Changes in calcium metabolic indices during long-term treatment of patients with essential hypertension

1988 ◽  
Vol 75 (5) ◽  
pp. 543-549 ◽  
Author(s):  
Andreas Hvarfner ◽  
Reinhold Bergström ◽  
Hans Lithell ◽  
Claes Mörlin ◽  
Leif Wide ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Essential Hypertension ◽  
Parathyroid Hormone ◽  
Free Fatty Acids ◽  
Calcium Metabolism ◽  
Elevated Blood Pressure ◽  
Ionized Calcium ◽  
Elevated Blood ◽  
Metabolic Indices

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.

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
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Lipid Profile ◽  
Vascular Reactivity ◽  
Bay K 8644 ◽  
Elevated Blood Pressure ◽  
Male Rats ◽  
Elevated Blood ◽  
Lipid Abnormalities

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.

scholarly journals Role of oxidative stress in elevated blood pressure induced by high free fatty acids

2009 ◽  
Vol 32 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Hui Wang ◽  
Hongliang Li ◽  
Zhiqiang Hou ◽  
Lin Pan ◽  
Xiaoxia Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Elevated Blood Pressure ◽  
Elevated Blood

scholarly journals Elevated blood pressure: Our family’s fault? The genetics of essential hypertension

2014 ◽  
Vol 6 (5) ◽  
pp. 327 ◽  
Author(s):  
Aniket Natekar ◽  
Randi L Olds ◽  
Meghann W Lau ◽  
Kathleen Min ◽  
Karra Imoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Genetics Of Essential Hypertension

Nature of Elevated Blood Pressure in Normoalbuminuric Type I Diabetic Patients Essential Hypertension?

1993 ◽  
Vol 6 (10) ◽  
pp. 830-836 ◽  
Author(s):  
Kirsten Nørgaard ◽  
Else Rasmussen ◽  
Tonny Jensen ◽  
Jorn Giese ◽  
Bo Feldt-Rasmussen
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Elevated Blood Pressure ◽  
Diabetic Patients ◽  
Type I ◽  
Elevated Blood

Alterations of dietary calcium intake as a therapeutic modality in essential hypertension

1986 ◽  
Vol 64 (6) ◽  
pp. 803-807 ◽  
Author(s):  
Lawrence M. Resnick
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Calcium Metabolism ◽  
Calcium Supplementation ◽  
Ionized Calcium ◽  
Therapeutic Modality ◽  
Dietary Calcium Intake ◽  
Vitamin D Metabolites ◽  
Dietary Salt ◽  
Hypertensive Disease

Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin–angiotensin system and in the pathophysiology of human hypertension.

Diagnosis, assessment, and treatment of essential hypertension

2010 ◽  
pp. 3039-3057
Author(s):  
Bryan Williams ◽  
John D. Firth
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Subsequent Treatment ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Assessment And Treatment

Essential hypertension is almost invariably symptomless, and usually detected by routine screening or opportunistic measurement of blood pressure. Key questions to answer in the assessment of a person presenting with an elevated blood pressure are: (1) Do they have hypertension, i.e. is the blood pressure persistently elevated? (2) Are there any associated clinical features that might warrant further evaluation to exclude secondary causes of hypertension? (3) Are there factors that might be contributing to an elevated blood pressure, including lifestyle or dietary factors or concomitant medication? (4) Is there any associated target organ damage or comorbidity that influences the overall cardiovascular disease risk and subsequent treatment of the patient?...

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