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

We evaluated the need for erythropoietin (EPO) treatment in 134 end-stage renal disease patients assuming a level of hemoglobin below 6 mmol/l (9.6 g/dl) as indication for treatment. 91 patients (68%) fulfilled this criterion. Absolute contraindications in 2 patients were previous thrombotic encephalopathy and refusal of treatment. Relative contraindications due to cardiac disease were found in 3 patients. In 15 patients additional treatment was required because of hypertension (5) or deficiency states (10). The implications of elevated serum PTH and aluminum overload are discussed.
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PMID:On the need for erythropoietin treatment in dialysis patients. A Copenhagen City Dialysis Unit study. 222 88

Determination of the concentration of ionized calcium in the blood of metallurgists and miners with arterial hypertension (AN) revealed a tendency to reduction of calcemia that was more pronounced in high arterial pressure and low consumption of calcium with food. A tendency to reduce calcemia by stimulating PTH secretion has a pathophysiological significance in the development of AH. A calcium-enriched diet may be of value in the prophylaxis of AH.
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PMID:[The calcium concentration of the blood in arterial hypertension patients]. 228 60

The relationship between 24-h recumbent blood pressure levels and secretory patterns of catecholamines was investigated in 4 patients with pseudohypoparathyroidism (PsHP) and hypertension and in 9 patients with essential hypertension. A clear circadian rhythm of blood pressure and catecholamines was documented in both groups with lowest levels of blood pressures and catecholamines occurring during sleep. During the 24-h period of recumbency mean arterial blood pressure (MAP) was correlated (r = 0.63, p less than or equal to 0.01) with plasma norepinephrine (N) in the patients with essential hypertension, but this correlation was weaker in patients with PsHP (r = 0.38, p less than or equal to 0.05). MAP was more closely related to plasma epinephrine (E) (r = 0.62, p less than or equal to 0.01) than to plasma NE in patients with PsHP. Plasma NE and E levels were considerably lower in patients with PsHP than in patients with essential hypertension throughout the 24-h recumbent period. The sleep-related decline in blood pressure and NE was less than in patients with essential hypertension. These results suggest that while the sympathetic nervous system may have a role in hour-to-hour maintenance of blood pressure in patients with PsHP and hypertension, it does not appear to be responsible for the elevated arterial pressure in these patients. Factors other than those investigated, such as obesity, alterations in sodium homeostasis of refractoriness of the vascular smooth muscle to the vasodilatory effect of PTH may be involved in the pathogenesis of hypertension in PsHP.
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PMID:Circadian variations of catecholamines and blood pressure in patients with pseudohypoparathyroidism and hypertension. 235 Sep 86

Returning to the patient presented today, perhaps we can now understand some of his findings. As I noted, men are more likely to demonstrate alterations in calcium metabolism associated with elevations in blood pressure. Furthermore, blacks are more likely than whites to develop hyperparathyroidism, particularly in the third and fourth decades of life. It is unlikely, however, that parathyroid hormone was responsible for the increase in this patient's arterial pressure because PTH has a vasodilating action. Moreover, the long-term response to parathyroidectomy is more likely to be an increase rather than a decrease in blood pressure. It is also unlikely that the mild elevations in the serum total calcium observed in this patient were responsible for his hypertension. Correction of hypercalcemia by surgical intervention failed to improve the blood pressure. There is little evidence that mild, protracted hypercalcemia can account for increases in arterial pressure. Finally, the patient's alcohol abuse might have contributed to his elevated blood pressure; it is possible that his hypertension was in part a reflection of the abnormal calcium metabolism he developed as a consequence of the alcohol abuse. Answers to some questions we faced when we first studied this patient more than a decade ago can be provided by the wealth of basic research and clinical investigation that has occurred since. We now know that calcium metabolism is a factor in blood pressure regulation in some humans and in some experimental models. Epidemiologic studies document a consistent association between lower dietary calcium intake and higher blood pressures in humans. An additional non-pharmacologic approach has been identified that can produce a modest but important lowering of blood pressure in a subset of hypertensive individuals. Much data show that calcium-regulating hormones have important cardiovascular actions that might account for some of the mechanisms by which increased dietary calcium lowers blood pressure. Research in this area also has set the stage for exploring another theoretical mechanism for sodium-chloride-sensitive hypertension. Finally, a theoretical mechanism(s) has emerged that could provide a pathophysiologic link between hypertension and certain high-risk populations such as blacks, the elderly, type-II diabetics, and pregnant women. The principal clinical implication derived from this work to date is the following: In patients with mild to moderate hypertension, the level of dietary calcium intake should be assessed. Patients whose intake is deficient should be encouraged simply to maintain calcium intake at 800 to 1000 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium metabolism and hypertension. 254 Mar 74

