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

Sodium-lithium countertransport (Na-Li CT) has been reported to be increased in essential hypertension (EHT) but the nature and degree of distinction from normal controls in unclear. Of 44 unselected patients with EHT in the hospital hypertension clinic 36% had Na-Li CT greater than the normal control range and 70% of these had a family history of hypertension. Almost all the patients with normal Na-Li CT had no family history of hypertension. Analysis of variance showed that raised Na-Li CT was related to both a family history of hypertension and a family history of a cardiovascular event. Of 23 patients with hypertension secondary to renal disease, 43% had Na-Li CT greater than the normal control range and raised Na-Li CT was related to both a family history of hypertension and a family history of cardiovascular event in the same way as EHT. Raised Na-Li CT was not characteristic of EHT but identified a subgroup of patients with EHT and a family history of hypertension, some of whom also had renal disease.
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PMID:Erythrocyte sodium-lithium countertransport in primary and renal hypertension: relation to family history. 249 56

Atrial natriuretic factor was infused in a low dose (0.2 microgram/min) during 5 days in six patients with essential hypertension. Atrial natriuretic factor infusion caused plasma levels of atrial natriuretic factor to increase from 49 +/- 10 to 106 +/- 19 pg/ml. Within 4 hours after the start of the atrial natriuretic factor infusion, urinary sodium excretion increased in all subjects. Sodium balance was regained after 24 hours with a net loss of 72.3 +/- 14.6 mmol. However, systolic as well as diastolic blood pressure started to decrease gradually in all subjects only after 12 hours of atrial natriuretic factor infusion, reaching a stable level after 36 hours with a decrease of 11.5 +/- 1.5% and 10.3 +/- 0.8%, respectively. Heart rate increased in parallel by 12.6 +/- 3.1%. Hematocrit rose 7.1 +/- 2.3%. After cessation of atrial natriuretic factor infusion, plasma atrial natriuretic factor levels, sodium balance, and hematocrit returned to baseline within 24 hours, whereas blood pressure slowly returned toward baseline values over 3 days. These data show that chronic atrial natriuretic factor infusion in patients with essential hypertension causes a negative sodium balance and a rise in hematocrit, followed by a smooth decrease in blood pressure with a rise in heart rate until a new equilibrium is reached after approximately 2 days. Thus, atrial natriuretic factor in low doses appears intimately involved in the regulation of sodium balance and blood pressure in humans. Moreover, these data suggest that atrial natriuretic factor-like substances will eventually become useful antihypertensive drugs.
Hypertension 1989 Jun
PMID:Antihypertensive effect of a 5-day infusion of atrial natriuretic factor in humans. 252 24

Obesity, diet and alcohol consumption constitute major environmental determinations of blood pressure elevation. The long term setting of blood pressure in response to these factors will be determined by genetic susceptibility, and interactions with effects of physical fitness and smoking. Dietary changes which independently influence both atherosclerosis and hypertension are likely to be of greatest value in helping to control morbidity and mortality from hypertensive cardiovascular disease. Recommendations should focus on diets low in total and saturated fat intake and high in fruit and vegetables, containing potassium and fibre, coupled with weight control, alcohol moderation to less than two drinks per day in drinkers and regular physical exercise. Sodium restriction will help lower blood pressure in older hypertensives in particular. The role of dietary calcium or fish oils in blood pressure regulation is still uncertain. Dietary and related recommendations on smoking and exercise should be 'first line' treatment in mild hypertensives, and complimentary to therapy in all patients requiring drugs.
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PMID:Diet, alcohol and hypertension. 255 47

The extent to which the natriuretic effect of a prolonged low dose infusion of atrial natriuretic factor (30 ng/kg/min) is dependent on interference with the prevailing intrarenal actions of angiotensin II was examined before and after blockade of angiotensin production with the converting enzyme inhibitor enalaprilat (5 mg/kg). Lithium clearance was used to assess proximal tubular sodium and water reabsorption. Atrial natriuretic factor and enalaprilat caused similar increases in sodium excretion (10-fold and sevenfold, respectively) and glomerular filtration rate (each 34%) and similar decreases in fractional proximal reabsorption of sodium (17% and 13%, respectively) and blood pressure. Each also caused a major disruption in the effectiveness of proximal glomerulotubular balance (30% and 50% of perfect balance). Infusion of atrial natriuretic factor during converting enzyme inhibition increased glomerular filtration rate further by 23%, reaching 63% above control without change in renal blood flow but with a rise in filtration fraction to 0.48. Sodium excretion increased further but fractional proximal sodium reabsorption remained constant and proximal glomerulotubular balance appeared to improve. Atrial natriuretic factor therefore possesses a glomerular action that persists during converting enzyme inhibition and is indeed additive to the removal of angiotensin II when the proximal effect of atrial natriuretic factor is no longer apparent. It is concluded that failure of atrial natriuretic factor to further suppress fractional proximal sodium reabsorption during converting enzyme inhibition is caused by either prior removal of the stimulatory action of angiotensin II on proximal tubular transport or extreme changes in peritubular physical factors consequent on the high filtration fraction.
Hypertension 1989 Dec
PMID:Atrial natriuretic factor modulates proximal glomerulotubular balance in anesthetized rats. 255 4

