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)

The prevalence of arterial hypertension in primary hyperparathyroidism (PHPT) is higher than in the general population. With the aim of determining the evolution of hypertension associated with PHPT, we analyzed a group of 56 patients followed for a mean of 60 months (range 10-101 months) after successful parathyroidectomy for PHPT. The study group consisted of 16 men and 40 women. The mean age was 49 +/- 12 years (range 18-73 years). None of the patients had renal impairment. Two hypertensive patients died during the follow-up from complications related to their hypertension. Twelve (21.8%) patients were hypertensive before parathyroid surgery (systolic greater than 160 mmHg and/or diastolic greater than 90 mmHg). Pre-operative midregion serum parathyroid hormone concentration was higher in the hypertensive patients than in normotensive patients (2.7 +/- 2.4 vs 0.82 +/- 0.4 mu iEq/l, p = 0.018). Pre-operative creatinine clearance was lower in the hypertensive patients than in normotensive patients (65.4 +/- 27.5 vs 86.7 +/- 26 ml/min, p = 0.002). There were no significant differences between normotensive and hypertensive patients in age, sex, body weight, clinical manifestations, weight of parathyroid tissue removed, and calcium metabolism, or in plasma concentrations of magnesium, uric acid, cholesterol, proteins, or albumin. During follow-up, none of the patients with pre-operative hypertension became normotensive, whereas 32% of the patients who were normotensive preoperatively developed clinical hypertension. The global prevalence of postoperative hypertension was thus 48%. The patients that developed hypertension after parathyroidectomy were followed for a longer period than the normotensive patients (76 +/- 17 vs 53 +/- 10 months, p = 0.005), had a lower postoperative creatinine clearance (74 +/- 28 vs 90 +/- 25 mg/min, p = 0.07), and higher cholesterol levels (6.2 +/- 1.5 vs 5.5 +/- 0.9 mmol/L, p = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of parathyroidectomy for primary hyperparathyroidism on arterial hypertension. 141 42

Recently, a parathyroid hypertensive factor was postulated to play a role in the pathogenesis of hypertension in genetically hypertensive rats. Therefore it was examined, whether in human parathyroid glands a vasopressor substance can be detected. For this purpose, homogenates of hyperplastic parathyroid glands from 20 patients with tertiary hyperparathyroidism were deproteinized and fractionated by gel chromatography. The fractions obtained were tested for vasopressor activity in isolated perfused rat kidneys. A vasopressor fraction containing substances of 0.6-2.5 kDa was identified in the parathyroid glands. The responsible product was heat sensitive, peptidase-, trypsin- and carboxypeptidase y- sensitive and hydrophilic, as it did not bind to hydrophobic reversed-phase gel. These results suggest that parathyroid glands contain a hydrophilic peptide-like vasopressor substance different from the parathyroid hormone.
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PMID:A vasopressor factor partially purified from human parathyroid glands. 141 52

Essential hypertension has been associated with disturbed calcium metabolism, but the available data are controversial. We measured parameters of calcium metabolism in groups of untreated male subjects (n = 78) with elevated diastolic blood pressure (101 +/- 6 mmHg, mean +/- SD) and age-matched male subjects (n = 79) with low diastolic blood pressure (62 +/- 4 mmHg). The participants of the study were drawn from a random population sample. Subjects with high diastolic blood pressure had significantly higher carboxy-terminal parathyroid hormone (PTH) plasma concentrations than controls with low diastolic blood pressure (median 114 vs. 43 pmol/l, P less than 0.01). The 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were comparable in both groups. Individuals with high diastolic blood pressure had significantly lower total serum calcium (2.41 +/- 0.10 vs. 2.47 +/- 0.10 mmol/l, mean +/- SD; P less than 0.01). PTH concentrations were correlated with diastolic pressure (r = -0.39, P less than 0.001). The data are compatible with increased parathyroid activity despite unchanged concentrations of vitamin D metabolites in human hypertension.
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PMID:Disturbed calcium metabolism in subjects with elevated diastolic blood pressure. 848 30

Recent evidence suggests a pathogenetic link between hypertension and insulin resistance. In addition, disturbances of vitamin D/parathyroid hormone axis have been reported in various hypertensive and insulin-resistant states. Chronic renal failure is characterized by high incidence of hypertension, insulin resistance and disturbances in the vitamin D/parathyroid hormone axis. Preliminary studies in both patients and rats with end-stage renal disease who were hypertensive, insulin resistant and 1,25-dihydroxycholecalciferol deficient with hyperparathyroidism; parenteral administration of pharmacological doses of 1,25-dihydroxycholecalciferol led to reversal of hypertension and insulin resistance without significant changes in serum calcium or parathyroid hormone concentrations. Thus, vitamin D deficiency may be an important factor in the pathogenesis of hypertension and insulin resistance in end-stage renal disease.
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PMID:The vitamin D/parathyroid hormone axis in the pathogenesis of hypertension and insulin resistance in uremia. 146 50

