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

A 52-year-old woman was admitted to our hospital for further examination of central obesity, hypertension and hirsutism suggesting Cushing's syndrome. Hirsutism had been remarkable for two years, and muscle weakness of the lower extremities gradually developed during the past year. CT scan revealed a tumor in the left adrenal gland which was 1 cm in diameter, round, well-circumscribed, homogeneous and not enhanced. Endocrine data disclosed increased urinary 17-OHCS (11.5-16.4 mg/day) and elevated plasma ACTH (125 pg/ml) and cortisol (19 micrograms/dl) with a lack of diurnal rhythm. Administration of the single-dose dexamethasone (1mg) did not suppress plasma cortisol. However, consecutive administration of either 2mg or 8mg of dexamethasone for 2 days suppressed both plasma cortisol and urinary 17-OHCS. Administration of metyrapone raised both urinary 17-OHCS and plasma ACTH levels. Rapid ACTH test resulted in a hyperresponse of plasma cortisol. CRF injection raised plasma ACTH and cortisol. Bilateral adrenal glands were well demonstrated by 19-iodocholesterol (I-131) scintigraphy during the administration of dexamethasone. MRI with Gd-contrast revealed a microadenoma in the sella turcica. With the diagnosis of Cushing's disease, the microadenoma was removed by the transsphenoidal approach and adrenal function was normalized. However, the left adrenal tumor remained on CT scan but was not demonstrated by scintigraphy. These findings indicate that this is a very rare case of Cushing's disease which was associated with an unilateral non-functioning adrenal tumor.
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PMID:[A case of Cushing's disease associated with a non-functioning adrenal tumor]. 129 36

A humoral inhibitor of the membrane calcium pump was studied in plasma from 28 normal controls, 33 patients receiving long-term hemodialysis, and 26 with chronic renal failure (CRF; creatinine clearance range was 6 to 97 ml/min). Calcium pump activity was measured as the rate of Sr2+ efflux in normal erythrocytes (RBCs) loaded with Sr2+ (a substitute of Ca2+ in the calcium pump). Plasma, and plasma ultrafiltrates from hemodialysis patients strongly inhibited calcium pump activity compared with controls without plasma (36 +/- 18 vs. 25 +/- 12, %INHIBITION/CONTROL, P < 0.05). Inhibition markedly decreased with acute hemodialysis (16 +/- 12 vs. 5 +/- 14, %INHIBITION/NORMAL PLASMA, N = 15, P < 0.001). In CRF, degree of inhibition correlated with the serum creatinine concentration (r = 0.75, P < 0.001). A kinetic study showed that plasma decreased the maximal rate of the Ca2+ pumps (Vmax) without affecting the apparent affinity for internal cations (KSr). Moreover, the plasma inhibitory factor had a low molecular weight, and was dialyzable and heat stable. In conclusion, we found evidence for an RBC membrane calcium pump inhibitor in uremic plasma, which correlates with the degree of renal insufficiency. Possibly, it may increase calcium content in RBCs and other cells and could thus be related to uremic toxicity and/or hypertension.
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PMID:A circulating inhibitor of the RBC membrane calcium pump in chronic renal failure. 133 28

The use of anthropometric measurements of triceps (TSF) and subscapular skinfolds (SSF) and mid-upper arm muscle circumference (MAMC) was examined as far as the diagnosis of energy-protein malnutrition (EPM) is concerned. The study was undertaken in five groups of patients (n = 231): arterial hypertension (AH, n = 63), chronic obstructive pulmonary disease (COPD, n = 17), hemodialyzed chronic renal failure (CRF, n = 19), critically ill patients with an acute event (CA, n = 42) and critically ill patients with chronic diseases (CCD, n = 90). The results were compared to those obtained in a group of healthy individuals (control group, n = 102). The control group and the group of patients were allocated in subgroups according to sex and age (less than 50 and more than 50 years). It was expected that significant differences would be found for the anthropometric values between the control subgroups and the COPD, the CRF and the CCD subgroups of patients. For the skinfold thicknesses (TSF and SSF), significant differences were found between CRF, CCD subgroups and the control subgroups under fifty years of age; however, the differences were not significant when the subgroups over fifty were analyzed. Concerning the MAMC, significant differences were found: 1 degree) between the CRF subgroups (males and females) and the control subgroups under fifty years of age; 2 degrees) between the CCD male subgroups (younger and older subgroups) and the respective control subgroups and 3 degrees) between the COPD and the control subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The use of skinfolds and of the muscle circumference of the upper arm in the diagnosis of protein-energy malnutrition in adults patients: a critical study]. 134 Jun 6