Echocardiography was studied in 83 uremic patients on maintenance hemodialysis and 18 normal subjects. Cardiac systolic and diastolic functions were evaluated according to Yamaguchi's method. Systolic functions such as ejection fraction and fractional shortening decreased in the patients receiving hemodialysis for less than 3 months. However, they remained within normal range in the patients under hemodialysis for more than 3 months. There were no significant correlations between systolic functions and mean blood pressure or various serum biochemical parameters such as urea nitrogen, creatinine, Na, K, Ca, P, hematocrit and PTH-C. Diastolic functions such as rapid filling rate/endosystolic volume, mean velocity of circumferential fiber lengthening during rapid filling, diastolic descent rate and diastolic posterior wall velocity also decreased in the patients receiving hemodialysis for less than 3 months. However, they increased slightly in the patients under hemodialysis for more than 3 months, although they were still lower than those in normal subjects. They were not related to mean blood pressure or various serum biochemical parameters. Hemodialysis patients had left ventricular hypertrophy regardless of duration of hemodialysis. Diastolic dysfunction in hemodialysis patients seemed to be due to systolic dysfunction, left ventricular hypertrophy and diminished ventricular compliance with myocardial degeneration. It was also suggested that increasing slow filling and atrial contraction in diastole might be related to diastolic dysfunction. These cardiac changes may be compensatory reactions of cardiac muscle to various uremic environments such as anemia, hypertension, fluid retention, electrolytes disturbance or uremic toxins.
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PMID:[An echocardiographic study of cardiac function in chronic hemodialysis patients]. 258 30

The purpose of this study was to determine if alterations of calcium and calcium regulating hormones precede the onset of NaCl induced hypertension in the Dahl salt sensitive (S) rat. After a 5 day balance study, serum ionized calcium, PTH, and 1,25 dihydroxy vitamin D concentrations were measured in Dahl-S and salt resistant (R) rats that had been maintained on a "normal" (1%) or high (7%) NaCl intake. Blood pressure was higher in Dahl-S than R (P less than .01), but was not affected by 5 days of high NaCl. On both NaCl intakes, urine calcium excretion was increased, serum calcium was decreased, and serum PTH and 1,25 dihydroxy vitamin D were increased in Dahl-S compared to Dahl-R (P less than .01). On the high NaCl intake, fecal calcium was greater in Dahl-S than in Dahl-R, and net 5 day calcium balance was less positive in Dahl-S (P less than .05). In contrast to NaCl, a high dietary intake of sodium with anions other than chloride (NaAA) fails to produce hypertension in the Dahl-S rat. NaAA loading resulted in decreased urine calcium excretion (P less than .01), and after 5 days of the high NaAA diet, serum calcium and PTH did not differ in Dahl-S and Dahl-R. Thus, alterations of calcium, PTH, and vitamin D precede NaCl-induced hypertension in Dahl-S. These alterations may contribute to the development of hypertension in this animal model.
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PMID:Calcium and calcium regulating hormones in the "prehypertensive" Dahl salt sensitive rat (calcium and salt sensitive hypertension). 280 69

We report the clinical and biological picture of 34 primary hyperparathyroidism (PHT) cases, diagnosed in rheumatology. It concerned 25 women and 9 men, aged 61 + 11 years. The PHT was often asymptomatic (47 p. cent of cases) at the time of diagnosis. The clinical manifestations were dominated by asthenia (50 p. cent) and renal lithiasis (47 p. cent). We found a chondrocalcinosis in 29 p. cent of patients. No patient presented any bony manifestations of cystic osteitis; 7 out of 34 patients (including 6 women between 57 and 74 years) presented vertebral compression. The mean calcemia was 117 +/- 9 mg/l. There were no hypercalcemic attack. The dosage of PTH and cyclic AMP were elevated in 29 out of 32 and 28 out of 31 patients respectively. In all patients, the level of either of these two tests was increased. The chloremia/phosphoremia ratio was also extremely predictive of HBP, since it was increased, exceeding 3.3 in 33 out of 34 patients. The 25-hydroxyvitamin D levels (25 (OH) D) were normal. The levels of 1,25 (OH) 2D were markedly spread (37 +/- 16 pg/ml) and not significantly different from the reference group. Patients with lithiasis did not present a higher level of 1,25 (OH) 2D. A bone histomorphometry carried out in 15 patients showed a bone trabecular volume similar to that of the reference with the same age. The osteoclastic resorption was increased in all cases and was not correlated with the PTH level, but was significantly correlated with the level of 1,25 (OH) 2D (r = 0.79 p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Primary hyperparathyroidism seen in rheumatology. Clinical symptoms and the relation between bone histologic signs and biological parameters]. 326 11