Sodium regulation of alpha 2-adrenoreceptors was investigated in inbred salt-sensitive (S) and inbred salt-resistant (R) rats fed a high or low salt diet. The systolic blood pressure was higher in S rats than in R rats, and this difference was obviously greater on a high salt diet. In rats fed a low or high salt diet, S rats had higher alpha 2-adrenoreceptor density in the kidneys compared with R rats as measured by [3H]yohimbine binding and Scatchard analysis. The affinity of the receptors in the kidney for the antagonist, yohimbine, was nearly the same in these two strains either on a low or high salt diet. In the brain, the affinities or the numbers of receptors were not significantly different whether these two strains were fed a low or high salt diet. Inclusion of NaCl up to 80 mM in the assay medium did not alter the in vitro binding of [3H]yohimbine in the kidney or brain. On the other hand, inclusion of NaCl in the assay medium reduced the ability of epinephrine in competing with [3H]yohimbine for the receptor sites in the kidney and in the brain, and this effect of NaCl was the same in a given tissue between S and R rats, whether they were fed a low or high salt diet. These results suggest that: (1) in the kidneys, the receptor density and not the receptor affinity was different between S and R strains whether they were fed a low or high salt diet; (2) in the brain, the receptor density and affinity were the same between S and R rats regardless of the diet (low or high salt), indicating that the sodium salt diet modulates the peripheral but not the central alpha 2-adrenoreceptors; and this modulatory effect was observed only in S rats; (3) Na+ was able to reduce the affinity of the agonist (epinephrine) for the receptors in both S and R rats, and this effect of Na+ on central and peripheral alpha 2-adrenoreceptors was similar in prehypertensive rats and rats with salt-induced hypertension; and (4) the resistance of R rats to salt-induced hypertension was not due to the absence of Na+ binding component involved in the regulation of alpha 2-adrenoreceptor-adenylate cyclase complex.
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PMID:Sodium regulation of alpha 2-adrenoreceptors in Dahl rats. Effect of feeding a low or high salt diet. 255 32

Cerebral and renal alpha 2-adrenoceptors are implicated in the control of sympathetic activity and of sodium reabsorption respectively. In addition, sodium ions play an important role in the regulation of either alpha 2-adrenoceptor densities and affinities for adrenergic agonists. In the present study, alpha-adrenoceptor properties were investigated in genetically predetermined salt-sensitive and salt-resistant Dahl and Sabra rats. Cerebral alpha 2-adrenoceptor densities were higher in salt-resistant than in salt-sensitive Dahl and Sabra rats. In contrast, renal alpha 2-adrenoceptor density was higher in salt-sensitive than in salt-resistant rats. No difference in cerebral and renal alpha 1-adrenoceptor densities was observed between Dahl and Sabra substrains. Noradrenaline content in cerebral and renal cortex were also similar in both these rat substrains. Sodium ions markedly increased cerebral and renal high-affinity alpha 2-adrenoceptor densities in salt-sensitive but not in salt-resistant rats. Cerebral and renal alpha 1-adrenoceptor densities were unchanged in salt-sensitive and salt-resistant substrains of Dahl and Sabra rats. In addition, sodium ions reduced the affinity of adrenaline for renal alpha 2-adrenoceptors in salt-sensitive rats but not in salt-resistant rats. We can conclude that there exist genetically determined differences in the densities and properties of cerebral and renal alpha 2-adrenoceptors between salt-sensitive and salt-resistant rat strains. Abnormal densities of alpha 2-adrenoceptors may play a primary role in the role in the development of hypertension in salt-sensitive animals. These results also suggest an association between absence of sodium regulation of alpha 2-adrenoceptors and resistance to salt-induced hypertension. The absence of sodium regulation in salt-resistant rats may be linked either to a particular receptor conformation or to an abnormal structure of the receptor system. This property may represent a genetically-mediated change responsible for the resistance to the development of salt-induced hypertension.
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PMID:Alpha-adrenoceptor properties in rat strains sensitive or resistant to salt-induced hypertension. 255 64