The anionic component of sodium salt has been reported to contribute to hypertension in some animal models and hypertensive patients. In the present study, the anionic effects on exacerbation of hypertension in spontaneously hypertensive rat (SHR) were investigated by chronic loading tests with two sources of sodium, viz. sodium chloride (NaCl; 0.9% solution) and sodium bicarbonate (NaHCO3; 1.28% solution), using SHRs with normal renal function (NRF) and with chronic renal failure (CRF; produced by cryosurgery). In addition, extracellular fluid volume (ECFV: inulin space) was measured in SHRs with NRF and CRF. In the NRF groups, systolic blood pressure (SBP) reached 230 mmHg at Week 13, and there was no significant difference in SBP between the NaCl and NaHCO3 groups. In the CRF groups, SBP of the NaCl group was significantly higher (p less than 0.01) than that of the NaHCO3 group (280 mmHg vs. 230 mmHg at Week 15). ECFV was also greater in the NaCl group than in the NaHCO3 group (ECFV: NaCl vs. NaHCO3, 15.9 +/- 1.7 vs. 14.0 +/- 0.9 at Week 13; and 16.2 +/- 1.1 vs. 14.2 +/- 1.2 at Week 15, respectively). These results indicate that chloride ion plays an important role in the pathogenesis of hypertension in SHR with CRF. Expansion of ECFV is considered to be one of the mechanisms whereby the hypertension is exacerbated.
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PMID:Effect of dietary chloride on spontaneously hypertensive rat. 177 41

We investigated lipoprotein profile of 18 non-dialysis patients with CRF and 17 patients on hemodialysis, and studied effect of LPD plus EAA on lipid metabolism of 18 non-dialysis patients with CRF. The results revealed that total triglyceride, cholesterol, LDL, VLDL, and semi-quantity of ApoCII, ApoCIII were significantly increased, and HDL, ApoAI ApoAI/ApoB rate, semiquantify of ApoCI were significantly reduced in non-dialysis patients and patients on hemodialysis; VLDL and Ccr were closely negative related in non-dialysis patients. The lipid abnormalities were more severe in non-dialysis patients complicated with hypertension than without hypertension. After 6 to 10 weeks' LPD plus EAA treatment in 18 non-dialysis patients, total triglyceride, cholesterol, LDL, VLDL were significantly reduced, and HDL, ApoAI, ApoAI/ApoB were significantly increased. We conclude that it is characterized by type IV hyperlipidemia in lipid abnormalities of patients with CRF, and LPD plus EAA treatment may improve it effectively.
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PMID:[Effect of low protein diet, plus essential amino acids on lipid metabolism in patients with chronic renal failure]. 186 71

We have retrospectively examined 324 patients with chronic renal failure and evaluated the probable underlying causes of neurologic complications, laboratory data and therapeutic interventions. The common neurologic problems in our patients were alterations in consciousness (40.7%) and convulsions (35.1%). When BUN concentration was above 135 mg/dl and creatinine clearance was below 8 m/min/1.73 m2, alteration of consciousness was observed and when BUN concentration was 200 mg/dl and creatinine clearance was below 7 m/min/1.73 m2, abnormal convulsives appeared. Changes in deep tendon reflexes and pathologic reflexes were associated with hypertension. All of the patients with cortical atrophy using computerized cranial tomography aluminum hydroxide at least for 18 months, and six of them had hemodialysis. Fourteen patients who underwent dialysis developed convulsions and were thought to have disequilibrium syndrome. These findings are consistent with the suggestion that the metabolic and biochemical derangements associated with CRF may be particularly detrimental to the still developing CNS of the child.
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PMID:Neurologic complications in chronic renal failure: a retrospective study. 224 42

Renal function was evaluated in normal and after 30 days of 5/6 renal mass reduction (CRF) in Munich-Wistar (MW) rats, spontaneously hypertensive rats with superficial glomeruli (EPM), and in Brattleboro rats with congenital diabetes insipidus (DI). Mean arterial pressure was higher in EPM-Control and EPM-CRF rats as compared with MW and DI rats. MW and EPM rats with CRF showed increases of 120% and 196%, respectively, in single nephron glomerular filtration rate as compared with their controls. However, DI rats with CRF did not show any increase in single nephron glomerular filtration rate as compared with the control group. Therefore, the data suggest that the presence of hypertension enhances the adaptive mechanisms on remnant kidney's function. Conversely, in the absence of antidiuretic hormone, adaptive mechanisms of remnant nephrons did not occur. In addition, it was observed that rats with CRF submitted to prostaglandin blockade with indomethacin showed for MW rats a 55% and 20% reduction in ultrafiltration coefficient and in single nephron glomerular filtration rate, respectively. Decreases of 60% and 30% in ultrafiltration coefficient and single nephron glomerular filtration rate, respectively, were observed for EPM rats. In contrast, DI rats did not show any alteration on renal function after indomethacin. It seems, therefore, that prostaglandins play a role in remnant nephron function of MW and EPM rats, but in the absence of antidiuretic hormone, prostaglandins do not affect remnant glomerular hemodynamics.
Hypertension 1990 Feb
PMID:Effects of systemic hypertension, antidiuretic hormone, and prostaglandins on remnant nephrons. 229 77

