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)

In order to determine whether pharmacologically-induced alterations in the spontaneous activity of neurons in the locus coeruleus are associated with changes in blood pressure, the activity of the locus coeruleus and blood pressure were recorded simultaneously in anesthetized rats after the administration of agents known to affect both of these parameters. Spontaneous activity of the locus coeruleus was decreased by intracerebroventricular (i.c.v.) administration of both clonidine and St 91, [2,(2,6-diethyl-phenylimino)imidazolidine chloride], a charged analogue of clonidine. However, only clonidine decreased the mean blood pressure after intracerebroventricular administration suggesting that either the receptors mediating decreases in the activity of the locus coeruleus are different to those mediating hypotension, or that St 91 does not distribute to sites involved in the control of blood pressure even after intracerebroventricular administration. Intravenous administration of clonidine, but not of St 91, decreased the activity of the locus coeruleus and produced a prolonged hypotension, thus suggesting a central mechanism for these effects. Both clonidine and St 91 administered intravenously, produced a brief initial period of hypertension which was not associated with consistent changes in the spontaneous activity of the locus coeruleus. Thus, noradrenergic agonists can decrease the activity of the locus coeruleus without affecting blood pressure, and increase blood pressure without affecting the activity of the locus coeruleus. The spontaneous activity of cells in the locus coeruleus was increased by 100% after the intracerebroventricular administration of corticotropin-releasing factor (CRF; 3.0 micrograms).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation of locus coeruleus activity and blood pressure. Effects of clonidine and corticotropin-releasing factor. 348 98

We performed computerized tomography (CT) of the brain in 22 patients, 2 to 18 years of age, with stable chronic renal failure (n = 6), on dialysis (n = 14) and after renal transplantation (n = 2). None suffered from a systemic disease known to affect the central nervous system (CNS) and none had overt CNS dysfunction at the time of the CT examination. The most striking pathological finding was brain atrophy, which was present in 13 patients (59%). In two patients cortical infarcts were present and one patient was found to have a hypodense area in the basal ganglia. The brain atrophy could not be related to the type of basic renal disease, the age of the patient, corticosteroid dosage, the duration of the renal failure or the presence of hypertension However, the mode of treatment, i.c. hemodialysis, seemed to be a risk factor. We assume that metabolic derangements and/or the accumulation of toxic substances due to the uremic state may be responsible for the brain atrophy in young patients with CRF. Recurrent osmotic changes of the brain during hemodialysis may aggravate the process of brain atrophy.
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PMID:Computerized tomography of the brain in children with chronic renal failure. 403 Feb 22

Early diagnosis of chronic renal failure in childhood is difficult, since the course of CRF shows in children with congenital renal diseases unspecific symptoms. The active cooperation of the practical pediatrician with a pediatric nephrologist enables this team for prevention of complications of chronic uremia. The integration of treatment between general pediatrician and specialist also prevents long hospitalisation and makes the prevention of the child for the best mode of treatment possible, i.g. ambulant hospital dialysis, home dialysis or CAPD. Pediatric dialysis should be performed in one of the established 14 pediatric dialysis centres in our country, because psychological, somatic and technical problems in children differ from those in adults. In dialysed children the general pediatrician should be further involved in treatment and may contribute worthy help in medical (control of drug compliance, hypertension) and psychosocial (school, employment) care of the chronic sick children. Even after successful renal transplantation the local pediatrician should continue to be involved in patient care, in spite of more frequent check up controls at hospital.
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PMID:[Integrated treatment of children with chronic renal insufficiency]. 636 10

The authors studied the blood aldosterone, cortisol, and kalium levels, the plasma renin activity and the aldosterone urinary excretion following L-Dopa (0,50 g per os) administration in five patients affected by hypertension and six healthy control subjects, before and after the CRF-ACTH system suppression. The observed pattern shows that the aldosterone biosynthesis is inhibited also after the CRF-ACTH system has been suppressed. Therefore the authors conclude that the inhibiting action of L-Dopa on the aldosterone biosynthesis is mediated by the dopaminergic system stimulation.
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PMID:[The dopaminergic system and aldosterone secretion. II. Effect of L-dopa and dexamethasone on aldosterone biosynthesis]. 701 72

