Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the role of the parathyroid gland (PTG) in the long-term development of blood pressure (BP) in stroke prone spontaneously hypertensive rats (SHR/SP) and Wistar Kyoto (WKY) rats. After ablation of their own PTGs, SHR/SP animals received PTGs from WKY rats and vice versa. Transplantation resulted in a normal calcium and parathyroid hormone status without signs of hypoparathyroidism. All animals received a high salt diet (8% NaCl) for 4 weeks after transplantation of PTGs. In SHR/SP, which received PTGs from WKY, development of high BP was clearly attenuated when compared to sham-operated SHR/SP rats. WKY rats with PTGs from SHR/SP rats became hypertensive, while WKY sham-operated animals remained normotensive. PTGs from SHR/SP rats are able to induce hypertension in normotensive WKY rats.
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PMID:Development of hypertension in WKY rats after transplantation of parathyroid glands from SHR/SP. 170 92

Na(+)-H+ exchange activity is increased in hypertensive rat strains and could be a predisposing factor in the pathogenesis of essential hypertension. Previously we demonstrated that proximal nephron Na(+)-H+ exchange is stimulated by alpha-adrenergic agonists and angiotensin II (ANG II) and inhibited by parathyroid hormone (PTH) and dopamine (DA). To test the hypothesis that hormonal regulation of proximal nephron Na(+)-H+ exchange could differ with hypertension, alterations in Na(+)-H+ exchange were determined by 1) amiloride analogue-suppressible 22Na+ uptake and 2) change in intracellular pH (pHi) as monitored with the fluorescent probe 2',7'-bis(carboxyethyl)-5(6)carboxyfluorscein acetoxymethyl ester. Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats had similar tail-cuff pressures at 4 wk, but SHR blood pressure was significantly elevated at 8 and 16 wk compared with WKY. No significant differences were observed between SHR and WKY basal ethylisopropyl amiloride-suppressible 22Na+ uptakes or rates of pHi change. alpha-Adrenergic agents and ANG II significantly increased (P less than 0.05) Na(+)-H+ exchange, but, in contrast, 8- and 16-wk-old SHR tubules lacked responsiveness to PTH (10(-8) M) and DA (10(-6) M) observed in WKY. A significant reduction (57-79%, P less than 0.05) in norepinephrine and ANG II stimulation was observed with 8- and 16-wk-old WKY tubules incubated in combination with PTH or DA, but only a 3-33% reduction was produced in 8- and 16-wk-old SHR tubules. PTH- and DA-stimulated adenosine 3',5'-cyclic monophosphate accumulation was significantly reduced in SHR compared with WKY tubules at 4 and 8 wk. It appears that proximal nephron Na(+)-H+ exchange activity is a balance between ANG II and NE activation and PTH and DA inhibition. The data suggest SHR proximal hormone responses are different from WKY and may alter the balance of net Na(+)-H+ exchange activity, possibly contributing to the development or maintenance of hypertension in the SHR.
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PMID:Hormone responses of proximal Na(+)-H+ exchanger in spontaneously hypertensive rats. 171 62

Patients with mild asymptomatic primary hyperparathyroidism who do not meet currently accepted guidelines for surgery may be followed medically. General medical management of these individuals should be directed toward maintaining adequate hydration, therapy of hypertension, and avoiding immobilization. Diuretics should be used only with caution. Moderate dietary calcium intake (500-800 mg/day) should be encouraged. Propranolol and cimetidine are not useful in the therapy of primary hyperparathyroidism. Oral phosphate is efficacious in lowering serum and urinary calcium. However, because of concerns related to ectopic calcification, phosphate is usually reserved for those patients who meet surgical guidelines but who are not to undergo surgery. Bisphosphonates, potent inhibitors of osteoclast-mediated bone resorption, have been shown to lower serum and urinary calcium in patients with primary hyperparathyroidism. However, long-term data on their efficacy in this disorder are not yet available. The use of bisphosphonates at the present time is generally restricted to the research setting. More potent bisphosphonates as well as the design of newer agents that interfere with parathyroid hormone secretion may become very useful in future approaches to the medical management of primary hyperparathyroidism.
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PMID:Medical management of asymptomatic primary hyperparathyroidism. 176 64

Primary hyperparathyroidism (PHPT) is characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia. PTH acts by binding to cell surface receptors coupled to G proteins. Cyclic AMP is the classic second messenger of PTH action, but substantial evidence indicates that PTH also acts to stimulate formation of the dual second messengers, inositol trisphosphate and diacylglycerol, thereby mobilizing intracellular calcium. The physiologic actions of PTH include (1) an increase in extracellular fluid ionized calcium through direct actions on kidney and bone, the classic target organs for PTH, and (2) a decrease in extracellular fluid phosphate primarily through renal action. The pathophysiologic effects of PTH arise from (1) direct actions of PTH on bone and kidney, and possibly on nonclassic target organs, and (2) indirect effects of altered mineral homeostasis. PTH hypersecretion in PHPT can lead to bony demineralization, nephrolithiasis, and hypercalcemic crisis. PHPT may also be associated with mental disturbances, neuromuscular disease, hypertension, and glucose intolerance.
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PMID:Pathophysiology of primary hyperparathyroidism. 176 67

