was to define quantitative trait loci (QTL) for blood pressure that differ between two widely used hypertensive rat strains, the Dahl salt-sensitive (S) rat and the spontaneously hypertensive rat (SHR). A genome scan was done on an F2 (S × SHR) population fed 8% NaCl for 4 wk. Three blood pressure QTL were detected, one on each of rat chromosomes (chr) 3, 8, and 9. For the chr 3 QTL the SHR allele increased blood pressure, and for chr 8 and 9 the S allele increased blood pressure. The QTL on chr 9 was exceptionally strong, having a LOD score of 7.3 and accounting for 30% of the phenotypic variance and a difference of 40 mmHg between homozygotes. A review of the literature in conjunction with the present data suggests that S and SHR are not different for the previously described prominent blood pressure QTL on chr 1, 2, 10, and 13. QTL for body weight on chr 4, 12, 18, and 20, each with an effect of about 30 g, were incidentally observed.


1982 ◽  
Vol 60 (8) ◽  
pp. 1098-1103 ◽  
Author(s):  
Heinz Rupp ◽  
Ruthard Jacob

Cardiac muscle can adapt to different functional demands, as evidenced by polymorphism of myosin. Pressure load in spontaneously hypertensive rats induced a shift of the myosin isoenzymes towards myosin V3 (18% V1, 27% V2, 55% V3) relative to normotensive Wistar rats (49% V1, 29% V2, 22% V3). A swimming routine with Wistar rats resulted in a shift towards myosin V1 (72% V1, 18% V2, 10% V3). The training effect is not restricted to normotensive rats, since spontaneously hypertensive rats subjected to the same swimming routine exhibited a myosin isoenzyme pattern (38% V1, 31% V2, 31% V3) approaching that of the sedentary Wistar rats. Swimming training can, therefore, prevent the myosin isoenzyme redistribution towards myosin V3 found in sedentary spontaneously hypertensive rats. Furthermore, systolic blood pressure was significantly reduced (130 ± 8 mmHg (1 mmHg = 133.322 Pa)) in the swim-trained compared with the sedentary spontaneously hypertensive rats (157 ± 12 mmHg). The training-induced changes in myosin polymorphism and systolic blood pressure are, at least partially, attributed to substantially normalized sympathetic activity. The functional relevance of swimming training in the spontaneously hypertensive rat is seen in the increased potential of coping with situations requiring fast contraction which may occur during sudden physical exertion or emotional stress.


1980 ◽  
Vol 59 (s6) ◽  
pp. 79s-82s ◽  
Author(s):  
J. S. Hutchinson ◽  
A. E. Doyle

1. Neurosecretion of peptides from superfused neurohypophyses in vitro was inhibited by dopamine. 2. This inhibition was dose-dependent. 3. Intravenous injection of the dopamine agonist, bromocriptine, lowered blood pressure in spontaneously hypertensive rats within 15 min. 4. Saralasin or captopril also lowered blood pressure of spontaneously hypertensive rats, but progressively over a period of 3 h. 5. The results suggest that dopamine and angiotensin have opposite effects on the neurosecretion of vasopressin. 6. Vasopressin appears to be involved in maintenance of blood pressure in the spontaneously hypertensive rat but is apparently not the only factor.


1994 ◽  
Vol 267 (4) ◽  
pp. H1250-H1253 ◽  
Author(s):  
S. Verma ◽  
S. Bhanot ◽  
J. H. McNeill

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.


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