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)

Parathyroid hormone's cardiovascular effects were assessed in a model of experimental hypertension with known abnormalities of calcium metabolism. Mean arterial pressure (MAP) changes and serum ionized calcium responses were measured in the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto (WKY), following injections of synthetic human PTH 1-34. Six 22-wk-old SHR and six WKY were given intra-arterial serial injections (0.1-100 micrograms/kg) of hPTH 1-34. Both the SHR (P less than 0.001) and WKY (P less than 0.001) demonstrated log dose-dependent hypotensive responses that were maximal at 1 min, with recovery occurring between 15 and 30 min. The slopes, however, of the dose-response curves differed (P less than 0.01). The SHR experienced a greater maximal delta MAP [-93.7 +/- 2.4 (SHR) vs. -71.2 +/- 1.6 mmHg (WKY), P less than 0.01]. Furthermore, the duration of the hypotensive action of hPTH 1-34 was significantly longer (P less than 0.001) in the SHR. Even when corrected for base-line MAP the SHR demonstrated a significant (P = 0.025) enhancement of this vasodilator response at doses of 5 micrograms/kg and greater at time intervals between 3 and 9 min after injection. A transient decrease [2.25 +/- 0.10 (pre) vs. 2.17 +/- 0.11 meq/liter (1 min post), P less than 0.01] in serum ionized calcium occurred at 1 min. We conclude that hPTH 1-34 is a potent vasoactive peptide in both the normotensive WKY and the SHR. The greater maximal hypotensive response to hPTH 1-34 and the prolongation of this cardiovascular effect in the SHR may be an additional manifestation of this experimental animal's acknowledged abnormalities of cellular membrane calcium and phospholipid metabolism.
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PMID:Vasodilation mediated by human PTH 1-34 in the spontaneously hypertensive rat. 669 83

PTH causes dose dependent transient vasodilatation in various vascular beds, specifically renal, coeliac, coronary, but not osseous. It has an acute dose-dependent hypotensive effect in the intact animal which is not mediated by alpha- or beta-adrenergic, cholinergic or histaminergic mechanisms. Aortic medial smooth muscle cells respond to PTH with an increase of cAMP, cGMP and, presumably via protein kinase, with activation of phosphorylase B kinase. The acute vasodilatory effect of PTH is antagonised by indomethacin and diclofenac as well as by ouabain, suggesting that the membrane Na-K pump and prostaglandins are involved in PTH-induced vasodilatation. Parathyroidectomy and a high calcium diet attenuate the rise of arterial pressure in experimental hypertension, pointing to some permissive effect of PTH for development hypertension. This is most likely due to long term effects of PTH on vessel wall calcium content and exchange. This chronic effect of PTH may explain the high prevalence of hypertension in patients with primary hyperparathyroidism.
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PMID:Vascular effects of parathyroid hormone (PTH). 675 27

Fourteen patients (six males and eight females) have been treated with chronic hemofiltration three times weekly for three to 27 months with the post-dilution technique. All patients had previously been on regular dialysis treatment. Patients were selected for hemofiltration because of dialysis-resistent hypertension (eight), symptoms of dialysis discomfort (five), hypertriglyceridemia (five) and polyneuropathy (seven). Hypertension improved in six of eight patients, symptoms of dialysis discomfort markedly diminished in all five patients, hypertriglyceridemia did not change consistently, polyneuropathy improved in six of seven patients. Balance studies of Na, Ca and Mg revealed a positive correlation to fluid balance. Phosphate, BUN, creatinine and uric acid increased. Loss of amino acids and protein is negligible. Hormone studies showed a decrease of T3, T4 and TSH though the pituitary-thyroid axis is intact, possibly indicating a decreased TRH activity. Vitamin D remained unchanged, PTH levels increased, possibly related to a diminished excretion of phosphate and diminished intake of calcium, respectively, during hemofiltration treatment as compared to hemodialysis.
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PMID:Chronic hemofiltration treatment. 736 95

