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

This study attempts to understand the various factors involved in the pathophysiology of hypertension in black Beduins. Parameters known to differentiate US black from white hypertensives were examined. Sixty Beduin families (thirty families each of black and white, total of 205 subjects) were evaluated for environmental risk factors: a traditional nomad shepherd life-style compared with working in a city, living in tents or in western style housing and dietary habits related to cardiovascular risk factors. Blood pressure, body mass index (BMI), sodium-lithium counter transport rate and 24 hour urinary sodium excretion (UNa) were measured and the data obtained were compared between normotensives and hypertensives, within each racial group. The mean value of the BMI of the white population was greater than that of the black population while the BMI of hypertensives was greater than that of the normotensives in each of the racial groups. The mean systolic BP of black hypertensives was greater than that of the corresponding whites. There were no significant differences in UNa between the four groups. Sodium-lithium countertransport was significantly higher in the hypertensive whites compared with the normotensive population (0.46 versus 0.22 mmol Li efflux/IRBC/hr). The countertransport rate for black hypertensives was lower than that of white hypertensives (0.20 versus 0.46). Black families had lower socio-economic scores than did white families and families with a hypertensive member scored lower than did families with a normotensive history. These results demonstrate some similarities between the American and Beduin black hypertensive populations, in spite of entirely different life-styles, indicating that in these populations genetic factors, rather than environmental influences, appear to be dominant in the pathophysiology of hypertension.
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PMID:Environmental and genetic factors of hypertension in a biracial Beduin population. 159 43

The long-term roles of dietary sodium and potassium on the renal end-organ damage of hypertension were investigated in Wistar-Kyoto (WKY) and in spontaneously hypertensive (SHR) rats. Eight rats from each strain were maintained since 1 month of age on one of four dietary combinations of either low (0.4%) or high (6.0%) NaCl and low (0.51%) or high (7.6%) KCl providing sodium/potassium molar ratios of 1:1, 1:15, 15:1, and 15:15, respectively. Urinary sodium/potassium excretion ratios confirmed the proportion of salts consumed. Systolic blood pressures (SBP) were similar at 5 months of age and at the completion of the study at 9.5 months; SBP was significantly higher in SHR than in WKY rats and was not attenuated by dietary potassium supplementation of a magnitude that raised plasma potassium concentrations. Albumin excretion rate (AER) was also higher in SHR than in WKY rats (P less than 0.0001). In SHR, AER rose further with high sodium intake (P less than 0.035) but, contrary to SBP, was ameliorated by an equimolar addition of potassium (P less than 0.01). Morphologic lesions were generally absent in WKY rats and were more common in SHR as a group (P less than 0.001). In all four SHR groups, the graded histopathologic injury correlated well with measured AER but a major improvement in hypertensive renal lesions occurred largely in the KCl-supplemented, salt-loaded SHR group. These results show a disassociation between the effects of dietary monovalent cations on the level of SBP and their effect on renal injury. Sodium aggravates renal injury and potassium protects against this renal effect of sodium independent of SBP effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potassium supplementation attenuates experimental hypertensive renal injury. 160 Jan 25

Sodium (Na+)-dependent hypertension was studied in hypoxia in an effort to determine the basis for hypoxia-mediated attenuation of hypertension. Hypoxia attenuated spontaneous hypertension while Na+ increased blood pressure in SHR. A lack of interaction between the effects of hypoxia and Na+ indicated additivity of effects. As a result, hypoxia-exposed, Na(+)-supplemented SHR had similar blood pressure as did normoxic, nonsupplemented SHR although both groups had lower blood pressure than normoxic, Na(+)-supplemented SHR. Hypoxia decreased serotonin turnover (5-HIAA/5-HT) in the brain stem of SHR while supplemental Na+ had no influence on this measurement. Hypoxic exposure in DOCA-treated rats failed to prevent the development of hypertension although hypoxia decreased 5-HIAA/5-HT in the brain stem of hypoxic rats, irrespective of DOCA treatment. The finding in SHR that Na+ counteracts the protection of hypoxia could be argued to support a similar mechanism of action for hypoxia and sodium. However, the results with DOCA treatment clearly refute such an interpretation. Our findings indicate that the pressor influence of Na+ does not occur through the modulation of brain stem 5-HIAA/5-HT.
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PMID:Hypoxic attenuation of brain stem serotonin does not influence sodium-induced hypertension. 160 Jun 39

