Blood Pressure Responses to Sucrose Ingestion in Four Rat Strains

Preuss, Harry G.; Zein, Mohmed; Knapka, Joseph J.; MacArthy, Philip; Yousufi, Ayub K.; Gleim, Gilbert W.; Glace, Beth W.; Zukowska‐Grojec, Zofia

doi:10.1093/ajh/5.4.244

Cited by 28 publications

(11 citation statements)

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“…Consistent with this epidemiologic observation is the reduction of systolic and diastolic blood pressures clinically observed with improved metabolic control of diabetes (12). Experimentally, even in the absence of clinical diabetes, excess sucrose ingestion may elevate blood pressure in different rat strains ( 13). Our group has attempted to understand the relationship between diabetes and hypertension from a cellular point of view, proposing that hypertension, peripheral insulin resistance, and hyperinsulinemia may be different clinical manifestations of a common underlying cellular defect of mineral ion metabolism, represented at least in part by elevated cytosolic free calcium and suppressed intracellular free magnesium levels (7,14,15).…”

Section: Discussionmentioning

confidence: 99%

Glucose-induced alterations of cytosolic free calcium in cultured rat tail artery vascular smooth muscle cells.

Barbagallo¹,

Shan²,

Pang³

et al. 1995

J. Clin. Invest.

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We have previously suggested that hyperglycemia per se may contribute to diabetic hypertensive and vascular disease by altering cellular ion content. To more directly investigate the potential role of glucose in this process, we measured cytosolic free calcium in primary cultures of vascular smooth muscle cells isolated from Sprague-Dawley rat tail artery before and after incubation with 5 (basal), 10, 15, and 20 mM glucose. Glucose significantly elevated cytosolic free calcium in a dose-and time-dependent manner, from 110.0±5.4 to 124.5±9.0, 192.7±20.4, and 228.4+21.9 nM at 5, 10, 15, and 20 mM glucose concentrations, respectively. This glucose-induced cytosolic free calcium elevation was also specific, no change being observed after incubation with equivalent concentrations of L-glucose or mannitol. This glucose effect was also dependent on extracellular calcium and pH, since these calcium changes were inhibited in an acidotic or a calcium-free medium, or by the competitive calcium antagonist lanthanum.We conclude that ambient glucose concentrations within clinically observed limits may alter cellular calcium ion homeostasis in vascular smooth muscle cells. We suggest that these cellular ionic effects of hyperglycemia may underlie the predisposition to hypertension and vascular diseases among diabetic subjects and/or those with impaired glucose tolerance. (J. Clin. Invest. 1995. 95:763-767.)

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Section: Discussionmentioning

confidence: 99%

Glucose-induced alterations of cytosolic free calcium in cultured rat tail artery vascular smooth muscle cells.

Barbagallo¹,

Shan²,

Pang³

et al. 1995

J. Clin. Invest.

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“…Simple sugars such as glucose, sucrose and fructose represent carbohydrates with high-glycemic indices. Furthermore, there is abundant evidence to suggest that a high glucose, sucrose or fructose diet elevates risk of developing cardiovascular disease, including hypertension, atherosclerosis, and ischemic heart disease [8,9,10,11,12,13,14,15,16,17,18,19,20,21]. …”

Section: Introductionmentioning

confidence: 99%

Effect of Dietary Chromium on Resistance Artery Function and Nitric Oxide Signaling in the Sucrose-Fed Spontaneously Hypertensive Rat

