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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the present study was to attempt to correlate four calcium diets (0.02, 0.1, 0.5 and 2.5%) with changes in the development of hypertension in both spontaneously hypertensive and Wistar-Kyoto rats. Our findings confirm that an inverse relationship exists between dietary calcium content and the development of hypertension. The relationship does not rely upon altered serum ionized sodium, potassium, or calcium or parathyroid hormone levels. In addition, no consistent dietary calcium-dependent changes were noticed in cardiovascular reactivity. In contrast, anesthesia with pentobarbital completely abolished the relationship. These data support the hypothesis that dietary calcium influences autonomic tone through some, as yet, undefined processes.
Magnesium 1989
PMID:Dietary calcium and development of hypertension in spontaneously hypertensive rats. 261 20

Hypertension is a complex, heterogeneous disorder of which the exact etiology is unknown. The difficulty in ascribing an independent role to a single dietary constituent in blood pressure regulation may be due to interactions among nutrients which influence blood pressure. The effect of any one nutrient, particularly magnesium, on hypertension should be considered within the context of overall nutrition in each patient. Clinical, experimental and epidemiologic studies support the role of magnesium in hypertension, whereas a few studies negate this role. Magnesium ions are important in arterial smooth muscle contraction. Since magnesium is found mainly at the inner surface of the cell membranes, it could play a role in cell membrane permeability for sodium and calcium which is important in the etiopathogenesis of hypertension. Magnesium deficiency can predispose to increased contractility of the arteries and its excess can modulate smooth muscle contractility caused by bradykinin, angiotensin II, serotonin, prostaglandins and catecholamines. Magnesium therapy can prevent the development of resistant hypertension and arrhythmias in hypertensives with diuretic-induced hypomagnesemia. It might also reduce blood pressure at least up to 10/5 mm Hg provided adequate magnesium salts are given for an adequate period of time. In view of the still ill defined role of magnesium in hypertension, magnesium supplementation is advised only to those hypertensives who are receiving diuretics and develop resistant hypertension or who have frank magnesium deficiency. A diet rich in magnesium may be used for prevention of hypertension in predisposed communities because of the other advantages of such a diet in prevention.
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PMID:Magnesium metabolism in essential hypertension. 267 48

Alcohol use is associated with an increased prevalence of hypertension although the responsible mechanisms and hemodynamic correlates have not been well-defined. Disorders of electrolyte and water metabolism with resultant retention of sodium and water are common in alcoholics. However, although volume relates to cardiac output, and cardiac output to blood pressure, plasma volume expansion does not appear to be important in the development of the hypertension associated with chronic alcoholic use. Most available evidence suggests that the primary underlying mechanism is increased vascular resistance. Chronic alcohol administration may produce an increased accumulation of cytoplasmic calcium in vascular smooth muscle with vascular hyperreactivity, vasoconstriction, and increased peripheral resistance. Although precise mechanisms have not been elucidated, this may result from (1) a direct effect of alcohol on plasma membrane permeability, sodium transport, and Na+/Ca2+ exchange, and/or (2) impaired calcium transport due to a secondary abnormality such as magnesium depletion, which is present in alcoholics.
Magnesium 1989
PMID:Role of electrolytes in the etiology of alcohol-induced hypertension. 268 40