The differential diagnosis of hypercalcemia has expanded to over 25 separate disease states, with primary hyperparathyroidism and malignancy accounting for 80-90% of all hypercalcemic patients. Primary hyperparathyroidism comprises the majority of hypercalcemic patients among the ambulatory population, but malignancy accounts for up to 65% of such patients in the hospital. Factors favoring primary hyperparathyroidism include a family history of hyperparathyroidism or multiple endocrine neoplasia, a history of childhood radiation to the head and neck, the postmenopausal state, a history of renal calculi or peptic ulcer, hypertension, the induction of hypercalcemia by thiazides, or an asymptomatic patient with a prolonged, stable mild hypercalcemia. The usefulness of the serum calcium, parathyroid hormone, chloride, phosphorus, serum 25-OHD, and 1,25-(OH)2D, and urinary calcium in the differential diagnosis of hypercalcemia is discussed. The pitfalls of an excessive reliance on the serum PTH in diagnosing hyperparathyroidism are stressed. The discriminant values of the serum calcium, chloride, phosphorus, and parathyroid hormone are explored, with the serum parathyroid hormone, chloride, and calcium proving most useful in separating primary hyperparathyroidism from other forms of hypercalcemia. Multivariate discriminant analysis using the serum calcium, phosphorus, and chloride and the hematocrit achieves an accuracy of 95-98% and is the most economical method of identifying hyperparathyroidism. The addition of the amino-terminal or intact PTH assay increases the accuracy to 99% and is essential in the presence of renal insufficiency.
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PMID:Differential diagnosis of hypercalcemia. 176 70

Over the last 25 years, the perceived clinical spectrum of primary hyperparathyroidism (HPT) has changed dramatically from a disorder characterized by severe bone and renal disease to one typically manifested by few or mild symptoms and little evidence of organ damage. Reasons for this change in spectrum include changing demographics (primary HPT is primarily a disease of the middle-aged and elderly), diffusion of medical knowledge leading to a higher index of suspicion, and improved clinical laboratory technology (especially inexpensive and accurate determination of serum calcium and parathyroid hormone). In the first 343 cases of primary HPT seen at the Massachusetts General Hospital, 57% had renal stones, 23% had hyperparathyroid bone disease, and less than 1% had no symptoms. By contrast, studies dating from the availability of automated serum calcium measurement found renal stones and hyperparathyroid bone disease in less than 5% of cases, and about half of cases had few or no symptoms. Most patients with primary HPT today have mild, nonspecific symptoms, such as weakness, fatigue, and mental depression, and such signs as arterial hypertension and osteopenia, and detection of their hypercalcemia is generally serendipitous. The mildness and slow progression seen in many cases of primary HPT has resulted in much controversy about appropriate management.
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PMID:Clinical spectrum of primary hyperparathyroidism: evolution with changes in medical practice and technology. 176 71

In order to clarify the pathophysiological significance of changes in intracellular ionized calcium and sodium levels in pregnancy induced hypertension (PIH), the intracellular ionized calcium concentration in platelets (p-[Ca2+]i) and the intracellular ionized sodium concentration in red blood cells (r-[Na+]i) were measured simultaneously in PIH women in the third trimester. p-[Ca2+]i in the first trimester showed a slightly greater increase than in the women of normal luteal phase. In the second trimester, p-[Ca2+]i decreased significantly compared to first trimester, and the third trimester and first trimester levels were the same. In women with mild and severe PIH, the levels in both groups were significantly increased compared with that in normal pregnant women. Thus mechanisms not associated with platelet activation were considered as the cause of the increase of p-[Ca2+]i of women with PIH. r-[Na+]i in mild and severe PIH were also significantly increased compared to normal pregnancy. No correlation between p-[Ca2+]i and r-[Na+]i and diastolic blood pressure was observed in normal pregnancy, but a positive correlation was observed in PIH. When the male platelets were incubated with serum from non-pregnant or normal pregnant women, p-[Ca2+]i did not show any significant changes. On the other hand, p-[Ca2+]i was significantly increased after the incubation with serum from PIH women. Moreover, p-[Ca2+]i was significantly increased after the incubation with 17 beta-estradiol, parathyroid hormone (PTH), or endothelin-1 (ET-1). These data suggest that the increase of p-[Ca2+]i and r-[Na+]i in PIH is important in the initiation and maintenance of hypertension by influencing peripheral vascular resistance, and also various factors in the serum of PIH women may contribute to the accumulation of intracellular ionized calcium in patients with PIH.
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PMID:[Cation metabolism and the effects of circulating factors in pregnancy induced hypertension]. 178

