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)

Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.
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PMID:Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up. 898 42

In senescence renal function is thought to decline markedly even in the absence of renal disease. It has also been proposed that the changes in renal function with age are not uniform and that confounding factors such as hypertension or atherosclerosis may play a role. We performed a comprehensive study to compare several aspects of renal function in four groups: (i) young healthy normotensive subjects (N = 24; 13 males; mean age 26 +/- 3 years); (ii) elderly healthy normotensive subjects (elderly NT; N = 29; 13 males; 68 +/- 7 years); (iii) elderly treated and untreated hypertensive patients (elderly HT; N = 25; 13 males; 70 +/- 6 years); and (iv) elderly patients with compensated mild to moderate heart failure (elderly HF; N = 14; 6 males; 69 +/- 6 years). Compared to young subjects mean GFR (C(In)) and ERPF (C(PAH)) were significantly lower in the elderly, despite similar mean plasma creatinine levels (young, 121 +/- 11, 650 +/- 85 ml/min/1.73 m2; elderly NT, 103 +/- 11, 486 +/- 102; elderly HT, 103 +/- 13, 427 +/- 55; elderly HF, 92 +/- 14, 377 +/- 103). Nevertheless, GFR was within the normal range in the majority of elderly NT and HT, but not in elderly HF. ERPF was significantly lower in elderly HT as compared with elderly NT, and still lower in elderly HF. Mean renovascular resistance and filtration fraction were significantly higher in the elderly, particularly in elderly HT and HF as compared with the young. Mean fractional excretion of Na+ was similar in all groups studied, but the lithium clearance was significantly lower in the elderly, suggesting a greater proximal and less distal sodium reabsorption in senescence. In the elderly, mean PTH concentration and urinary excretion of pyridoline cross-links were significantly higher and mean 25-(OH)D3, calcitriol and phosphate concentrations significantly lower; the correlation between PTH and GFR was significant (r = -0.432, P < 0.001). The results document that the decrease in renal hemodynamics with senescence is less marked than suggested by some studies using less stringent methodology and inclusion criteria. Comorbid conditions confound renal function in the elderly. Age-associated changes in renal hemodynamics are accompanied by significant alterations of renal hormones and of renal sodium handling.
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PMID:Renal function in the elderly: impact of hypertension and cardiac function. 908 86

Na+/H+ exchange (NHE) was measured as maximal initial velocity of pH-dependent H+ efflux from red cells into an alkaline medium containing Na+ in patients with insulin-dependent or noninsulin-dependent diabetes, with and without hypertension and in normoglycemic, essential hypertensives and normal controls (50 subjects in each subgroup). Maximal velocities of NHE were found in microalbuminuric patients in all subgroups, and NHE correlated with the rate of micro-albuminuria (r = 0.61, p = 0.02). Daily insulin requirements were greater in those with elevated NHE (84 +/- 8 vs 42 +/- 4 U/day). There was no correlation between NHE and levels of plasma glucose, HbA1 and plasma aldosterone and lipid profile and PRA. NHE was correlated with plasma prolactin (r = 0.51, p = 0.02) and PTH r = 0.24, p = 0.05). In uremic patients, NHE was inversely correlated with creatinine clearance (r = -0.48, p = 0.03). Since calphostin C, a selective inhibitor of protein kinase C, lowered increased NHE in vitro, the protein kinase C-dependent pathway of the exchanger regulation was concluded to be responsible for NHE activation in diabetes mellitus and essential hypertension.
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PMID:[Red cell Na+/H+ exchange and role of protein kinase C in its stimulation in diabetes mellitus, essential hypertension and nephropathy]. 922 70

Based on our studies at the Hypertension research unit, we have found that the renin-angiotensin aldosterone. System (RAAS) undergoes several changes being the following the most relevant: Low plasma renin concentration (LPRC), while the plasma Aldosterone concentration is high (HPAC). At the same time we found calcium metabolism alterations: High urine calcium excretion, low serum ionic calcium and high PTH level. This alterations are more evident if the elder patient become hypertensive. We have found this changes in several groups in our community: black, ancient, obese and diabetic patients; who more often suffer hypertension and they must be followed up closely. In this group there are the sodium dependent hypertensive and they are the one who can get beneficial effects from the low salt diet and high calcium intake. When we studied the low plasma renin hypertensive we found the calcium changes mentioned before in ancient patient, as well as, high urine Zinc excretion. When we gave and oral calcium supplement to these patients, we saw that the calcium and Zinc alterations mentioned before were corrected. The high plasma renin concentration hypertensive patients showed low serum magnesium concentration and high urine magnesium excretion. A brief comment on the possible role of oxidative stress on essential hypertension is made.
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PMID:[Alterations of calcium, magnesium, and zinc in essential hypertension:their relation to the renin-angiotensin-aldosterone system]. 947 Dec 28