Many different classification systems for Ca2+ antagonists were proposed. They are mostly based on structural aspects or profiles of biological activity. 1,4-dihydropyridines, with Ca2+ channel antagonistic activity, including nifedipine and nitrendipine, are highly effective as antihypertensive agents. Although Ca2+ antagonists have multiple sites of antihypertensive action, their main mechanism of action is inhibition of Ca2+ entry into the vascular smooth muscle cells. Ca2+ channel antagonists bind to specific receptors at Ca2+ channels and stabilize the channels in a mode unavailable for opening. Their effect is enhanced by depolarization of the cell membrane. Currently used pharmacological methods for detection of Ca2+ antagonistic action of drugs include: (1) inhibition of 45Ca2(+)-uptake; (2) displacement of [3H]nitrendipine from isolated membranes, and (3) inhibition of Ca2+ current in single cells or channels. Ca2+ antagonists were reported to prevent hypertension-induced vascular changes and other vascular pathology, probably related to Ca2+ overload. Vascular lesions in Dahl salt-sensitive hypertensive rats and in spontaneously hypertensive rats were prevented by chronic administration of nifedipine or nitrendipine. Hemodynamic effects of Ca2+ antagonists are characterized by reduction in total peripheral vascular resistance, increase in cardiac output, reduction in systemic left ventricular end-diastolic, pulmonary arterial and capillary wedge pressures. Ca2+ antagonists differ in potency, duration of action and their therapeutic ratios. DHPs enhance sympathetic tone and have little or no negative dromotropic action. They are, therefore, safer in combination with beta-adrenoceptor antagonists than either verapamil or diltiazem. In comparison with other Ca2+ antagonists nitrendipine is highly potent as a vasodilator. As a negative inotropic agent, it is, however, less potent than either verapamil or nifedipine. Nitrendipine has, therefore, a better therapeutic ratio than some of the other well-known Ca2+ antagonists. Unlike older vasodilators, e.g. hydralazine and minoxidil, Ca2+ antagonists have diuretic properties which are primarily due to inhibition of tubular reabsorption of salt and water. Under certain experimental conditions, e.g. infusion of angiotensin II, DHPs can increase GFR. Nitrendipine has also renal cytoprotective activity. It protected rats from aminoglycoside-induced nephrotoxicity and antagonized proliferative glomerular changes in nephritic rats.(ABSTRACT TRUNCATED AT 400 WORDS)
Magnesium 1989
PMID:Pharmacological basis for use of calcium antagonists in hypertension. 269 46

The roles of sodium, potassium and magnesium in the etiology of high blood pressure are reviewed. Mechanisms of action for these cations in alterations of systemic blood pressure are discussed. A rationale for the introduction of a new Na-K-Mg salt for the prevention and treatment of hypertension in human subjects is presented. Preliminary results with this new Na-K-Mg salt are promising.
Magnesium 1989
PMID:New oral salt in treatment of high blood pressure. 269 47

Deranged magnesium concentrations in serum and cardiovascular structures have been implicated in the pathophysiology of hypertension, ischemic heart disease, arrhythmias, and sudden death. This study was conducted to determine the status and interrelation of serum and tissue concentrations of magnesium in patients with congestive heart failure, a clinical setting purportedly predisposed to the development of depleted levels of this cation. Magnesium concentrations of serum, circulating mononuclear cells, skeletal muscle, and myocardium were measured in 23 patients with heart failure on standard therapy. Two patients were hypomagnesemic (less than 1.6 meq/l). Poor or no correlations were found between serum and tissue magnesium concentrations and among the magnesium concentrations of the three tissues studied. Strong direct correlations were, however, noted between magnesium and potassium concentrations of the tissues examined. The prevalence of hypomagnesemia in this typical ambulatory heart failure population is relatively low (9%) and serum, circulating mononuclear cell, skeletal muscle, and myocardial magnesium concentrations correlate poorly with each other. Serum, circulating mononuclear cell, and skeletal muscle magnesium concentrations are thus of little predictive value in assessing the status of myocardial magnesium in humans with heart failure.
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PMID:Magnesium content of serum, circulating mononuclear cells, skeletal muscle, and myocardium in congestive heart failure. 276 10

The interaction between magnesium, calcium, sodium, potassium and blood pressure (BP) was assessed in three urban male groups (n = 463). Each group was at a different phase of urbanisation. 27% of black labourers (n = 296), 37% of city blacks (n = 94) and 14% of "coloureds' (mixed race;n = 73) were hypertensive. In the black labourers, serum Mg, K, Ca and erythrocyte Mg were inversely related to BP. Of all the cations, Mg correlated most closely with BP. In the coloured group, there was a weak inverse relationship between serum magnesium and BP. There were no biochemical abnormalities in the city blacks. During urbanisation or in the early phases of hypertension changes occur in blood cation levels. Mg and its interactions with Ca, Na and K may, in certain individuals, play an important role in the pathogenesis of hypertension.
Magnesium 1989
PMID:The relationship between magnesium, calcium, sodium, potassium and blood pressure in South African adult males. 281 77

