Bezafibrate, an anti-hypertriglyceridemic drug, attenuates vascular hyperresponsiveness and elevated blood pressure in fructose-induced hypertensive rats

1999 ◽  
Vol 77 (10) ◽  
pp. 755-762 ◽  
Author(s):  
Xiaochen Si ◽  
R Clinton Webb ◽  
Joyce M Richey

A high fructose diet induces hypertension, hyperinsulinemia - insulin resistance, and hypertriglyceridemia (syndrome X). In this study, we investigated the role of an abnormal lipid profile in mediating fructose-induced hypertension. We hypothesized that bezafibrate, a lipid-lowering drug, would reduce elevated blood pressure and inhibit increased vascular reactivity in fructose-fed rats. Male rats were placed on four different diets: group 1 was fed standard chow (n = 6); group 2 was fed 60% fructose (n = 5); group 3 was fed fructose plus bezafibrate (30 mg·kg-1·day-1; drinking water; n = 5); and group 4 was fed standard chow plus bezafibrate (n = 6). In addition, the direct effects of very low density lipoprotein (VLDL) on vascular reactivity were examined. Bezafibrate treatment lowered blood pressure, free fatty acids, and triglycerides in the fructose-fed group, suggesting that lipid abnormalities play a role in the elevation of blood pressure in the fructose-induced hypertensive rat. Aortae from fructose-fed rats were hyperresponsive to the calcium channel agonist Bay K 8644, which was normalized with bezafibrate treatment. Incubation of aortae in a VLDL medium resulted in increased responsiveness to Bay K 8644, lending further support to lipid abnormalities altering vascular reactivity. An altered lipid profile evidenced by elevated triglycerides and free fatty acids is causally related to the development of high blood pressure and increased vascular reactivity in the fructose-induced hypertensive rat.Key words: Sprague-Dawley rats, hypertriglyceridemia, free fatty acids, vascular reactivity, aortae.

1988 ◽  
Vol 75 (5) ◽  
pp. 543-549 ◽  
Author(s):  
Andreas Hvarfner ◽  
Reinhold Bergström ◽  
Hans Lithell ◽  
Claes Mörlin ◽  
Leif Wide ◽  
...  

1. Disturbances of calcium metabolism, mimicking mild, compensated secondary hyperparathyroidism, accompany essential hypertension, but it is not known whether these alterations are primary or only secondary to the elevated blood pressure. 2. Indices of systemic calcium metabolism were followed prospectively during 6 months' treatment with either propranolol, bendroflumethiazide or verapamil in 35 patients with essential hypertension. Multivariate statistical methods were employed to study the effects of blood pressure reduction upon the metabolic indices with adjustment for the effects of the different antihypertensive agents. 3. Propranolol treatment increased the plasma ionized calcium and serum phosphate concentrations, and reduced the serum levels of parathyroid hormone, free fatty acids and glycerol. Neither the total nor the total albumin-modified serum calcium concentration was significantly affected. Thus, presumably the decrease in free fatty acids reduced the calcium complex and the calcium binding to albumin, and consequently increased the plasma ionized calcium, thereby suppressing the secretion of parathyroid hormone. 4. Bendroflumethiazide caused a reduction of the fasting renal calcium excretion to half the pretreatment level, but produced no other significant changes in the various indices of calcium metabolism. 5. During verapamil treatment, the fasting renal excretion of calcium and magnesium increased, whereas the free fatty acids and glycerol concentrations in serum were reduced. These two changes presumably balanced each other, as the plasma ionized calcium and serum parathyroid hormone concentrations were not significantly altered. 6. There were no consistent relationships between the decrease in blood pressure and the changes in the metabolic indices, either in the total sample or within any subgroup. These findings indicate that disturbances of calcium metabolism in essential hypertension are primary to, and not induced by, the elevated blood pressure per se.


2009 ◽  
Vol 32 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Hui Wang ◽  
Hongliang Li ◽  
Zhiqiang Hou ◽  
Lin Pan ◽  
Xiaoxia Shen ◽  
...  

Author(s):  
Maryam Hani Abduljalal ◽  
Nuha Abdulkadir Shareef ◽  
Sarmad Osama Alfeel

Leptin is a hormone secreted from adipose tissue, proved to be related to inflammatory, hemostatic, and metabolic factors, and thought to be involved in the development of hypertension. We aim to evaluate serum leptin levels and lipid profile in males with elevated blood pressure to be compared with healthy controls males of matched body mass index (BMI) and age. The present study were included 50 subject, 24 healthy controls males whose BMI (Mean±SD 27.6±4.9) as control group and 26 hypertensive males with essential hypertension whose BMI (Mean±SD 28.3±3.4), those two groups were aged and BMI matched Fasting serum leptin level, triglyceride (TG), total serum cholesterol, high density lipoprotein(HDL) and low density lipoprotein(LDL) were measured. Leptin was found to be significantly higher in the hypertensive males (group2) when compared with the control group (group1) (21.5±2.3ng/ml against 14.3±1.4 ng/ml, respectively; p0.03), while a very high significant difference in triglyceride, systolic and diastolic blood pressure (p 0.0001) and a significant difference in cholesterol was (p 0.01), LDL was (p0.01) and HDLwas (p0.05). The present study concluded that male patients with elevated blood pressure had significantly higher serum leptin level compared with healthy subjects of a same BMI. More over patients with hypertension had an unfavorable lipid profile.