Rats with 5/6 nephrectomy develop hypertension and progressive deterioration in renal function. Several mechanisms may contribute to hypertension and to progressive renal disease in these rats. We have shown that increased activity of the sympathetic nervous system may contribute to hypertension in rats we chronic renal failure. However, the role of the sympathetic nervous system activity in the progression of renal disease has not been investigated. We have evaluated whether neurogenic factors contribute to the progression of renal disease in the renal ablation model of chronic renal failure in the rat. Sprague-Dawley rats underwent 5/6 nephrectomy and dorsal rhizotomy or sham rhizotomy (CRF). Age-matched normal rats were used as controls. Six weeks after surgery, rats with chronic renal failure and dorsal rhizotomy had lower blood pressure and serum creatinine than rats with sham rhizotomy. In addition, kidneys from rats with 5/6 nephrectomy and rhizotomy manifested less severe glomerulosclerosis than kidneys from rats without dorsal rhizotomy. These studies have demonstrated in rats with renal ablation. Although normalization of blood pressure may definitely play a role, the data raise the possibility that neurogenic impulses to the kidneys may contribute to the progression of renal disease.
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PMID:Renal afferent denervation prevents the progression of renal disease in the renal ablation model of chronic renal failure in the rat. 748 45

The metabolic syndrome is discussed in terms of insulin resistance linked to an increased regulation of metabolism by cortisol and fatty acids. This change in hormonal balance is associated with diabetes, android (visceral) obesity, hypertension, hypertriglyceridemia, hyperapobetalipoproteinemia and low concentrations of HDL; a cluster of risk-factors that predisposes to the development of premature atherosclerosis. It is proposed that the metabolic syndrome is accompanied by a derangement in the hypothalamic-pituitary-adrenal-axis such that the effects of cortisol are exaggerated relative to those of CRF. Excessive action of fatty acids and cortisol causes insulin resistance and increase the hepatic secretion of glucose and VLDL. Furthermore, cortisol can decrease the uptake of LDL by the liver. Cortisol in the presence of relatively high insulin concentrations can promote the deposition of energy and lead to obesity. Chronic treatment of rats with D-fenfluramine has been shown to decrease the release of cortisol and fatty acids in response to stress, and to improve insulin sensitivity. The effects of D-fenfluramine were also tested in male JCR:LA corpulent rats which are prone to develop atherosclerosis and myocardial lesions. D-fenfluramine improved insulin sensitivity, decreased the hypertriglyceridemia, and prevented the development of necrotic myocardial lesions caused by ischemia. The data presented demonstrates a link between excessive action of cortisol and fatty acids in predisposing to insulin resistance and the pathologies that are associated with the metabolic syndrome.
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PMID:Role of glucocorticoids and fatty acids in the impairment of lipid metabolism observed in the metabolic syndrome. 755 May 41

The present study describes the relationship between the whole blood Pb, plasma Al and plasma V levels and the arterial hypertension, for four groups of individuals: 20 normotensive azotemic patients in periodic hemodialysis (CRF), 20 hypertensive azotemic patients in periodic hemodialysis (CRF-AHT), 20 individuals with severe essential hypertension and normal renal function (AHT) and 20 individuals with normal renal function and normal blood pressure (controls) evaluated during a period of 1 year. The renal population's blood Pb was comparable with that found in the non-renal groups. Blood Pb in the essential AHT was higher than in controls (P < 0.05). CRF and CRF-AHT showed higher Al levels than those individuals with normal renal function (P < 0.01). In CRF, plasma Al did not correlate with the arterial hypertension. Plasma Al was increased in the AHT individuals (P < 0.05) with respect to the control group, suggesting the possible influence of this metal in the appearance of the arterial hypertension. In this study, the CRF-AHT patients had plasma V statistically higher (P < 0.005) than controls. However, no differences were found between plasma V of CRF and CRF-AHT groups or between AHT and controls. These results suggest that V in AHT is of doubtful significance, except maybe when the renal failure and the arterial hypertension appear together. In summary, high levels of blood Pb and plasma Al are associated with arterial hypertension in individuals without renal disease. Higher plasma V levels were not found in hypertensives with normal renal function with respect to controls.
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PMID:The influence of the blood levels of lead, aluminum and vanadium upon the arterial hypertension. 775 2

