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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A primary role for the kidney in hypertension has long been recognized, but the pathogenetic interactions among renal hemodynamics, hormonal and hereditary factors, and dietary sodium intake remain ill defined. Reduction in the filtration surface area, whether acquired in the course of intrinsic renal disease or after surgical renal ablation, leads to systemic hypertension as well as to progressive renal insufficiency, sequellae made even more severe by dietary sodium excess. Moreover, hypertension and progressive renal disease occur in some individuals born with a solitary kidney, and occur almost invariably with more severe degrees of dysgenesis. Hypertension is also commonly observed in certain inbred rat strains in which the filtration surface area is congenitally deficient. Based on these and other lines of evidence reviewed herein, we postulate that a renal abnormality that contributes to essential hypertension in the general population is a reduced number of glomeruli and tubules, the consequences of which are limitations in the ability to excrete sodium and thus salt-sensitive hypertension. Furthermore, congenitally decreased filtration surface area may explain why only some, but not all, patients exposed to potentially injurious renal stimuli eventually manifest chronic nephropathy, and may also account for the susceptibility of subsets of type I and type II diabetics to develop overt glomerulopathy. Clinically, tests of renal reserve capacity may serve as a useful guide to identification of those patients at risk for the development of hypertension and progressive renal disease.
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PMID:The interrelationships among filtration surface area, blood pressure, and chronic renal disease. 138 55

To assess the relation of the two natriuretic hormones, atrial natriuretic peptide (ANP) and digitalis-like natriuretic factor (DLF), to hypertension, levels of ANP and DLF were measured under basal conditions and after salt and water loading in 31 normal subjects and 36 and 57 patients with Stage I or II essential hypertension (EH). DLF levels were higher in normal women than men; in EH-II patients, DLF levels were elevated among men but subnormal in women (P less than .02) and rose with water loading in both genders. In all groups ANP levels tended to be higher in women. Water loading increased ANP levels in EH-I patients (P less than .001) and caused less marked increases of ANP in control and EH-II women and men. ANP also tended to increase with salt loading. Both DLF and ANP were related to blood pressure in the subject groups (r = 0.75 to 0.96 and r = 0.27 to 0.75, respectively) and were also related to each other (r = 0.20 to 0.47). The role of ANP and DLF in hypertension are likely to be compensatory and directed against water-electrolyte metabolism disorders associated with elevated arterial pressure.
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PMID:Atrial and digitalis-like natriuretic hormones in essential hypertension under functional loading. 138 63

We have investigated the cellular basis for the clinical and epidemiologic linkage of hypertension, left ventricular hypertrophy (LVH), obesity, and non-insulin-dependent diabetes mellitus (NIDDM) and have studied cytosolic free calcium and free magnesium levels in these syndromes. Specifically, intracellular free calcium is elevated and free magnesium is deficient in hypertension, and both are related (directly and inversely, respectively) to the ambient level of blood pressure, to LV mass index (and thus to the degree of cardiac hypertrophy), and to the hyperinsulinemia and insulin resistance of essential hypertension. Dynamically, the ability of dietary salt loading to elevate blood pressure corresponds to its ability to elevate cytosolic free calcium and reciprocally to suppress free magnesium levels. Conversely, the ability of calcium channel blockade to reverse salt-induced hypertension is related to its ability to prevent these transmembrane ionic effects. Higher steady-state free calcium or lower free magnesium, or both, are also observed in clinical states linked to hypertension, such as obesity and NIDDM. Oral glucose loading in normal subjects itself elevates free calcium and suppresses free magnesium levels, as does hyperglycemia in vitro. These data suggest an ionic hypothesis of cardiovascular and metabolic disease, in which a generalized defect in cell ion handling is present in all tissues, resulting in higher steady-state free calcium and lower free magnesium levels. In pancreatic beta cells, this would produce hyperinsulinemia; in fat and skeletal muscle, cause peripheral insulin resistance; and in renal tissue, increase proximal sodium resorption and increase urinary calcium excretion--all features of essential hypertension. In vascular smooth muscle, high cytosolic free calcium would increase smooth muscle tone and cause vasoconstriction, and in heart muscle, independent of blood pressure, would increase contractility and predispose to LVH. Therefore, what may appear clinically to be the separate syndromes of hypertension, obesity, and NIDDM may pathophysiologically be different manifestations of the same underlying cellular defect, thus explaining their frequent clinical coexistence. Therapeutically, reversal of this excess free calcium accumulation and/or free magnesium deficit with ion-specific agents, such as calcium channel blocking drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent excess morbidity and mortality of the concurrent cardiac, vascular, and metabolic aspects of the hypertensive state.
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PMID:Cellular calcium and magnesium metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders. 138 62