The effects of i.v. 1,25-dihydroxycholecalciferol (DHCC) on blood pressure and insulin sensitivity were studied in 7 patients on maintenance hemodialysis and compared with 7 healthy controls. Three days after discontinuing oral 1,25-DHCC, the dialysis patients were evaluated by glucose clamp studies to quantitate insulin sensitivity, with (+D) and without (-D) a prior single dose of i.v. 1,25-DHCC at 2 micrograms/m2. Blood pressure was measured just before the glucose studies. During -D studies, the patients were hypertensive (mean arterial blood pressure 108 +/- 2 mmHg, controls 84 +/- 4 mmHg, P less than 0.02) and insulin resistant (insulin sensitivity index 7.5 +/- 0.4 mg/kg.min per microU per ml, controls 14.2 +/- 0.7, P less than 0.01). i.v. 1,25-DHCC significantly reduced the mean arterial blood pressure (96 +/- 3 mmHg, P less than 0.05) and increased insulin sensitivity (10.9 +/- 0.5 mg/kg.min per microU per ml, P less than 0.02) in the dialysis patients. I.V. 1,25-DHCC did not change blood pressure and insulin sensitivity in the control subjects. During -D studies, serum concentrations of 1,25-DHCC were significantly lower in patients than controls (P less than 0.02). Serum 1,25-DHCC during the +D studies increased to supraphysiological levels in both patients and controls. Serum concentrations of intact parathyroid hormone, total and ionized calcium, magnesium, potassium, urea nitrogen and creatinine were not different between the +D and -D studies in either the dialysis patients or the controls. These results suggest that pharmacological doses of 1,25-DHCC may have therapeutic value in the treatment of hypertension and insulin resistance in dialysis patients.
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PMID:Amelioration of hypertension and insulin resistance by 1,25-dihydroxycholecalciferol in hemodialysis patients. 149 3

To determine whether obvious hemodynamic advantages of continuous ambulatory peritoneal dialysis (CAPD) over intermittent hemodialysis are reflected in superior cardiac structure and function, 16 of 55 analyzed CAPD patients (CAPD duration: 28 months) were followed over 35 months with echocardiography in a prospective analysis: 26 patients had died. LV dimensions (end-diastolic: 52 +/- 7 vs. 51 +/- 8 mm; control vs. follow-up) and systolic function (ejection fraction: 63 +/- 10 vs. 59 +/- 14%) were normal. Major findings were an increase in the amount of initially observed LV hypertrophy (251 +/- 68 vs. 342 +/- 135 g; p less than 0.03) and a decrease in mean LV volume/mass ratios (0.73 +/- 0.17 vs. 0.54 +/- 0.13; p less than 0.001). Excluding patients with dilated cardiomyopathy and valve disease, the amount of progression in LV hypertrophy was related directly to mean arterial pressure and cardiac output (n = 12; p less than 0.02) despite extensive use of antihypertensive medication (1.9 +/- 1.3 vs. 1.5 +/- 1.4 drugs/patient). No correlation was found with diastolic blood pressure, hemoglobin, serum parathyroid hormone, creatinine, urea, age, or CAPD duration. We conclude that LV hypertrophy is frequent in CAPD patients and further increases during long-term CAPD treatment. Factors contributing to the progression of LV hypertrophy are hypertension and hypercirculation.
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PMID:Progression of left ventricular hypertrophy in end-stage renal disease treated by continuous ambulatory peritoneal dialysis depends on hypertension and hypercirculation. 153 53