Plasma parathyroid hormone levels (pPTH) have been measured by radioimmunoassay (RIA) in young spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY) aged from 6 to 16 weeks to assess the possible role of PTH during the development of hypertension. Three antisera were used in the RIAs. One antiserum was directed toward the inactive C-terminal fragment of PTH, another toward the bioactive N-terminal fragment (PTH 1-34), and a third was obtained by immunization against intact PTH 1-84. Blood pressures were measured by tail-cuff plethysmography with prewarming. Blood ionized calcium and sodium concentrations (b[Ca2+] and b[Na+]) were determined by ion-selective electrolyte analysis. No significant differences were observed between pPTH in the SHR compared with WKY during the development of hypertension. Neither were significant differences in b[Ca2+] or b[Na+] present at any age. The expected progression of hypertension in SHRs was observed and blood pressure was significantly greater in SHR than in WKY at all times. The results suggest that differences in pPTH and b[Ca2+] in SHR reported in other studies may be secondary phenomena to the establishment of hypertension. Our data suggest that PTH is not involved in the pathogenetic processes occurring during the development of spontaneous hypertension in rats.
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PMID:Plasma parathyroid hormone during the development of spontaneous hypertension in rats. 344 94

In children with blood pressure levels persistently in the upper part of the distribution and without evidence for known causes of hypertension, one may ask which approach should be used to lower blood pressure. In general, non-pharmacological intervention will be preferred over drug treatment as a first choice in children with primary hypertension. No specific non-pharmacological treatment is available for children with high blood pressure. The main objective of this review is to underscore the need for further intervention studies in hypertensive children. Although the scientific evidence is rather scanty, some general recommendations concerning body weight, physical activity and fitness, dietary intake of electrolytes and relaxation procedures can be made. In obese children, weight reduction, combined with increase of physical activity, is the measure of first choice to lower blood pressure. In children with a high sympathetic outflow, as evidenced by high levels of circulating catecholamines, increase of physical activity and use of relaxation procedures may be the first approach to lower blood pressure. In children with evidence for disturbances in electrolyte metabolism, as evidenced by high intralymphocytic sodium, low serum calcium, or high PTH, a dietary approach to high blood pressure may be used. In these children, an increase of potassium intake or calcium intake seems a promising way to lower blood pressure.
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PMID:Non-pharmacological intervention in primary hypertension in childhood. 353 May 55

Plasma parathyroid hormone (pPTH) levels have been assessed in three separate radioimmunoassay systems in samples from Wistar-Kyoto rats. The animals were subjected to one of three dietary regimens throughout the study period: Group 1 animals consumed normal rat chow and drank tap water; Group 2 animals consumed normal rat chow and tap water was replaced with 0.5% saline solution; Group 3 animals consumed normal rat chow to which 2.5% CaCO3 (by weight) had been added and also drank 0.5% saline solution. Animals had consumed these diets for approximately 7 months prior to sacrifice for blood collection. Blood pressure was measured by tail cuff plethysmography in these animals and, as previously reported, saline consuming animals showed a moderate hypertension (Gp 2) only when diets did not contain added calcium (Gp 3). In the week prior to sacrifice, mean blood pressures were: Gp 1: 128.0 +/- 3.46 mmHg; Gp 2: 140.2 +/- 3.15 mmHg; and Gp 3: 133.5 +/- 2.90 mmHg. Three assay systems were used to measure pPTH levels from trunk blood samples obtained by guillotine decapitation. One assay used an antiserum directed toward the vasoactive N terminal fragment 1-34 and produced pPTH measurements of 0.74 +/- 0.05 ng/ml in Gp 1 animals, 1.04 +/- 0.07 ng/ml in Gp 2 animals and 1.12 +/- 0.08 ng/ml in Gp 3 animals. This pattern was consistent with that obtained by another antiserum which had been raised against the intact 1-84 PTH molecule and produced values of 0.25 +/- 0.03 ng/ml in Gp 1 animals, 0.55 +/- 0.07 ng/ml in Gp 2 animals and 0.74 +/- 0.04 ng/ml in Gp 3 animals. Antiserum raised against the C-terminal did not show any difference in pPTH across groups. We conclude that saline consumption may increase some portions of circulating PTH. Such elevation of pPTH may not be a pathophysiological component in the sodium dependent elevation of blood pressure since animals concurrently consuming both saline and calcium supplemented diets retained elevated pPTH levels even though blood pressures did not differ from controls. Rather, elevation of circulating PTH levels may be a response to prolonged increases in sodium consumption.
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PMID:Parathyroid hormone in sodium-dependent hypertension. 362 62


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