The paper is concerned with evaluating the efficacy of sanitary and health measures carried out within the framework of the program of secondary prophylaxis of arterial hypertension (AH) in an open rural population in terms of changes in the information of the community about hypertension. The program included regular radio transmissions, talks and lectures pertaining to the problems of essential hypertension prevention and treatment. During 4 years, the information of the respondents about hypertensive action of table salt increased 4-fold (from 8 to 32.3%), especially among persons suffering from AH. The number of persons who referred to overweight as one of AH causes rose 6-fold (from 2.6 to 18.1%). The information did not depend on the sex, age, or the presence of hypertensive factors in the examinees. Alterations were recorded in the attitude of the examinees to AH and its treatment: the portion of those who took hypotensive drugs increased more than 2-fold (from 10.9 to 23.4%) whereas the percentage of subjects treated successfully from 6.8 to 10.1%. The data obtained attest to a high enough efficacy of sanitary and health measures in relation to AH in the rural population.
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PMID:[An increase in the knowledgeability of the population on the problem of arterial hypertension as a result of conducting a secondary prevention program in a nonorganized rural population]. 138 88

The postulate of a natriuretic factor inhibiting the sodium pump in the kidney led to the detection of increased concentrations of endogenous digitalis-like factors in blood after salt loading, in essential hypertension, in pregnancy-induced hypertension and in chronic hypervolaemia. The recent isolation of ouabain or a close isomer thereof from human plasma and the demonstration of a compound similar if not identical to digoxin in adrenals and human urine shows that mammals like non-vertebrates and toads may synthesize cardiac glycosides in their adrenals and possibly in hypothalamus. The hypothalamus also forms other compounds of unknown structure which bind to the cardiac glycoside receptor site. The differential functions of endogenously formed ouabain and of a digoxin-like substance are unclear. The detailed knowledge of the physiological role of both endogenously formed cardiac glycosides in the regulation of blood pressure has still to be worked out.
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PMID:Endogenous digitalis-like factors. 139 72

To elucidate the importance of diastolic blood pressure in the definition of salt-sensitive hypertension, we studied 54 male subjects, 36 of whom had untreated, mild essential hypertension. The subjects received a 120 mmol/d Na (as the chloride salt) diet for six days. Thereafter they received a 10 mmol/d Na diet for eight days followed by a 400 mmol/d Na diet for another 8 days. Blood pressure was measured hourly "around the clock" on the last day of each diet; the averaged systolic, diastolic and mean blood pressure values were compared. In 22 subjects diastolic blood pressure increased, when salt intake was increased from 10 to 400 mmol/d. In 18 of these 22 subjects systolic blood pressure increased as well. In 20 subjects, systolic blood pressure increased with salt loading while diastolic blood pressure decreased. In 13 subjects both systolic and diastolic blood pressure decreased with increased salt intake. We defined those subjects showing an increase in diastolic blood pressure as salt-sensitive. If mean blood pressure were used to define salt-sensitivity, 8 of our subjects would have been labeled as salt-sensitive who actually decreased their diastolic blood pressure with salt loading. We suggest that consideration of systolic and diastolic blood pressure responses gives better insight into identifying volume and resistance-related phenomena in salt-sensitive hypertension, than does the consideration of mean blood pressure alone. The definition of salt-sensitivity may require reassessment.
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PMID:Definitions and characteristics of salt-sensitivity and resistance of blood pressure: should the diagnosis depend on diastolic blood pressure? 142 17