Sodium restriction by 50 to 100 mmol/day in populations with intakes averaging 150 to 180 mmol/day would likely lead to a reduction of population mean blood pressures, and less of a tendency for blood pressures to rise with age. Fewer people would require antihypertensive drug therapy, and those who did would require less drugs. The extent of any blood pressure fall would be greatest in the elderly or those with established hypertension. A corresponding reduction in stroke incidence might be anticipated, with less certain effects on coronary deaths and diseases. Other factors, such as weight control, alcohol moderation and increased physical activity, may be of greater importance in preventing hypertension in many populations, while cessation of smoking, control of obesity, increased physical fitness and reduction in dietary saturated fat consumption should probably receive the highest priority in terms of overall reduction in the risk of atheromatous cardiovascular disease. In countries such as Japan, which has a relatively high incidence of stroke and a low incidence of coronary disease, a high sodium intake assumes relatively greater importance, in conjunction with obesity and alcohol, as a risk factor for cerebrovascular disease.
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PMID:Dietary salt and risk factors for cardiovascular disease. 163 79

Over the last four decades there has been extensive research into the links between diet and coronary heart disease. The most recent literature is reviewed in this position statement. The clinical and public health aspects of the National Heart Foundation's nutrition policy are based on this review. The key points are as follows: 1. Saturated fatty acids A high intake of saturated fatty acids is strongly associated with elevated serum cholesterol and LDL-cholesterol levels and increased risk of coronary heart disease. 2. The n-6 polyunsaturated fatty acids The n-6 polyunsaturated fatty acids (principally linoleic acid) lower serum cholesterol levels when substituted for saturated fats and probably have an independent cholesterol-lowering effect. 3. The n-3 polyunsaturated fatty acids (fish oils) The n-3 polyunsaturated fatty acids reduce serum triglyceride levels, decrease the tendency to thrombosis and may further reduce coronary risk through other mechanisms. 4. Monounsaturated fatty acids Monounsaturated fatty acids reduce serum cholesterol levels when substituted for saturated fatty acids. It is not clear whether this is an independent effect or simply the result of displacement of saturates. 5. Trans fatty acids Trans fatty acids may increase serum cholesterol levels and can be reckoned to be equivalent to saturated fatty acids. 6. Total fat Total fat intake, independent of fatty acid type, is not strongly associated with coronary heart disease but may contribute to obesity. Associations between total fat intake and coronary heart disease are primarily mediated through the saturated fatty acid component. 7. Dietary cholesterol Dietary cholesterol increases serum cholesterol levels in some people and may increase risk of coronary heart disease. 8. Alcohol A high intake of alcohol increases blood pressure and serum triglyceride levels and increases mortality from cardiovascular disease. Light alcohol consumption reduces the risk of coronary heart disease. 9. Sugar The consumption of sugar is not associated with coronary heart disease. 10. Sodium and potassium High salt intake is related to hypertension especially in the subset of "salt-sensitive" people. Potassium intake may be inversely related to hypertension. 11. Overweight and obesity Abdominal obesity increases the risk of coronary heart disease probably by adversely influencing conventional risk factors. 12. Vegetarianism A high intake of plant foods reduces the risk of coronary heart disease through several mechanisms, including lowering serum cholesterol and blood pressure levels.
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PMID:Diet and coronary heart disease. The National Heart Foundation of Australia. 163 Mar 69