This study is aimed at examining the role of non-hemodynamic factors on the impaired microcirculation in patients with moderate essential hypertension. In a series of 31 patients (mean age, 47.8 +/- 1.1 years) with newly diagnosed untreated moderate essential hypertension (mean systolic blood pressure 161.7 +/- 2.0 mm Hg, mean diastolic blood pressure 102.4 +/- 1.5 mm Hg), parameters of the capillaroscopic examination of the finger microcirculation (mean number of capillaries, NRCAP), length of the capillaries (LECAP, microns), diameter micron) of the efferent (EFDI) and afferent (AFDI) apillaries, and mean red blood cell velocity (RBCV, microns/sec), which was measured by the flying spot technique, were correlated with a number of hormones (sampled after an overnight fast) including: plasma renin activity, aldosterone, and parathyroid hormone (PTH). A significant correlation (P less than .05) could be obtained between several parameters of the microcirculation and PTH:PTH (23.8 +/- 1.4 pg/mL)-NRCAP (14.9 +/- 0.5): r = -0.440, P = .013; PTH-AFDI (4.0 +/- 0.5 microns): r = 0.442, P = .012; PTH-EFDI (2.8 +/- 0.5 microns): r = 0.416, P = .019; PTH-RBCV (711 +/- 69 microns/sec): r = -0.351, P = .05. Furthermore, 24-h urinary norepinephrine (U-NOR) and afferent and efferent diameter of the capillaries intercorrelated significantly: U-NOR (46.0 +/- 6.2 micrograms/24 h)-AFDI: r = 0.439, P = .034; U-NOR-EFDI; r = 0.462, P = .025. This study shows that in patients with moderate essential arterial hypertension nonhemodynamic factors have an influence at the level of the microcirculation.
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PMID:Influence of nonhemodynamic factors on the microcirculation in moderate arterial essential hypertension. 178 51

Urinary excretion of sodium and calcium was examined in hypertensive (n = 8) and normotensive (n = 7) subjects following infusion of 2% saline at a rate of 11 mL/min for 90 min. The urinary sodium excretion was 204 +/- 38 (mean +/- SEM) muEq/min in normotensives and 233 +/- 28 muEq/min in hypertensives before infusion of saline and increased maximally to 499 +/- 114 muEq/min (P less than .05) and to 928 +/- 68 muEq/min (P less than .01), respectively, after saline infusion. In normotensives, urinary calcium excretion did not change significantly; however, in hypertensives excretion increased markedly (P less than .01) from 6.1 +/- 0.7 muEq/min to 12.3 +/- 1.6 muEq/min. Plasma atrial natriuretic peptide (ANP) levels increased significantly (P less than .05) in both groups. Serum ionized calcium and plasma parathyroid hormone (PTH) levels did not change significantly. The increments of urinary sodium and calcium and of plasma ANP, as well as the preinfusion plasma PTH level, were significantly (P less than .05) higher in hypertensives than in normotensives. The present study showed that exaggerated natriuresis was accompanied by hypercalcinuria and an enhanced rise in plasma ANP in hypertensives. Basal levels of plasma PTH were elevated in hypertensives. The calcium deficiency may be attributable to a close relationship between urinary sodium and calcium, and causally related to the disturbance of sodium and volume homeostasis in hypertension, which results in exaggerated natriuresis.
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PMID:Effect of saline infusion on urinary calcium excretion in essential hypertension. 182 96

Hypocalciuria is a feature of preeclampsia. The roles of parathyroid hormone (PTH) and vitamin D 1,25(OH)2D3 (calcitriol) in its pathogenesis have not yet been determined. Fourteen preeclamptic women were compared with 12 women with chronic hypertension and 11 normotensives, all in the third trimester. Preeclamptics had the lowest urinary calcium excretion rate (62.1 +/- 32.8 mg/24 hours) compared with chronic hypertensive women (162.6 +/- 97.8 mg/24 hours) and normotensive controls (225.6 = 146.9 mg/24 hours) (P less than .05). Serum PTH was lowest in preeclamptics (9.8 +/- 5.5 pg/mL), in contrast to the chronic hypertensives (18.5 +/- 2.7 pg/mL) and normotensives (16.4 +/- 3.2 pg/mL) (P less than .005). Similarly, urinary cyclic adenosine monophosphate (cAMP) excretion was 2.9 +/- 1.4 mumol/24 hours in the preeclamptics, 5.1 +/- 1.7 mumol/24 hours in the chronic hypertensives, and 4.6 +/- 1.3 mumol/24 hours in the normotensive group (P less than .05). These data suggest that the mechanism of hypocalciuria in preeclampsia is independent of the PTH-calcitriol axis. Therefore, it is suggested that the hypocalciuria of preeclampsia is due to intrinsic renal tubular dysfunction.
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PMID:Hypocalciuria of preeclampsia is independent of parathyroid hormone level. 184 25


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