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

Several steroid hormones act in the kidney. We have examined, by autoradiography, the precise distribution of receptors for aldosterone, glucocorticoids, vitamin D (1-25(OH)2D3) and estrogens, in the different epithelia of the nephron isolated by microdissection. Specific nuclear binding sites are localized in the distal parts of the nephron, with some variations according to the steroid hormone considered: target cells for aldosterone are located in the distal tubule and cortical collecting duct, glucocorticoid receptors are present in all distal segments, whereas those of 1-25(OH)2D3 are restricted to the thick ascending limb of Henle's loop and to the medullary collecting tubule. Thus, it appears that several receptors coexist in some cell types. No specific nuclear binding sites for estrogens could be detected along the nephron. On the other hand, a non nuclear specific binding for glucocorticoids was observed in the proximal tubule, where specific glucocorticoid effects have been described. By autoradiography on intact target cells, it appeared that aldosterone receptors are essentially (or exclusively) located in nuclei, as was recently described for other steroid hormones. Binding sites for aldosterone are already present in its target cells in the fetal kidney before their functional differentiation. Aldosterone is weakly metabolized in the kidney, without specific tubular localization. It is possible to show some modifications of aldosterone binding sites, at the level of its target cells, in some pathological states, such as hypertension.
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PMID:[Receptors of steroid hormones in the kidney]. 304 46

The effects of dietary sodium upon serum and urinary calcium and selected vitamin D metabolites were studied in two groups (n = 10 each) of age and gender matched, white normotensive subjects and patients with normal-renin hypertension. Isocaloric diets were consumed on a metabolic ward with sequential daily sodium intake of 109 meq for 5 days and 9 meq and 259 meq for 6 days each. Values for serum and urinary calcium, phosphorus, magnesium and electrolytes, creatinine clearance, plasma immunoreactive parathyroid hormone, and serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were similar in both study groups on each diet. Measurements of plasma renin activity and serum aldosterone levels were higher in the hypertensive than in the normotensive group on each diet (p less than .05-.01). Serum 1,25-dihydroxyvitamin D and urinary calcium increased on the high sodium diet in the normotensive (p less than .05) and the hypertensive groups (p less than .01). When the data for normotensive subjects and hypertensive patients were pooled by gender, males had a 1 1/2 to 3 times the urinary calcium excretion than females, regardless of diet. The present study indicates that there are no differences in the selected components of calcium and vitamin D metabolism in response to sodium intake in patients with essential hypertension and normal plasma renin activity as compared to normal controls.
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PMID:Normal vitamin D and mineral metabolism in essential hypertension. 305 8

Intestinal calcium transport rate and response to treatment with a vitamin D agonist [24,24-difluoro-1,25-dihydroxycholecalciferol, F2-1,25-(OH)2D3)] were studied in the spontaneously hypertensive (SH) rat-Wistar Kyoto (WKy) rat model of hypertension. We used the everted duodenal sac to study untreated, orally treated, and parenterally treated groups of SH and WKy rats. In untreated groups, net calcium transport was lower (P less than 0.05) in the SH rat than in the WKy rat (0.46-0.66 vs 0.81-1.04, all data mumole/g segment wet wt per hr). Both groups responded to treatment (SH vs WKy; 0.84-0.90 vs 1.56-1.57, P less than 0.05), but even in treated groups net calcium transport by the SH rat was lower than that by the WKy rat (P less than 0.05). Net water transport increased 3- to 8-fold in response to treatment in the WKy but not in the SH rat. The increased water transport prevented demonstration of treatment-mediated increased calcium transport based on serosal/mucosal concentration ratio in the WKy rat. We conclude that (i) both the SH and the WKy rat have the capability to increase calcium transport when treated with an agonist having vitamin D activity; (ii) the unstimulated and stimulated transport rate is lower in the SH rat than in the WKy rat; and (iii) water transport responds to treatment in the WKy rat but not in the SH rat.
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PMID:Calcium transport in the spontaneously hypertensive rat is responsive to vitamin D. 319 30

Disturbances of calcium or vitamin D metabolism have been suggested to be of pathogenetic importance both for hypertension and impaired glucose tolerance, two disorders that are commonly associated. In the present study 65 men, aged 61-65 years, with impaired glucose tolerance were enrolled in a prospective, double-blind, placebo-controlled study over 12 weeks evaluating the effects of 0.75 microgram alphacalcidol, a synthetic analog to the active metabolite of vitamin D. In the 26 patients with blood pressure greater than or equal to 150/90 mmHg before treatment a significant reduction (p less than 0.01) of both the systolic (SBP) and diastolic (DBP) blood pressure was found after therapy (from 171/95 to 150/88 mmHg). The effect was additive to concomitant antihypertensive treatment and was correlated (p = 0.03) to a reduction of serum levels of parathyroid hormone. Also in the whole group of patients given alphacalcidol blood pressure was moderately lowered from a mean of 152/87 +/- 22/10 (SD) to 143/84 +/- 17/8 mmHg. There were no relationships between the changes in body weight, blood glucose or insulin parameters and the changes in blood pressure during the trial. The findings are compatible with the concept that calcium metabolism influences blood pressure regulation and suggest that supplementation with a physiologic dose of active vitamin D could be beneficial for patients with high blood pressure.
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PMID:Reduction of blood pressure by treatment with alphacalcidol. A double-blind, placebo-controlled study in subjects with impaired glucose tolerance. 328 11