We performed an echocardiographic and hemodynamic study in 10 patients with cath proven pulmonary arterial hypertension (PAH). The results show that the echocardiographic pattern of PTH such as flat diastolic pulmonary echo, premature closing, flutter, abscense of "A" wave, in creased opening velocity and changes in the right ventricular systolic time intervals, are equivocal. The most common echo finding in our study, was the increased opening velocity. Other echo data could be absent despite the true presence of pulmonary hypertension in a particular case. This report shows similar findings to a recent one published elsewhere (12) with no correlation between echo and hemodynamic data.
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PMID:[Echocardiographic evaluation of pulmonary arterial hypertension]. 746 12

Although calcium (Ca) is pivotal for the prevention of osteoporosis, its role in the prevention of other unrelated diseases such as arterial hypertension, cancer of the colon and nephrolithiasis is perplexing. No unitarian hypothesis explaining these unrelated effects of Ca has been postulated. Cytosolic Ca concentration is 10,000-fold lower than in the extracellular space, and this gradient is tightly maintained. Abnormal elevation of cytosolic Ca causes cell damage and death. Parathyroid hormone is a Ca agonist and the suppression of its secretion by Ca could explain the beneficial role of Ca intake in multiple diseases. Thus, parathyroid ablation improves hypertension in rats and cardiomyopathy in hamsters. Since anthropologic data suggests a higher Ca intake, of approximately 1,600 1,600 mg/day, in preneolithic than in modern diets, it is likely that our levels of PTH on genetically predisposed subjects with a loose cellular Ca control may aggravate frequent modern diseases and the process of aging. A higher Ca intake in both sexes should be one of the goals of preventive medicine of our time.
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PMID:Calcium, why and how much? 756 57

Primary hyperparathyroidism (HPTH) is frequently associated with hypertension. To date, the relationship between these two conditions is still not clear. We have studied 34 consecutive patients with primary HPTH due to a parathyroid adenoma. The diagnosis was later surgically confirmed in 32 cases. Ten of thirty-four HPTH patients were hypertensive. Before adenomectomy (PTHX) and 1-2 months after PTHX, we measured the following parameters in all patients: circulating levels of total and ionized Ca, intact immunoreactive parathormone (iPTH) (1-84), plasma renin activity (PRA), aldosterone, and daily total urinary catecholamine excretion. Moreover, 10 hypertensive HPTH patients, 10 normotensive HPTH patients, compared to 10 to 10 sex- and age-matched healthy normotensive subjects, underwent an acute norepinephrine test to assess vascular reactivity to a pressor agent. Before PTHX, no significant difference was observed between normotensive and hypertensive patients in all the above-mentioned variables, except for PRA and plasma aldosterone levels which were higher in hypertensive patients. Furthermore, the pressor response to the norepinephrine test was significantly greater in hypertensive HPTH patients than in the other 2 groups. After PTXH, serum Ca and intact iPHT (1-84) levels were reduced to normal values in all patients, while blood pressure, PRA and plasma aldosterone levels became normal in 8 of 10 hypertensive patients. The pressor response to the norepinephrine test was similar in the 2 groups. These results are consistent with the hypothesis of a direct effect of PTH on renin secretion which could contribute to the pathogenesis of hypertension and to the vessels sensitization to pressor agents.
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PMID:Hypertension and primary hyperparathyroidism: the role of adrenergic and renin-angiotensin-aldosterone systems. 756 68

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalalgic women. It is often asymptomatic but may be associated with ophthalmologic, neurologic and non-characterizing endocrine disorders. We report here 43 cases of primary ESS observed and assessed in our Departments of Internal Medicine from June 1983 to May 1993. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. Clinical, neurologic (skull radiographs, sellar stratigraphy, computed tomography scan and magnetic resonance), and ophthalmologic (fundus, visual fields) assessments were also made. Our findings fit with the data in the literature concerning common symptoms of ESS, associated endocrinopathies and other illness. We found obesity (62.7%), oligo-amenorrhea (16.6%), galactorrhea (14.6%), hyperPRL (11.6%), hypopituitarism (9.3%), hypogonadism (4.6%), diabetes insipidus (2.3%), (micro-)polycystic ovary syndrome (19%), hyperACTH (2.3%). In 9.3% of the cases, endocrinopathy referred to pituitary adenomas. Moreover, we noted a high frequency of psychological disorders, to our knowledge not previously reported in the literature, including anxiety or dysthymic disorders with altered behavior (chiefly oral compulsion). We also make the hypothesis that obesity (occurring in 62.7% of our patients) and hypertension (62.7%) may be related to hypothalamic alterations.
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PMID:[43 cases of primary empty sella syndrome: a case series]. 761 55