2001 ◽  
Vol 280 (6) ◽  
pp. R1674-R1679 ◽  
Author(s):  
Milos P. Stojiljkovic ◽  
Da Zhang ◽  
Heno F. Lopes ◽  
Christine G. Lee ◽  
Theodore L. Goodfriend ◽  
...  

Evidence suggests lipid abnormalities may contribute to elevated blood pressure, increased vascular resistance, and reduced arterial compliance among insulin-resistant subjects. In a study of 11 normal volunteers undergoing 4-h-long infusions of Intralipid and heparin to raise plasma nonesterified fatty acids (NEFAs), we observed increases of blood pressure. In contrast, blood pressure did not change in these same volunteers during a 4-h infusion of saline and heparin. To better characterize the hemodynamic responses to Intralipid and heparin, another group of 21 individuals, including both lean and obese volunteers, was studied after 3 wk on a controlled diet with 180 mmol sodium/day. Two and four hours after starting the infusions, plasma NEFAs increased by 134 and 111% in those receiving Intralipid and heparin, P < 0.01, whereas plasma NEFAs did not change in the first group of normal volunteers who received saline and heparin. The hemodynamic changes in lean and obese subjects in the second study were similar, and the results were combined. The infusion of Intralipid and heparin induced a significant increase in systolic (13.5 ± 2.1 mmHg) and diastolic (8.0 ± 1.5 mmHg) blood pressure as well as heart rate (9.4 ± 1.4 beats/min). Small and large artery compliance decreased, and systemic vascular resistance rose. These data raise the possibility that lipid abnormalities associated with insulin resistance contribute to the elevated blood pressure and heart rate as well as the reduced vascular compliance observed in subjects with the cardiovascular risk factor cluster.


1991 ◽  
Vol 261 (4) ◽  
pp. R945-R949 ◽  
Author(s):  
K. E. Scrogin ◽  
D. C. Hatton ◽  
D. A. McCarron

Blood pressure increases associated with salt loading in the spontaneously hypertensive rat (SHR) are attenuated with increased dietary calcium. To assess the cardiovascular effects of these nutrients during stress, blood pressure and sympathoadrenal responses to stress were compared in salt-sensitive SHRs fed diets containing normal (0.73%) or high (8.0%) NaCl combined with either low (0.2%) or high (2.0%) calcium. NaCl-loaded rats showed increased blood pressure and exaggerated plasma epinephrine changes during restraint stress. Elevated blood pressure responses to exogenous NE were also observed with high salt intake. Supplementary calcium reduced blood pressure and attenuated the hypertensive effect of NaCl during restraint stress. Animals fed the high calcium diets had lower plasma epinephrine levels while vascular reactivity was not affected. The results indicate that increased sympathoadrenal activity and vascular reactivity contribute to elevated blood pressure and exaggerated pressor responses produced by NaCl loading in the salt-sensitive SHR. However, the hypotensive effects of dietary calcium appear to be related to sympathoadrenal activity but not vascular reactivity.


1960 ◽  
Vol XXXIV (III) ◽  
pp. 411-429 ◽  
Author(s):  
Melvin J. Fregly ◽  
Kenneth M. Cook

ABSTRACT The anti-thyroid drugs, thiouracil, propylthiouracil, and methimazole, prevented both development of elevated blood pressure and cardiac hypertrophy usually accompanying kidney encapsulation with latex envelopes. These drugs also reduced elevated blood pressure of rats with hypertension of 13 to 40 weeks' duration prior to drug administration. Addition of desiccated thyroid powder to diet containing an anti-thyroid drug overcame the anti-hypertensive effect of the latter. Withdrawal of thyroid powder only was followed by return of blood pressure to previous low level within 3 weeks. The results suggest that the anti-hypertensive effect of these drugs is related directly to the hypothyroidism produced rather than to extrathyroidal effects of the drugs. Comparison of potencies of the 3 drugs in terms of anti-hypertensive effect, inhibition of growth rate, increase in testicular size, and increase in thyroid size suggests that propylthiouracil and methimazole are equally potent per unit weight of drug. Thiouracil has approximately half the potency of the other two.


Sign in / Sign up

Export Citation Format

Share Document