The number and activity of erythrocyte ATPase-dependent sodium-potassium pump units were increased in obese subjects (p = 0.02). No link was observed between the number or activity of the pump units and hypertension. The ouabain-insensitive rubidium (i.e. potassium) transport was not associated with relative body weight or blood pressure status. Sodium-lithium countertransport correlated significantly with obesity but not with blood pressure status. In the hypertensive patients, before or after therapy with verapamil, hydrochlorothiazide, pindolol or atenolol there were no significant differences in cation transport. We propose that the correlation between obesity and essential hypertension cannot be explained by these two cation transport systems.
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PMID:Erythrocyte cation transport in obesity, hypertension, and during antihypertensive drug therapy. 257 70

Sodium intake from food and other sources must be carefully monitored in patients with hypertension and other disorders. Retention of sodium was measured during routine use of three commercially available, nonprescription mouthwashes: Cepacol, Plax, and Viadent. A test group of 17 adults rinsed with 15 ml of the three mouthwashes, and with 5% saline and distilled water as experiment controls. Sodium not recovered in the expectorate was considered to be retained for absorption by oral or other tissues. The sodium in each product (in mg/l) varied widely: Viadent, 144; Cepacol, 410; and Plax 5320. The analyzed expectorate revealed approximately 33% of the sodium in the 15 ml used for rinsing was retained, amounting to 0.7 mg for Viadent, 1.9 mg for Cepacol, and 28.3 mg for Plax. The results indicate that persons on sodium-restricted diets should be aware that some brands of mouthwash may be a potentially significant source of sodium.
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PMID:Sodium retention from mouthwashes. 260 65

Altered vascular reactivity to numerous vasoactive substances in hypertension formed the basis for studying the in vivo microcirculation of skeletal muscle tissue during high cardiac output bacteremia and low cardiac output sepsis. Large and small arteriole and venule diameters of the cremaster muscle were measured via videomicroscopy in normotensive and 1K-1C-renovascular hypertensive rats before and after the infusion of live Escherichia coli bacteria. During hyperdynamic bacteremia and during hypodynamic sepsis, large arterioles constricted and small arterioles dilated in normotensive animals. During hyperdynamic bacteremia, this differential arteriolar response was blunted in hypertension. In hypodynamic sepsis, large arterioles did constrict in the hypertensive animals, but small arteriolar dilation was still blunted. Sodium-nitroprusside, a postreceptor acting agent applied locally, maximally dilated small arterioles to the same level in all groups to indicate that the ability of vascular smooth muscle to relax is intact in hypertension. We conclude that the failure of the small arterioles to dilate during sepsis in hypertension is not due to a loss of vascular smooth muscle function, but that hypertension may functionally alter arteriolar reactivity at the receptor and/or endothelial level to interfere with E. coli-mediated responses in the skeletal muscle microvasculature.
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PMID:Hypertension alters microvascular responses in skeletal muscle to hyperdynamic bacteremia and hypodynamic Escherichia coli sepsis. 264 61

Short term angiotensin converting enzyme inhibition may induce a transient salt and water retention in patients with hypertension or heart failure. To verify the glomerular and tubular effects of short term converting enzyme inhibition, thirteen patients with mild to moderate essential hypertension (WHO I-II) were treated orally either with perindopril (4 mg o.d.) or captopril (25 mg b.i.d.) for one week. Both drugs reduced supine mean blood pressure significantly (p less than 0.01) (perindopril from 126 +/- 11 to 108 +/- 7 mmHg, mean +/- SD, and captopril from 132 +/- 12 to 121 +/- 16). Plasma volume (radio-iodinated albumin space) was unchanged while mean extracellular fluid volume (inulin space) increased although not significantly (from 5.05 +/- 1.32 l/sqm to 5.71 +/- 2.21 with perindopril and from 4.96 +/- 2.6 to 5.6 +/- 1.7 with captopril). Sodium clearance decreased (from 1.4 +/- 0.6 to 1.1 +/- 0.5 ml/min 1.73 sqm with perindopril, p less than 0.05, and from 0.97 +/- 0.44 to 0.88 +/- 0.51 with captopril, n.s.). In 9 patients (6 on captopril and 3 on perindopril) extra-cellular fluid volume increased simultaneously with reduction in glomerular filtration rate and in proximal tubule sodium re-absorption as well as an increase in distal tubule sodium reabsorption. In these patients the changes in proximal and distal tubule sodium reabsorption were significantly (p = 0.05) different from those of the patients with no extra-cellular fluid expansion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Volume of the extracellular liquid and renal function during short-term administration of angiotensin converting enzyme inhibitors in essential hypertension]. 267 Jun 57


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