Although PTH and PTH-related protein (PTHrP) are vasodilators, prolonged exposure to elevated levels of PTH is often associated with hypertension. We investigated the effects of prolonged incubation with PTH or PTHrP on arterial segments and cultured vascular smooth muscle cells (VSMC). PTH or PTHrP transiently relaxed precontracted arterial segments within 10 min. Additional PTH or PTHrP added after 40-min exposure to these peptides had little effect on vascular tone, whereas forskolin, isoproterenol, isobutylmethyl-xanthine, or acetylcholine were still potent. In fura 2-loaded VSMC, 5-min incubation with PTH or PTHrP attenuated angiotensin II (Ang II)-induced calcium mobilization, an effect that was reduced by preincubation of VSMC with PTH for 1.5 h. Similarly, 1.5-h preincubation with PTH or PTHrP decreased the cAMP response to these peptides but not to forskolin or NaF. Ang II potentiated the cAMP response to PTH and PTHrP but was also subject to desensitization. Nle8, 18Tyr34 bovine PTH(3-34) amide did not desensitize vascular tissue to PTH or PTHrP. Our results suggest that homologous desensitization to PTH or PTHrP in vascular tissue requires receptor stimulation, occurs proximal to G stimulatory protein, and impairs attenuation of calcium mobilization by PTH or PTHrP. This may be a mechanism by which vasodilator effects of these peptides are decreased with prolonged elevation of PTH levels.
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PMID:Desensitization of vascular tissue to parathyroid hormone and parathyroid hormone-related protein. 775 Apr 71

The present study was undertaken to examine the effect of parathyroid hormone-related peptide (PTHrP) on the vascular tone as well as the expression of its mRNA in the cardiovascular system and its regulation in response to systemic hypertension in Sprague-Dawley rats. In aortic rings precontracted with 0.3 microM norepinephrine PTHrP(1-34) caused a dose-dependent relaxation with the maximal response of 33% being observed at 10(-6) M. PTHrP was nearly equipotent to PTH or CGRP in the vasodilatory action. Ribonuclease protection assay and Northern blot analysis demonstrated that PTHrP mRNA levels in the heart and aorta were increased as a result of systemic hypertension induced by constant infusion of angiotensin II and salt loading. The results of our in vivo studies suggest an autocrine/paracrine role for PTHrP as a local regulator of the vascular tone.
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PMID:Parathyroid hormone-related peptide as a locally produced vasorelaxant: regulation of its mRNA by hypertension in rats. 788 63

We retrospectively studied clinical problems for 55 patients with primary hyperparathyroidism who were operated on at our hospital. The chance to discovery of primary hyperparathyroidism and its accompanied symptoms were various. Other than classical symptoms, hypertension was noted in 12 patients and malignant tumors in 9. Forty-four percent of patients who had no bone related symptoms were found to have decreased bone mineral density (BMD). Even the patients with normal BMD were seen to increase the BMD, postoperatively. We thought that the parathyroidectomy was indicated for the asymptomatic patients with normal BMD. Biochemical investigation showed that positive rate were 50% for PTH-C, 94% for PTH-HS, 78% for intact PTH, 87% for serum total calcium and 98% for serum ionized calcium. Serum ionized calcium and intact PTH were useful for the diagnosis of patients who had normocalcemia or slight elevation of serum calcium. The sensitivity was 61% for ultrasound sonography (US) and 49% for computer tomography (CT) and scintigram, respectively. The detection rate of US and CT was positively related to the size of the parathyroid glands, but scintigram was not. The rate with which the parathyroid glands can be recognized during operation increased from 30% in the former group to 52% in the later group. As a result, 11% of the patients with adenoma had too much surgery and 29% of the patients with hyperplasia had too little surgery.
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PMID:[Clinical study of primary hyperparathyroidism--diagnosis, parathyroidectomy and late result of operation]. 812 Nov 14


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