Among 838 consecutive patients who underwent abdominal CT scan, adrenal incidentalloma was detected in 41 cases (4.7%). We performed high (8 mg/day) and low dose (2 mg/day) dexamethasone (DXM) suppression test and diurnal rhythm of plasma cortisol in these patients. Autonomic cortisol production was observed in one hypertensive patient in whom Cushigoid appearance was absent, suggesting pre-clinical Cushing's syndrome. We reviewed the endocrine results of the 65 reported cases of pre-clinical or non-Cushigoid Cushing's syndrome in world and Japanese literature. Urinary cortisol excretion was normal in 77%, plasma cortisol rhythm was absent in 70%, and high dose DXM failed to suppress plasma cortisol in 95% of cases. Plasma ACTH and cortisol showed subnormal to low responses to CRF administration similar to overt Cushing's syndrome. Therefore, CRF-test alone was considered insufficient to differentiate the two disorders. Hypertension and glucose intolerance were present in approximately 50% of cases in otherwise asymptomatic patients. Post-surgical steroid replacement was required in 55% of cases in Japan and in 75% of the cases world-wide. Women were affected more with pre-Cushing's syndrome than men. Peak incidence of the pre-Cushing's syndrome in women was in the forties which was older than that of overt Cushing's syndrome, suggesting that pre-Cushing's syndrome is not the predisposing condition to clinically symptomatic Cushing's syndrome. We consider that endocrine test is necessary in incidentally discovered adrenal tumors to exclude the presence of pre-clinical Cushing's syndrome.
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PMID:[Pre-clinical Cushing's syndrome: report of a case and the review of the literature]. 795 80

The causes of left ventricular hypertrophy (LVH) in chronic renal failure are multifactorial. The tail arterial pressure, heart weight, maximum developed pressure and pressure-volume relationship in animals with 5/6 nephrectomy (CRF, n = 16) and CRF animals who received furosemide by oral gavage (CRF-F, n = 17) were studied. All CRF animals increased their blood pressure (Basal: 117.2 +/- 0.8; 6th week: 184.8 +/- 2.9, p < 0.001) but in those treated with furosemide the blood pressure stayed within normal levels (Basal: 118.23 +/- 1.3; 6th week = 118.8 +/- 1.6, p = 0.5734). SHAM animals served as control (SHAM, n = 15). All CRF and CRF-F animals increased their levels of serum creatinine (CRF = 1.81 +/- 0.05; CRF-F = 1.75 +/- 0.05; SHAM = 0.72 +/- 0.09 mg/dL p < 0.001). Cardiac weight was elevated in CRF and CRF-F when compared with SHAM rats. The operational maximum developed pressure was similar in the three groups (CRF = 221.2 +/- 7.04; CRF-F = 255.7 +/- 10.1; SHAM = 239.9 +/- 5.5 mmHg, n.s.). However, the end-diastolic volume was significantly increased in both CRF and CRF-F when compared with SHAM rats (CRF = 91.4 +/- 9.44; CRF-F = 70.9 +/- 6.22; SHAM = 28.75 +/- 3.12 microL. p < 0.001). These data demonstrate that LVH in chronic renal failure is not dependent of the arterial hypertension, that accompanies this condition. Moreover, the systolic work of LVH animals is similar to that of normal animals, but a greater utilization of Frank-Starling mechanism to maintain normal ventricular function is needed.
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PMID:[Ventricular function in animals undergoing renal mass ablation. Effect of blood pressure control]. 824 6

Dietary phosphorus restriction can prevent the progression of renal failure in subtotally nephrectomized rats or in rats with nephrotoxic serum nephritis, independent of protein and caloric intake. Conversely, diets high in phosphorus content result in a more rapid deterioration of renal function. The results are less compelling in indicating that phosphorus restriction can slow the progression of renal failure in the clinical setting. The toxicity of phosphate appears to be related to induction of calcium phosphate precipitation, resulting in tubulointerstitial disease. Most studies of prevention of renal calcification have addressed a single pathway in the development of nephrocalcinosis. These include inhibitors of calcium phosphate precipitation, calcium channel blockers, or an inhibitor of PTH secretion. All of these studies have shown a beneficial effect in preserving renal function. It is possible that a combination of these agents, started early in the course of CRF, may have an additive effect in preventing the progression to ESRD. The discussion of other factors associated with progression of renal failure is beyond the scope of this review. It is obvious that dietary protein restriction, treatment of systemic and intraglomerular hypertension and lipid abnormalities, and prevention of iron overload, all play roles in the preservation of renal function in CRF.
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PMID:Role of phosphate retention in the progression of renal failure. 832 Apr 87


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