Sodium ions markedly decreased in vitro renal alpha 2-adrenoceptor affinity for epinephrine in Sabra hypertensive (SBH) but not in normotensive (SBN) rats. Under these conditions, affinity of alpha 1-adrenoceptor for epinephrine was unchanged in SBH and SBN rats. If these data could be confirmed in vivo, the sodium ion, by acting as an inhibitor, could modify the effect of agonists on renal alpha 2-adrenoceptors in SBH rats. Conversely, the absence of sodium regulation in SBN rats might represent a genetically mediated change responsible for the resistance to the development of salt-induced hypertension.
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PMID:Sodium regulation in the affinity of renal alpha 2-adrenoceptors for epinephrine in Sabra salt-sensitive and salt-resistant rats. 164 80

The study was undertaken to clarify the role of atrial natriuretic polypeptide (ANP) in essential hypertension (EH). Plasma levels of alpha-human ANP (alpha hANP) were measured in 13 normal subjects, 25 patients with EH, 5 patients with primary aldosteronism (PA), 3 patients with renovascular hypertension (RVH) and 3 patients with pheochromocytoma (PC). Plasma level of alpha hANP (normal: 38.1 +/- 20.5pg/ml) was high in all hypertensive subjects. Synthetic alpha hANP was intravenously administrated to these subjects as follows: first a dose of 0.01 microgram/kg/min for 30 minutes, second a dose of 0.03 microgram/kg/min for 30 minutes, and then in normal subjects and EH 0.03 microgram/kg/min with a dose of 6.5 micrograms/kg/min of metoclopramide (MC) for 30 minutes. After the infusion of 0.01 microgram/kg/min alpha hANP, arterial blood pressure was significantly depressed in EH, RVH and PA, but not in PC. Marked diuretic and natriuretic responses were observed with increase in creatinine clearance and fractional sodium excretion in EH, RVH and PA, but not in PC. Sodium clearance/lithium clearance was slightly increased after infusion of 0.03 microgram/kg/min of alpha hANP in hypertensive subjects. Plasma renin activity did not change in low and normal renin EH and PA after infusion of either dose of alpha hANP, but was suppressed after 0.03 microgram/kg/min of alpha hANP in normal subjects and high renin EH, RVH and PC. Plasma aldosterone concentration was suppressed after either dose of alpha hANP in normal subjects and in EH, RVH and PC, but not in PA. Plasma cGMP concentration and urinary cGMP excretion were decreased after either dose of alpha hANP in both normal and hypertensive subjects. Furthermore, the decrease of PAC by alpha hANP was normalized by MC in normal subjects and EH. The rise in plasma cGMP by alpha hANP was suppressed by MC in both normal subjects and EH, but no changes were observed in arterial blood pressure and natriuretic response. These results suggest that alpha hANP secretion increases with elevation of blood pressure in EH, improving increase of circulatory blood volume, and alpha hANP may play a role in elevating blood pressure in EH. Moreover, it is considered that ANP increases sodium and water excretion through its effect on both renal glomeruli and distal tubules in EH. Hypotensive and natriuretic effects of ANP in EH may be concerned with dopaminergic activity which are probably related to the production of cGMP in the vascular wall and inhibition of the excretion of aldosterone in the adrenal cortex.
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PMID:[The significance of atrial natriuretic polypeptide in the cause of essential hypertension]. 165 13