Corticosteroid-dependent hypertension can be cured by surgical removal of steroid-producing adrenocortical adenomas or, in case of other etiopathologic factors, specific drug therapy may be introduced for preventing irreversible complications of the hypertension process. In most cases, corticosteroid-dependent hypertension fails to manifest itself with clearcut endocrine symptoms. Therefore, an endocrine evaluation is strongly recommended in all patients with hypertension who are susceptible to hypokalaemia and whose blood pressure is poorly controlled with conventional antihypertensive drugs. The increased blood pressure in corticosteroid-producing adrenocortical adenomas may be attributed not only to the main glucocorticoid, cortisol, and the main mineralocorticoid, aldosterone, but also to the actions of weak mineralocorticoids which may be occasionally predominant. Adrenocortical adenomas including incidentalomas produce in different quantities at least 6 corticosteroids which play direct or indirect roles in hypertension. These adenomas are lacking autonomous hormone secretion and they respond to different regulatory impacts (i.e. stress and, by analogy, CRF or ACTH administration) with markedly-increased hormone secretion. Consequently, hypertension and hypokalaemia develop, often in the absence of other endocrine symptoms. The weak mineralocorticoids may not entirely account for the hypertension, although they may be useful indicators or may serve as precursors for the generation of more potent hypertensinogen steroids and steroid metabolites. This is patently indicated by the disappearance of hypertension, hypokalemia and mineralocorticoid-excess induced suppression of the renin-angiotensin system after the surgical removal of adrenocortical adenomas which produce only weakly-hypertensinogen corticosteroids.
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PMID:[The hypertensive role of corticosteroids in the light of adenoma of the adrenal cortex]. 266 40

The case is described of a 61-year-old male who presented with hypertension and Cushing's syndrome which resolved on excision of a unilateral adrenal mass. Histology of the tumour revealed a benign phaeochromocytoma which immunostained for corticotrophin-releasing factor (CRF-41) but not for ACTH. Preoperative plasma concentrations of immunoreactive CRF-41 were increased, and gradients for both CRF-41 and ACTH were demonstrated across the tumour. Post-operatively, CRF-41 was undetectable in plasma. The tumour contained high concentrations of immunoreactive CRF-41 which co-eluted with synthetic human CRF-41 on reversed-phase high-performance liquid chromatography. Tumour CRF-41 stimulated the release of ACTH in a dose-dependent manner from isolated rat anterior pituitary cells. We conclude that this tumour secreted CRF-41 and ACTH and had the capacity to produce ACTH-dependent Cushing's syndrome directly by secreting ACTH and indirectly by secreting CRF-41 to stimulate ACTH secretion from the anterior pituitary.
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PMID:A phaeochromocytoma presenting with Cushing's syndrome associated with increased concentrations of circulating corticotrophin-releasing factor. 303 46

Angiotensin II and CRF are but two of the several regulatory peptides which exert specific actions in the brain that are complementary with their peripheral effects upon end organs such as the anterior pituitary and adrenal glands. In the pituitary, the two peptides act in a coordinate manner on the corticotroph to regulate ACTH release. In the adrenal gland, angiotensin II receptors are abundant in the zona glomerulosa but are also present in the medulla, where the occurrence of CRF receptors and actions on catecholamine release reveals an additional site at which the two peptides exert related actions, in this case in the peripheral neuroendocrine system. Within the brain, the mapping of AII and CRF binding sites by topical autoradiography has provided new information about the distribution and potential functions of receptors for the two peptides. The central receptors for AII are distributed in a characteristic pattern in brain regions concerned with drinking, regulation of adrenergic function and arterial blood pressure, and control of pituitary hormone secretion. Thus, in addition to its recognized modulatory effects in the peripheral adrenergic system, angiotensin II may be involved in the central control of catecholamine release and action. A central action of AII on the release of regulatory peptides such as vasopressin and CRF, both of which are present in neurones of the paraventricular nucleus, is indicated by the high concentration of AII receptors in this region. Also, the high density of AII receptors in the median eminence suggests that AII modulates the hypothalamic secretion of neuropeptides such as CRF by actions at their site of release, as well as on the cell bodies of neurones responsible for peptide synthesis. The highly localized pattern of AII receptors at numerous specific sites in the brain differs from the more general distribution of many other CNS receptors, and reflects the selective actions of AII on discrete neural systems that subserve precisely integrated functions within the central nervous system. The widespread distribution of CRF receptors, with prominent localization in the cortical and limbic regions, is consistent with the more general neuroregulatory actions of CRF in the brain, and with the presence of immunoreactive CRF in several regions of the brain including the cortex, limbic system, and centers involved in the control of autonomic function. The cortical and limbic receptors are clearly relevant to the effects of centrally administered CRF on both behavioral and visceral responses, with prominent autonomic changes including increased catecholamine release and hypertension.
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PMID:Brain receptors for hypothalamic hormones. 303 94


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