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

Several abnormalities of calcium metabolism have been described in patients with essential hypertension, and they have been linked to the pathogenesis of hypertension. Intestinal calcium absorption has been shown to be decreased in rats with spontaneous hypertension, but it has not been studied in patients with essential hypertension. In these studies we have for the first time measured intestinal absorption of calcium (using oral and intravenous administration of 47Ca), along with other parameters of calcium metabolism, in 14 patients with essential hypertension and normal renal function and in 16 normal subjects. There was no difference in serum total or ionized calcium, serum phosphorus, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), and 24,25-dihydroxy-vitamin D(24,25(OH)2D) among hypertensives and normotensives. The urinary excretion of calcium, on the other hand, was greater in hypertensive than in normotensive subjects (195 +/- 33 v 107 +/- 13 mg/24 h, P less than .05). There was also no difference in intestinal absorption of calcium after 2 and 24 h among hypertensives and normotensives. When hypertensive patients were stratified according to plasma renin activity (PRA) we found that patients with low PRA had higher intestinal absorption of calcium at 2 h (23 +/- 2.9 v 18 +/- 0.6%, P less than .05) but not at 24 h. Serum total and ionized calcium, PTH, and 1,25(OH)2D were not different between patients with low and those with normal-high PRA. The major derangement of calcium metabolism in patients with essential hypertension is hypercalciuria. This abnormality is more pronounced in patients with low PRA, and it may lead to increased vitamin D-dependent intestinal absorption of calcium.
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PMID:Intestinal absorption of calcium and calcium metabolism in patients with essential hypertension and normal renal function. 206 73

The decrease in arterial blood pressure in patients with essential arterial hypertension treated with clonidine is associated, in 88.9% of cases, with a rise in serum inorganic phosphorus. The increase of inorganic phosphorus in the serum of patients with hypophosphataemia, during clonidine therapy, is higher (P less than 0.001) than in hypertensive patients with normal values of serum phosphorus (P less than 0.01). This effect is more significant in overweight hypertensive patients (P less than 0.0005) than in normal weight hypertensives (P less than 0.02). No correlation was noted between the rise of serum inorganic phosphorus and the decrease in systolic and diastolic arterial blood pressure. The rise of serum phosphorus concentration in hypertensive patients is attributed to inhibition of insulin release and enhancement of growth-hormone secretion induced by clonidine.
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PMID:Effect of clonidine on serum inorganic phosphorus in patients with essential arterial hypertension. 209 11

The concentration of serum inorganic phosphorus was determined in 162 patients with essential arterial hypertension (EAH) and in 71 control subjects. The serum phosphorus level was lower in patients with essential arterial hypertension than in the control subjects, and the differences were higher in the advanced stages of the disease. The lowest level of serum phosphate concentration was noted in overweight hypertensive patients, probably in relation to an enhanced insulin secretion. In control subjects the serum concentration of phosphate decreased with advancing age.
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PMID:Hypophosphatemia in patients with essential arterial hypertension. 213 90

The effects of an orally active inhibitor (UK 79300) of the neutral metalloendopeptidase EC 3.4.24.11 were investigated in six healthy male volunteers maintained on a constant diet (150 mmol sodium/day and 80 mmol potassium/day). Subjects were studied in a random order, single-blind study on two occasions, each 48 hours in length, when they were given UK 79300 (25 or 50 mg p.o.) or placebo at 12-hour intervals (each agent for 24 hours). The endopeptidase inhibitor enhanced plasma concentrations of atrial natriuretic factor in association with suppression of both plasma renin activity and aldosterone concentrations. Twenty-four-hour urinary excretion of sodium was doubled by UK 79300, and the urinary excretion rates of phosphorus, atrial natriuretic factor immunoreactivity, and cyclic guanosine monophosphate were also significantly enhanced, whereas urinary aldosterone excretion was halved. The profile of biological effects closely paralleled those previously reported with low dose infusions of atrial natriuretic factor in humans and animals. Therapeutic trials of such inhibitors are now indicated for hypertension or heart failure together with further studies to clarify the underlying mechanisms of action.
Hypertension 1990 Sep
PMID:Inhibition of endopeptidase EC 24.11 in humans. Renal and endocrine effects. 214 60

To study the functional and metabolic correlates of left ventricular hypertrophy [LVH] in non-human primates, 7 hypertensive baboons [papio anubis] with 4.6 +/- 0.1 years of hypertension produced by a two-kidney one-clip model, and echocardiographically documented concentric LVH underwent serial phosphorus-31 [P-31] NMR Spectroscopy studies at rest and during inotropic cardiac stress produced by dobutamine infusion [5 micrograms/kg/minute]. Responses in LVH baboons were compared to those in 5 normotensive, sex and weight-matched control animals. The ratio of P-31 NMR-S derived inorganic phosphates [Pi] to phosphocreatine [PCr] was significantly greater at rest in LVH baboons [0.53 +/- 0.06 versus controls = 0.41 +/- 0.17; P less than 0.05]. With dobutamine drug stress, the Pi/PCr ratio rose significantly in LVH baboons [0.77 +/- 0.15 versus 0.56 +/- 0.16; P less than 0.05 at 15 minutes]. Despite hemodynamic recovery, the 5 minute post-dobutamine Pi/PCr ratio remained elevated compared to baseline in LVH baboons only [0.78 +/- 0.16 versus 0.53 +/- 0.06; P less than 0.05]. In pre-instrumented baboons [n = 5], the 'transfer function' of cardiac work [heart rate x LV end-systolic pressure x + dp/dt max] versus Pi/PCr ratio was abnormally shifted rightward and downward [r = 0.80] with LVH as compared to the linearly increasing response in controls. We conclude that in vivo P-31 NMR Spectroscopy studies during dobutamine stress demonstrate reduced PCr stores, delayed metabolic recovery following cessation of inotropic stress, and an abnormal rightward shift in the 'transfer function' in LVH baboons.
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PMID:In vivo phosphorus-31 NMR spectroscopy of abnormal myocardial high-energy phosphate metabolism during cardiac stress in hypertensive-hypertrophied non-human primates. 214 66