The hormone-sensitive adenylate cyclase system of plasma membrane is composed of at least three types of proteins: hormone receptors, activatory (Gs) and inhibitory (Gi) guanine nucleotide-regulatory proteins and the catalytic unit (C). Abnormal hormonal regulations of platelet adenylate cyclase in both humans and experimental animals have been reported to occur in hypertension. However, little is known about the mechanisms for these alterations. The aim of the present study was to compare the activity of C and the inhibitory capacity of Gi in platelet membranes from spontaneously hypertensive rats (SHR) and their normotensive controls (WKY). Adenylate cyclase activity of 40,000 g membranes was assessed at pH 7.5 with 0.1 mM (alpha-32P) ATP and an appropriate bivalent cation (Mn2+ or Mg2+). Under incubation conditions that uncoupled C from Gs and Gi (25 mM MnCL2, 100 microM forskolin), a significantly lower adenylate cyclase activity was measured in membranes from SHR rats (2.07 +/- 0.12 vs 2.36 +/- 0.1 nmol cAMP/mn/mg of protein, p less than 0.05). This difference between the two strains was also observed in platelet homogenates. In a second kind of experiments, membranes were incubated with 2.1 mM MgCl2 instead of MnCl2. In both strains of rats, low concentrations of Gpp (NH)p (10 to 300 nM) inhibited adenylate cyclase activity when stimulated by 50 microM forskolin. However, the maximal extent of inhibition was significantly reduced in hypertensive rats (49.7 +/- 2.4 vs 60.5 +/- 2.3 p. 100, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anomalies of the adenylate cyclase system in platelets of the SHR rat]. 284 72

It has recently been shown that human red blood cells possess a voltage-independent calcium channel which can be influenced by in vitro modification of the membraneous cholesterol content. To determine whether there is also a link between plasma lipids and the calcium influx through this channel under in vivo conditions, the calcium influx was measured in red blood cells from 51 male donors (aged 41 +/- 5 years). The influx through the channel was defined as the nitrendipine (15 mumol/l)-inhibitable part of 45Ca2+ influx. The Ca(2+)-ejecting ATPase was inhibited by vanadate. The results demonstrate a strong inverse relationship (r = -0.81; P < 0.001) between the plasma concentration of high density lipoproteins (HDL) and 45Ca2+ influx. No significant correlation was found between 45Ca2+ influx and triglycerides, low density lipoproteins (LDL), very low density lipoproteins (VLDL), total plasma cholesterol or extracellular electrolytes (K+, Na+, Ca2+, Mg2+). The results indicate that HDL are involved in the modulation of the calcium channel and provide a link between the cellular cholesterol turnover and the calcium influx in the pathogenesis of atherosclerosis and hypertension.
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PMID:High density lipoproteins--modulators of the calcium channel? 285 25

A prospective study of 53 nulliparous teenagers was conducted to determine differences in erythrocyte and plasma magnesium concentrations between subjects who had normal full-term deliveries (normal pregnant group) and those who developed pregnancy-induced hypertension. Magnesium content of monthly blood samples was determined by atomic absorption spectrophotometry. Socioeconomic data and information on use of supplements, medicines, tobacco, and alcohol were obtained by interview and medical chart review. Erythrocyte magnesium levels in both groups remained stable during pregnancy, whereas plasma magnesium showed a slight decline (P less than .08). Plasma and erythrocyte magnesium did not differ significantly between the normal pregnant (N = 30) and pregnancy-induced hypertension (N = 12) groups. Overall, mean arterial pressure was not significantly related to plasma or erythrocyte magnesium values. Within the pregnancy-induced hypertension group, there was a slight (P less than .05) inverse relationship between mean arterial pressure and plasma magnesium. The two groups were similar for socioeconomic characteristics, gynecologic age, previous use of oral contraceptives, and use of tobacco and magnesium-containing supplements. Pregnancy-induced hypertension subjects reported more alcohol use than did normal pregnant subjects (P less than .02). In conclusion, there was no evidence of magnesium depletion among teens who developed pregnancy-induced hypertension, by measurement of erythrocyte or plasma magnesium.
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PMID:Erythrocyte and plasma magnesium during teenage pregnancy: relationship with blood pressure and pregnancy-induced hypertension. 291 22


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