2007

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Background: Consumption of high-glycemic index foods contributes to the development of hypertension in some patients. Likewise, in spontaneously hypertensive rats (SHR), high sucrose promotes a secondary rise in systolic blood pressure (SBP). Chromium (III) (Cr³⁺) prevents sucrose-induced hypertension, but leaves the basal hypertension that characterizes SHR intact. Methods: Since hypertension entails increased peripheral resistance, we compared effects of Cr³⁺ on resistance arteries from SHR fed low-glycemic (starch) versus high-glycemic (sucrose) index diets. Subgroups of SHR also received Cr³⁺. Structure, stiffness, and vasodilation of mesenteric resistance arteries were studied using pressurized myography. Results: Sucrose increased SBP in SHR and, exclusively in sucrose-fed SHR, Cr³⁺ reduced SBP and augmented acetylcholine or nitroprusside-dependent vasodilation. Neither sucrose nor Cr³⁺ affected artery structure or stiffness. Since Cr³⁺ enhanced vasodilation, we assessed endothelial NO synthase (eNOS), guanylate cyclase, cGMP-dependent protein kinase (PKG-1α and 1β), and PKG activity by immunoblotting. Sucrose reduced eNOS, PKG-1β, and PKG activity. Cr³⁺ prevented the effects of sucrose on NO signaling. Conclusion: In hypertension exacerbated by high-glycemic index diet, Cr³⁺ reduces SBP. The BP-lowering effect of Cr³⁺, selectively on sucrose-induced but not basal hypertension in SHR, involves at least in part, improving vasodilatory function vis-à-vis restoration of NO signaling in resistance arteries.

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“…[1][2][3][4][5] In this regard, many investigators have suggested that increased insulin levels and/or resistance may be causally related to elevated BP. 6 -7 This possibility is supported by reports correlating hyperinsulinemia with hypertension.…”

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confidence: 99%

Potential Role of Glycerol Leading to Rat Fructose Hypertension

Damiano

Rosón²,

Armando³

et al. 1999

Hypertension

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Abstract-A fructose-enriched diet promotes hypertension in rats. We thought that an enhancement of the glycolytic and/or lipid disorder (s) that raise blood pressure could be the cause. Therefore, we studied 4 groups of Sprague-Dawley rats (Ϯ200 g): (1) control rats received a standard diet and tap water; (2) the glycerol group of rats received a standard diet and 0.54 mol/L glycerol in tap water; (3) the fructose group was given a fructose-enhanced diet (chow had 55% fructose instead of dextrin) and tap water; and (4) the fructose-glycerol group was given the fructose-enhanced diet and 0.54 mol/L glycerol in drinking water. At the end of the second week, the findings were as follows. Blood pressure was 149Ϯ2 mm Hg in the fructose-glycerol group versus 129Ϯ2 (PϽ0.001), 131Ϯ2 (PϽ0.001), and 140Ϯ3 (PϽ0.005) mm Hg in the control, glycerol, and fructose groups, respectively. Insulinemia was higher in the fructose-glycerol group than the control (PϽ0.001), glycerol (PϽ0.001), and fructose groups (PϽ0.001); triglyceridemia was higher in the fructose-glycerol (PϽ0.02), fructose (PϽ0.05), and glycerol groups (PϽ0.02) than the control group. Thoracic aorta rings showed a lower ED 50 to 12,13-phorbol dibutyrate in the fructose-glycerol group than in the control (PϽ0.001), glycerol (PϽ0.002), and fructose groups (PϽ0.001). In conclusion, glycerol-fructose administration resulted in hypertriglyceridemia, hyperinsulinemia, and increased vascular sensitivity to 12,13-phorbol dibutyrate (with respect to the control group), and significantly greater expression of protein kinase C ␣ and ␤II (with respect to the glycerol group

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Blood Pressure Responses to Sucrose Ingestion in Four Rat Strains

Cited by 28 publications

References 0 publications

Glucose-induced alterations of cytosolic free calcium in cultured rat tail artery vascular smooth muscle cells.

Glucose-induced alterations of cytosolic free calcium in cultured rat tail artery vascular smooth muscle cells.

Effect of Dietary Chromium on Resistance Artery Function and Nitric Oxide Signaling in the Sucrose-Fed Spontaneously Hypertensive Rat

Potential Role of Glycerol Leading to Rat Fructose Hypertension

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