In patients with chronic renal failure cardiovascular morbidity and mortality are higher than in non-uremic controls. Chronic renal failure influences a number of factors that promote atherogenesis: blood pressure, nitric oxide activity, advanced glycosylation, lipid metabolism, oxidant stress, homocysteine levels, glucose metabolism and PTH. How these factors are influenced by chronic renal failure, how they interrelate and how they promote atherogenesis is still debated. Published data are for and against accelerated atherogenesis. The use of only clinical endpoints may be partially responsible for these conflicting data. Measurement of atherosclerosis itself by computerized ultrasound imaging of the common carotid arteries can be used as an outcome variable. We conclude that there is still a need for prospective, controlled, epidemiologic studies to answer the question whether or not atherogenesis is accelerated in chronic renal failure and to clarify the role of hypertension and other risk factors.
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PMID:Hypertension and accelerated atherosclerosis in endstage renal disease. 970 69

Twenty-five patients on long-term regular hemodialysis treatment (RDT) at our dialysis unit who underwent diagnostic cerebral computed tomography (CCT) participated in a study aimed at clarifying the pathogenesis of cerebral atrophy occasionally found at their original scan. The upper age limit was 55 years to exclude the physiological involutive brain changes occurring with age. Cerebral atrophy (CA), as defined morphologically (enlargement of cerebral sulci or an increased Evan's Index), was detected in all cases. Seventeen patients underwent magnetic resonance imaging (MRI) to define possible white matter changes more accurately. No significant correlation was found between the degree of atrophy and the following uremia-altered hematoseric parameters: creatinine, hematocrit, cholesterol, triglyceridemia, albumin, PTH, calcium, inorganic phosphate. There was no correlation between degree of atrophy and number of months the patients had been on RDT or time that passed between the finding of a creatinine clearance <30 ml/min and the start of RDT. Very high correlations were found between the degree of CA and predialytic blood pressure values, and between CA and the duration of hypertension (n = 13, r = 0.66, p < 0.013). Thus, hypertension seems to be an early cause of cerebral parenchymal damage in RDT patients, and should be promptly corrected.
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PMID:Hypertension as an etiopathological factor in the development of cerebral atrophy in hemodialyzed patients. 988 14

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, cephalgic women, it is often asymptomatic but it may be associated with ophthalmologic, neurologic and sometime non-characterizing endocrine disorders. We report here 71 cases of primary ESS observed and assessed during the last fourteen years. 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. cortisolemia, Aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, insulin hypoglycemia, etc.; inhibition tests: "overnight" and high dose dexamethasone. Clinical, radiological (skull radiographs, CT and/or MRI) and ophthalmologic (fundus, visual fields) assessment were made. We found principally cephalgia (52/71: 73.2%), hypertension (42/71: 59.1%), obesity (47/71: 66.1%). But we found especially mental disorders (57/71: 80.2%), in our knowledge not previously reported in the literature, as anxiety or dysthymic disorders with behavioural disturbances (chiefly oral compulsion). We found endocrinopathies in 36/71 (50.7%), isolated or coexisting in some patients: hyperPRL (14%), hypopituitarism (10.4%), hypogonadism (7%), diabetes insipidus (2.8%), hyperACTH (1.4%), hypoGH (15.4%), pituitary adenomas (8.4%). Several hypothalamic illness show a clinical picture including mental disorders and obesity. The Authors hypothesize that the ESS may be a "new" hypothalamic syndrome (compression/stretching on hypophysis and/or hypophyseal stalk by arachnoidocele; disorder of some hormones and neurotransmitters as leptin, neuropeptide Y, orexins, POMC-derived peptides, etc).
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PMID:[Primary empty sella syndrome. Observations on 71 cases]. 1020 96