We previously reported that preeclampsia is associated with hypocalciuria (N Engl J Med 1987; 316:715). The purpose of this study was to determine whether alterations in calcium regulatory hormones are present in preeclampsia and, if so, whether they are responsible for hypocalciuria. Thirty-two pregnant women were studied in the second and third trimesters of pregnancy (11 women with preeclampsia, nine with chronic hypertension, and 12 normotensive women). 1,25-Dihydroxyvitamin D, C-terminal parathyroid hormone, ionized calcium, and urinary calcium excretion were measured. 1,25-Dihydroxyvitamin D was significantly lower in the women with preeclampsia in the third trimester when the disease developed (37.8 +/- 15 pg/ml) than in women with chronic hypertension (75 +/- 15 pg/ml, p less than 0.05) and normal women (65 +/- 10 pg/ml, p less than 0.05). Parathyroid hormone was higher, but not significantly, in those with preeclampsia. Ionized calcium was not significantly different among the three groups. Urinary calcium excretion was abnormally low for pregnancy (less than 50 mg/24 hr) in all but one women with preeclampsia. We conclude that 1,25-dihydroxyvitamin D is reduced in preeclampsia and may lead to hypocalciuria by causing decreased intestinal absorption of calcium, stimulation of parathyroid hormone, and increased distal renal tubular resorption of calcium. The cause of reduced 1,25-dihydroxyvitamin D in preeclampsia is unknown and may be due to either diminished renal or placental production of the hormone.
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PMID:Abnormal 1,25-dihydroxyvitamin D metabolism in preeclampsia. 156 88

Recent research provides evidence that parathyroid hormone is implicated in the pathogenesis of genetic hypertension. Abnormalities in calcium metabolism in genetic hypertension have been reported. These include hypercalciuria, depressed serum ionized calcium associated with enhanced serum parathyroid hormone levels. Calcium supplement resulted in normalization of calcium metabolism and reduction in blood pressure. In addition, removal of parathyroid glands attenuated the rise in blood pressure in genetic hypertensive rat. This review focuses on the links between calcium metabolism and calcium endocrine system abnormalities and the etiology of experimental genetic hypertension. The mechanisms by which dietary supplement and parathyroidectomy lower genetic hypertension are also discussed. Although the causality of raised parathyroid hormone in genetic hypertension is not yet fully understood, we conclude that this hormone may play a permissive effect in the development of hypertension.
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PMID:Parathyroid hormone and genetic hypertension. 161 92

Cloned rat parathyroid cells (PTr cell line) that produce parathyroid hormone-related peptide plus endothelin 1 and primary cultures of human parathyroid cells were tested for growth and differentiation responses to atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). High- and low-affinity binding sites for ANP were found on PTr cells; BNP appeared to bind to the same receptors with similar affinities. Either ANP or BNP stimulated production of cGMP and caused a 30% decrease in Na(+)-K(+)-Cl- cotransport. Each peptide increased synthesis and secretion of endothelin 1 by PTr cells in a dose-dependent fashion, but cell growth was not affected. Human parathyroid cells (normal and pathological) also responded to ANP or BNP with an increase in cGMP production. The finding of receptors for natriuretic hormones on parathyroid cells with consequent effects on release of endothelin 1 might be of relevance in understanding the clinical association between hyperparathyroidism and hypertension.
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PMID:Natriuretic peptide receptors regulate endothelin synthesis and release from parathyroid cells. 165 Apr 71

The effects of insulin on Na(+)-H+ exchange were examined in isolated proximal segments from normotensive Sprague-Dawley (SD) and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with monitoring of rates of intracellular pH change (delta pHi/min) and ethylisopropyl amiloride (EIPA)-suppressible 22Na+ uptakes. A 12-min insulin preincubation was necessary for steady-state 22Na+ uptake and rate of pHi change. Insulin responses were similar for 4-wk (prehypertensive) SHR and WKY tubules; 8- (rising hypertension) and 16-wk (established hypertension) SHR responses were increased (P less than 0.05) 23 and 36% with 10(-6) M insulin, respectively. Insulin-like growth factors (IGF-I, IGF-II; 10(-10)-10(-7) M) had no effect on Na(+)-H+ exchange activity. Incubation with physiological concentrations of insulin in combination with hormones that stimulate Na(+)-H+ exchange (angiotensin II; alpha-adrenoceptor agonists) demonstrated no synergistic increases in SHR or WKY tubules; incubation with hormones that inhibit Na(+)-H+ exchange [parathyroid hormone (PTH), dopamine (DA)] indicated that insulin stimulation was decreased with PTH or DA in WKY segments, but PTH or DA reduction of insulin stimulation was lacking in SHR tubules. In summary, these data indicate a direct stimulation by insulin of Na(+)-H+ exchange in the proximal nephron, indicate an increased responsiveness in SHR compared with WKY tubules, and suggest a modulatory role of insulin with other hormones in regulating proximal nephron Na(+)-H+ exchange.
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PMID:Insulin increases Na(+)-H+ exchange activity in proximal tubules from normotensive and hypertensive rats. 167 43


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