This article reviews aspects in the clinical presentation of nephrotic syndrome that are not generally considered characteristics of the syndrome's definition. The importance of various general clinical aspects such as hematuria, hypertension, and other laboratory or histologic findings are discussed. The clinical relevance and management of other specific aspects such as lipid alterations, coagulation abnormalities, calcium and vitamin D metabolism, and nutritional complications derived from the nephrotic syndrome also are included in this review.
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PMID:Less commonly recognized features of childhood nephrotic syndrome. 329 18

There is epidemiologic evidence of a relationship between calcium deficiency and hypertension. The present study evaluated the effects of alphacalcidol, a synthetic analogue of active vitamin D, given to 29 patients with marginal, intermittent hypercalcaemia. Before therapy there was an inverse relationship between serum calcium levels and diastolic blood pressure (p less than 0.02). Treatment with 1 microgram alphacalcidol raised the serum calcium by 0.07 mmol/l during a 6-month, double-blind, placebo-controlled trial and caused a significant reduction of diastolic blood pressure by 9.2 mmHg compared with placebo (p less than 0.01). The study extends previous observations, in normocalcaemic subjects, of inverse relationships between serum calcium and blood pressure indicating a primary disturbance of calcium homeostasis in hypertension. The observation that a physiologic amount of active vitamin D has hypotensive effects agrees with such a concept and suggests a new principle for the treatment of hypertension.
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PMID:Blood pressure is lowered by vitamin D (alphacalcidol) during long-term treatment of patients with intermittent hypercalcaemia. A double-blind, placebo-controlled study. 332 26

Prior studies report that plasma membranes of the spontaneously hypertensive rat (Okamoto-Aoki strain) bind less calcium than do the corresponding preparations from Wistar Kyoto controls. The possibility that the differences result from a decrease in the content of integral membrane calcium-binding protein (IMCAL) was explored by the application of immunoassays with polyclonal antisera and a mouse monoclonal antibody. IMCAL binds calcium with relatively high affinity, and its content in many rat tissues is regulated by vitamin D and the level of dietary calcium. Immunoassays of tissue IMCAL demonstrate significant reductions in content in the erythrocyte ghost, intestinal mucosa, kidney, heart, testis, and liver of the spontaneously hypertensive rat as compared to the control strains. The decreases are observed both at 4-5 weeks of age, before the onset of severe hypertension and at 8-9 weeks in the presence of severe hypertension. Moreover, the magnitude of the decrease in erythrocyte IMCAL can account for much of the decrease in the calcium-binding capacity of erythrocyte membranes reported by others. The results are especially significant because an abnormality in the membrane binding of calcium and in the regulation of cytosolic calcium ion concentration could underlie the pathogenesis of the hypertension.
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PMID:Decreased content of integral membrane calcium-binding protein (IMCAL) in tissues of the spontaneously hypertensive rat. 345 64

To test the possible impairment of vitamin D metabolism in hypertension, we studied the effect of parathyroid hormone (PTH) on the renal production of 1,25-dihydroxyvitamin D [1,25(OH)2D] in spontaneously hypertensive rats (SHR) before (at 4 weeks of age) and after (at 12 weeks of age) the onset of hypertension. Basal serum of 1,25(OH)2D was normal in SHR at both ages. At 4 weeks of age, rise in serum 1,25(OH)2D following PTH injection (50 U subcutaneously every 2 h, four times) was also normal in SHR. By contrast, at 12 weeks of age it was approximately one-third of that in Wistar-Kyoto rats (WKY) in parallel with an attenuated response to PTH of renal production of 1,25(OH)2D. Basal 1,25(OH)2D production by the kidney in SHR was higher than that in WKY at both ages, which was abolished by thyroparathyroidectomy but not by parathyroidectomy. These data demonstrate that altered vitamin D metabolism exists even before the onset of hypertension in SHR.
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PMID:Altered vitamin D metabolism in the spontaneously hypertensive rat. 346 1

Previous studies suggest abnormalities in PO4 and perhaps vitamin D metabolism in the spontaneously hypertensive rat (SHR) compared with normotensive Wistar-Kyoto (WKY) control rats. The mechanism for the hypophosphaturia obscure, but intestinal malabsorption of P and/or the possibility of linkage to renal Na avidity has not been evaluated. Furthermore, if sustained, the potential effects of the hypophosphaturia on P balance are not known. The present investigation examined these issues. We found that the reduced P excretion occurs as early as age 22 days, the second day after weaning in the SHR, well before the onset of detectable hypertension. This phenomenon is dissociable from renal Na avidity, and sustained through the 12th week of age, the last week of our studies. Since P absorption is normal, external P balance is increased relative to the WKY control rats. The greater cumulative P retention from infancy to adulthood may explain the age-dependent fall in serum 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] reported in the SHR by some investigators.
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PMID:Nature and metabolic consequence of hypophosphaturia in spontaneously hypertensive rats. 347 94

Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin-angiotensin system and in the pathophysiology of human hypertension.
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PMID:Alterations of dietary calcium intake as a therapeutic modality in essential hypertension. 353 Apr 9


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