To determine the effects of age, sex, race, and family history of hypertension on cellular cation transport, we measured specific tritiated-ouabain binding (sodium/potassium pump number), and sodium/potassium pump-mediated rubidium-86 uptake in blood lymphocytes from 105 healthy normotensive adults, comprising 23 Chinese and 19 Indian subjects who had first-degree relatives with cryptogenic hypertension, and 40 Chinese and 23 Indian matched subjects without such history. Both Chinese and Indian subjects with family history had significantly fewer sodium/potassium pumps than control subjects. Sodium/potassium pump-mediated rubidium-86 uptake was similar in these four subject groups. Seven Indian patients with untreated cryptogenic hypertension had fewer sodium/potassium pumps than normotensive Indians without family history. Age did not affect sodium/potassium pump numbers in cells from normotensive subjects. In normotensive subjects without family history. Chinese women had more sodium/potassium pumps than Chinese men, but Indian subjects did not show this pattern. We conclude that a family history of cryptogenic hypertension is associated with fewer lymphocyte sodium/potassium pumps than normal. The reduction in cellular pump number might be only a marker, or an epiphenomenon. However, the reduction in pump number might contribute to the pathogenesis of cryptogenic hypertension if it produces sodium retention in renal tubular or peripheral vascular cells.
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PMID:Influence of family history of cryptogenic hypertension, age, sex and race on lymphocyte sodium/potassium pumps. 165 41

Exchangeable sodium is lower than normal in young male patients with essential hypertension. This may reflect a primary or secondary abnormality. To investigate this question, exchangeable body sodium was measured in 31 normotensive men with positive and 31 normotensive men with negative family history of essential hypertension on a normal sodium intake (150 mmol/day). Blood pressure (BP) tended to be higher in the former group (p less than 0.005) but age, urinary sodium excretion, plasma renin activity, and aldosterone levels or creatinine clearance were comparable. Exchangeable sodium averaged 100.8 +/- 7.1% in subjects with positive and 100.2 +/- 6% in those with negative family history. In both groups, exchangeable sodium was unrelated to arterial pressure. The response of exchangeable sodium to variations in dietary sodium intake was further investigated in 13 subjects with and 10 subjects without family history. The change from a low (17 mmol/day) to a high (270 mmol/day) sodium diet elevated exchangeable body sodium to a comparable extent, despite a greater increase in BP in subjects with positive family history. Sodium-dependent suppression of renin, angiotension II, aldosterone, and plasma catecholamines was comparable between the two groups. These findings suggest that body sodium is normal and adapts normally to variations in dietary sodium intake in normotensive subjects with familial predisposition to hypertension. Body sodium depletion in early hypertension appears to be a secondary rather than a primary event.
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PMID:Body sodium in normal subjects predisposed to hypertension. 170 25

This study examined whether the calcium antagonist nisoldipine can shift the relations between sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure toward lower pressures in spontaneously hypertensive rats. Mean arterial pressure decreased similarly by 9% and 12% in Wistar-Kyoto and spontaneously hypertensive rats after nisoldipine (0.5 microgram/kg bolus + 0.017 microgram/kg/min). Urine flow and sodium excretion increased by 35% and 24% in Wistar-Kyoto rats after nisoldipine. In contrast, urine flow and sodium excretion rose by 121% and 132% in spontaneously hypertensive rats, and fractional sodium excretion rose from 1.9 +/- 0.3 to 4.2 +/- 0.4%. Control sodium excretion, papillary blood flow, and renal interstitial pressure were significantly lower in spontaneously hypertensive rats than in Wistar-Kyoto rats when compared at similar renal perfusion pressures. Sodium excretion, papillary blood flow, and renal interstitial pressure all increased in spontaneously hypertensive rats after nisoldipine, whereas it had no effect on papillary blood flow or renal interstitial pressure in Wistar-Kyoto rats. The relations among sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure were shifted toward lower pressures in spontaneously hypertensive rats given nisoldipine and became similar to those seen in Wistar-Kyoto rats. These results indicate that nisoldipine normalizes the relations among sodium excretion, renal interstitial pressure, papillary blood flow, and renal perfusion pressure in spontaneously hypertensive rats perhaps by correcting the defect in renal medullary perfusion associated with resetting of pressure natriuresis in this model of hypertension.
Hypertension 1992 Jan
PMID:Normalization of pressure-natriuresis by nisoldipine in spontaneously hypertensive rats. 173 Apr 39


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