1. The salt sensitivity index (SSI) and family history of hypertension were studied in 140 hospitalized patients with essential hypertension to clarify whether salt sensitivity of blood pressure is related to familial disposition to hypertension. 2. SSI was calculated by dividing the change of mean blood pressure by that of urinary sodium excretion when salt intake was restricted from 15 to less than 3 g/day. 3. Family history of hypertension was classified into three groups depending on the presence or absence of hypertension in the father, mother and siblings. 4. The group without a family history of hypertension showed a significantly lower SSI value than other groups. 5. In multiple regression analysis undertaken within each gender, SSI showed significant partial correlations with blood pressure and family history of hypertension in the female group (r = 0.402 and 0.265, respectively), whereas in the male group it showed a positive correlation only with blood pressure (r = 0.501). These results indicate that salt sensitivity of blood pressure is related to familial disposition to hypertension. This association was more apparent in the female than male group and its gender difference can be partially attributed to the fact that blood pressure in the female group is more sensitive to salt.
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PMID:The association between salt sensitivity of blood pressure and family history of hypertension. 144 11

The clinical linkage of hypertensive cardiovascular disease, left ventricular hypertrophy, and accelerated atherosclerosis with a spectrum of metabolic disturbances including peripheral insulin resistance, hyperinsulinemia, obesity, and frank non-insulin dependent diabetes mellitus, has been increasingly appreciated. However, the underlying biologic basis mediating this clinical association remains unclear. Nuclear magnetic resonance techniques have been used to measure various intracellular ion species in human erythrocytes and have found that common, shared intracellular abnormalities of cytosolic free calcium, free magnesium, and pH occur in each of these clinical syndromes. Specifically, essential hypertension is characterized by higher fasting free cytosolic calcium concentrations and reciprocally lower intracellular free magnesium and pH levels compared with those of normotensive control subjects. Furthermore, for all subjects, free calcium and free magnesium levels were closely related both to the left ventricular mass and to the degree of insulin resistance present. Moreover, these same intracellular ionic lesions were found in normotensive obese and/or non-insulin diabetic individuals. Last, evidence has recently been provided that the cardiovascular consequences of increased dietary sugar and salt intake may well be determined by their concurrent influence on cellular ion metabolism. These data led to a hypothesis for a central role for altered cellular ion homeostasis in mediating the clinical linkage of cardiovascular and metabolic disease. According to this ionic hypothesis, essential hypertension, non-insulin dependent diabetes, and their frequently associated features of obesity, left ventricular hypertrophy, and accelerated atherosclerosis all derive from and reflect different clinical manifestations of the same underlying cellular lesion, characterized at least in part by elevated cytosolic free calcium and suppressed free magnesium levels.
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PMID:Cellular ions in hypertension, insulin resistance, obesity, and diabetes: a unifying theme. 145 64

A risk factor is a characteristic which is associated with a greater than average probability of developing coronary disease. Raised serum cholesterol and hypertension are two such factors. Intervention studies conducted to confirm the risk factor hypothesis have shown that reduction of serum cholesterol and essential hypertension may be associated with a small decreased CHD incidence, however there were almost as many deaths due to coronary disease in the intervention groups as in the control groups. These findings suggest that our approach to risk factor intervention may be a misguided attempt which needs modification. It is possible that the major risk factors develop in an attempt of our body to adapt to environmental factors such as increased intake of salt, saturated fat and cholesterol, physical inactivity, increased intake of calories and obesity and stress. Smoking may be the result of social changes. Since the body has to modify its metabolic mechanism depending upon the factor to which it adapts, development of hyperlipidemia and hypertension may be protective mechanisms of the body which it has developed while fighting against environmental factors. Reduction of major risk factors by drug therapy may mean that we are trying to prevent the body, fighting environmental factors. Thus our approach to control of the major risk factors should be to treat the causative environmental factors or alter the lifestyle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk factors for coronary heart disease: synthesis of a new hypothesis through adaptation. 149 21

1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16-18 g/day) and after 7 days of a low salt intake (1-3 g/day). 2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+ concentration: 147.7 +/- 0.4 mmol/L vs 145.3 +/- 0.5 mmol/L; P less than 0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period. 3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt-sensitive (n = 8) and the non-salt-sensitive (n = 7) subjects, but the changes in plasma NA and PRA were smaller in the salt-sensitive subjects. 4. These results indicate that the sympathetic nervous system is less suppressed in salt-sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central nervous system.
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PMID:Sodium and noradrenaline in cerebrospinal fluid and blood in salt-sensitive and non-salt-sensitive essential hypertension. 151 70


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