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

Captopril, an orally active angiotensin I-converting inhibitor, is an effective drug in the treatment of hypertension in adults and children. The use in newborn infants has been, nevertheless, short. We report five cases of hypertension in newborn infants poorly responsive to large doses of other potent antihypertensive agents: furosemide, propanolol and hydralazine. We have got a reduction in mean blood pressure in three cases, with doses of 0.1-0.2 mg/kg/day for a time lesser than a month. Another patient had a reduction with high doses (5 mg/kg), showing increase in mean serum urea, creatinin, potassium and phosphorus levels. This effect disappeared after captopril was discontinued. We suggest the use of captopril in hypertension non-responsive to other antihypertensive agents, mainly in those of renovascular cause.
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PMID:[Captopril treatment of neonatal arterial hypertension]. 218 32

Patients who lose more than 50% of their functioning renal mass are at risk to develop progressive deterioration of their remaining kidney function, even though the process that caused the original loss of kidney function may no longer be present. The glomerular capillary hyperperfusion, hypertension, and hyperfiltration that occur in the surviving nephrons may play an important role in the natural tendency for renal function to deteriorate. Nevertheless, recent studies suggest that these glomerular hemodynamic events may not be the final common pathway for the natural deterioration of renal function, as was once thought. With regard to the general management of patients with impaired renal function, recent evidence suggests that controlling systemic blood pressure, reducing dietary protein and phosphorus intake, and controlling hyperlipidemia may be effective in slowing the loss of renal function.
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PMID:On the natural tendency to progressive loss of remaining kidney function in patients with impaired renal function. 219 55

Alterations of calcium metabolism have been described in human essential hypertension and experimental hypertension. We investigated the interrelationship of parathyroid hormone (PTH) and 1,25(OH)2-vitamin D (1,25(OH)2D) in patients with untreated essential hypertension as compared to normotensive controls. The hypertensive subjects (n = 75; 43 men, 32 women) had a mean blood pressure of 138 +/- 8/95 +/- 5 mm Hg as compared with 120 +/- 11/80 +/- 8 in the normotensive group (n = 40; 22 men, 18 women). Serum PTH was measured with an intact molecule immunochemiluminometric assay and 1,25(OH)2D was measured with radioimmunoassay after HPLC separation. Hypertensive men had PTH levels that were 36% higher than normotensive men (5.3 +/- 2.9 v 3.9 +/- 0.8 pmol/L, P = .005). When blood pressure was analyzed as a continuous variable, there was a direct correlation between it and serum PTH in men (r = .31, P = .004). In women, by contrast, there was no difference in serum PTH between hypertensive and normotensive subjects and no relationship between blood pressure and the serum PTH concentration. Blood pressure was inversely correlated with serum phosphorus levels in both sexes (r = -0.20, P = .04). In men, the elevated serum PTH levels and depressed serum phosphorus levels would have predicted that serum 1,25(OH)2D would be higher in the hypertensive subjects. However, that was not observed, as serum 1,25(OH)2D was slightly lower in hypertensive (38.3 +/- 15.2 pg/mL) than normotensive men (42.7 +/- 11.3, P = .21).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium regulating hormones in essential hypertension. Importance of gender. 222 63

Little notice has been paid in the surgical literature to problems with psychoeffective lithium, which by interfering with adenylate cyclase affects thyroid and parathyroid function, causing hypercalcemia, hyperparathyroidism, and hypothyroidism. Seven patients with lithiumogenic hyperparathyroidism occurring after years of lithium therapy underwent treatment and manifested osteoporosis (n = 2), hypertension (n = 2), nephrolithiasis (n = 1), coma (n = 1), rising hypercalcemia (n = 1), goitrous myxedema (n = 4), nephrogenic diabetes insipidus (n = 2), renal failure (n = 2), and hyperlipidemia (n = 1). Disease-directed parathyroidectomy (without morbidity) was curative. Unique laboratory findings included normal serum phosphorus and reduced urinary calcium and cyclic adenosine monophosphate values. Three separate cases of thyroid carcinoma after long-term lithium therapy were also treated, being preceded by myxedema (n = 2) and concurrent with hyperparathyroidism (n = 1). There has been only one previous report of lithium-associated thyroid carcinoma. All patients taking lithium should undergo surveillance for thyroid and parathyroid dysfunction and neoplasia, and appropriate surgical and medical treatment should be considered in each situation. Although hyperparathyroidism may be reversible with lithium discontinuance, such therapy may be obligatory for patient well-being, thus dictating parathyroidectomy.
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PMID:Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. 224 24


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