We have previously demonstrated that genetically based leptin deficiency due to a missense leptin gene mutation in a highly consanguineous extended Turkish pedigree is associated with morbid obesity and hypogonadism. We have now performed detailed assessments of endocrine, sympathetic, and immune function. We have also identified a new adult female homozygous patient in this extended family who is severely obese and amenorrheic. In this family all wild-type and heterozgous individuals have normal body weight. Seven obese members of this family, whom we presume to have been leptin deficient, died during childhood. There are several findings that indicate potentially novel targets for leptin action in humans. Four homozygous patients (1 adult male, 2 adult females, and 1 child) have sympathetic system dysfunction, whereas all heterozygous subjects have normal sympathetic system function. Despite sympathetic system dysfunction and postural hypotension, 1 of 3 homozygous adult patients has impaired renin-aldosterone function. The patients also exhibit alterations in GH and PTH-calcium function, and 1 of them has decreased bone mineral density. Despite their obesity, these patients do not have risk factors for cardiovascular disease, such as hypertension, impairments in lipid metabolism, or hyperleptinemia [corrected]. These data support the hypothesis that the obese may have central, but not peripheral, resistance to the effects of leptin and that hyperleptinemia [corrected] may mediate the cardiovascular morbidity of the obese who are not leptin deficient. Furthermore, these data indicate that there may be several new targets for leptin action in human physiology. Such new targets may lead to novel pharmacological strategies for the use of leptin agonists and antagonists in the treatment of human disease. All 19 normal weight individuals in this family are alive, whereas 7 of 11 obese individuals died in childhood after infections. The odds ratio for mortality in the context of this obesity phenotype is 25.4, indicating that this mutation severely impairs key biological functions during childhood, negatively impacting on survival. We found that only the obese child in this family had thyroid function abnormalities. The oldest homozygous female patient started to menstruate, albeit with a luteal phase defect, 7 months ago, after a delay of over 20 yr, whereas the younger adult subjects are still hypogonadic. Thus, we conclude that due to their long life span, humans who survive the negative effects of leptin deficiency during childhood can, in contrast to ob/ob mice, over decades compensate some of the effects of leptin deficiency on immunity and endocrine function through mechanisms that remain to be elucidated.
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PMID:Human leptin deficiency caused by a missense mutation: multiple endocrine defects, decreased sympathetic tone, and immune system dysfunction indicate new targets for leptin action, greater central than peripheral resistance to the effects of leptin, and spontaneous correction of leptin-mediated defects. 1183 53

A family (a brother and a sister) of the familidal isolated hyperparathyroidism (FIH) was reported. The older brother with age of 58 year-old was pointed out hypercalcemic while examining his hypertension and proteinuria. He had high levels of serum total and ionized calcium, intact-PTH and gastrin, and hypophosphatemia. His neck CT scan revealed swelling of the two parathyroid glands in each side. He underwent resection of the tumors and the auto-implantation of the glands under diagnosis of primary hyper parathyroidism. Histopathology was diagnosed to be hyperplasia of the parathyroid glands. The younger sister with age of 52 year-old was referred to our clinic because she was suffering from recurrent urolithiasis. Biochemical examination of her blood sampling resulted in very resemble values of her brother mentioned above. Her neck CT scan showed three tumors consisting of each one at the bilateral parathyroid glands and one in the thymic region. She underwent resection of the tumors and the auto-implantation of the glands and histopathological diagnosis was hyperplasia as same as her brother's one. The postoperative courses of these cases have been uneventful for four years. FIH is a low significant disease of which ten lineages have been reported in Japanese literature although it should be differentiate with such a disease of multiple endocrine neoplasms.
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PMID:[Familial isolated hyperparathyroidism: a report of two cases]. 1068 81

The Dahl/Rapp rat model of hypertension is characterized by a marked increase in blood pressure and a progressive fall in glomerular filtration rate when salt-sensitive (S) rats are placed on an 8% NaCl diet. On the same diet, the salt-resistant (R) rat does not exhibit these changes. In previous studies we found that protein kinase C (PKC) upregulates Na(+)/Ca(2+) exchanger activity in afferent arterioles and mesangial cells from R but not S rats. One possible reason for the difference in PKC sensitivity may be due to differences in the S and R Na(+)/Ca(2+) exchanger protein. We now report the cloning of Na(+)/Ca(2+) exchangers from R (RNCX1) and S (SNCX1) mesangial cells. At the amino acid level, SNCX1 differs from RNCX1 at position 218 in the NH(2)-terminal domain where it is isoleucine in RNCX1 but phenylalanine in SNCX1. These two exchangers also differ by 23 amino acids at the alternative splice site within the cytosolic domain. RNCX1 and SNCX1 were expressed in OK-PTH cells and (45)Ca(2+)-uptake studies were performed. Acute phorbol 12-myristate 13-acetate (PMA) treatment (300 nM, 20 min) upregulated exchanger activity in cells expressing RNCX1 but failed to stimulate exchanger activity in SNCX1 expressing cells. Upregulation of RNCX1 could be prevented by prior 24-h pretreatment with PMA, which downregulates PKC. These results demonstrate a difference in PKC-Na(+)/Ca(2+) exchange activity between the isoform of the exchanger cloned from the R vs. the S rat. Lack of PKC activation of SNCX1 may contribute to a dysregulation of intracellular Ca(2+) concentration and enhanced renal vasoreactivity in this model of hypertension.
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PMID:Cloning of mesangial cell Na(+)/Ca(2+) exchangers from Dahl/Rapp salt-sensitive/resistant rats. 1089


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