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

A 48-year-old man was admitted for treatment of Cushing's syndrome due to right adrenal adenoma, associated with chronic renal failure (CRF) with a blood urea nitrogen level of 64.2 and serum creatinine level of 3.9 mg/dl. After removal of the adrenal adenoma, the CRF deteriorated with progressive symptoms of anorexia, vomiting and hypertension, and the patient was placed on hemodialysis. Prior to adrenalectomy, the 17 OHCS and 17 KGS in the urine were not so high. However, the urinary 17 KS was high with an elevated 11-oxy fraction. In comparison with 2 patients suffering from adrenal Cushing's syndrome with normal renal function, there were no large accumulated quantities of glucuronic conjugated and unconjugated metabolites in the plasma of the CRF Cushing's syndrome, with confirmation ascribable to the radioimmunoassayable cross-reactivity of the cortisol antiserum used in the radioimmunoassay kit. In the Cushing's syndrome with CRF, almost all the cortisol, which was hypersecreted from the adenoma, was presumed to be converted to the 11-oxy fraction of 17 KS, possibly by activation of hepatic enzymes.
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PMID:Cortisol and its metabolites in the plasma and urine in Cushing's syndrome with chronic renal failure (CRF), compared to Cushing's syndrome without CRF. 279 94

Corticosteroid 11 beta-dehydrogenase (11-DH) catalyzes the conversion of cortisol to the inactive metabolite cortisone. Absence of 11-DH activity leads to a potentially fatal form of childhood hypertension termed apparent mineralocorticoid excess. As a first step in elucidating the molecular basis of this disorder, we isolated and characterized a rat cDNA clone encoding 11-DH. This clone hybridized to a single mRNA species in liver, kidney, and testis RNA but not to RNA from heart. The insert was 1265 base pairs long and included an 861-base pair open reading frame encoding 287 amino acids. A search of sequence databases revealed that 11-DH is identical in about 27% of amino acid residues to ribitol dehydrogenase from Klebsiella and to the product of the nodG gene from the nitrogen-fixing bacterium, Rhizobium meliloti, thus defining a new superfamily of genes encoding dehydrogenases. The 11-DH cDNA was expressed by transfection into Chinese hamster ovary cells under the control of an SV40 promoter. The expressed enzyme mediated both 11 beta-dehydrogenation and the reverse 11-oxoreduction reaction. Southern blot analysis of rat and human DNA suggested that additional genes related to 11-DH exist in both species.
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PMID:Cloning and expression of rat cDNA encoding corticosteroid 11 beta-dehydrogenase. 280 2

The cardiovascular and metabolic responses to severe head injury were studied in the acute phase after severe head injury with the object of determining if a common response was present and, if so, its significance in the management of the patients' intracranial and systemic physiological states. The cardiovascular response to head injury was studied by measurement of cardiac output, pulmonary capillary wedge pressure, arterial blood pressure, arterial and mixed venous blood gases and arterial and mixed venous epinephrine and norepinephrine serially in 15 patients during the first three days after injury. A hyperdynamic state was found characterized by increased cardiac output and cardiac work, moderate hypertension, tachycardia, decreased or normal systemic and pulmonary vascular resistance, increased pulmonary shunting and increased oxygen delivery and utilisation. Arterial E and NE levels correlated well with the cardiac output, cardiac work, blood pressure, heart rate, oxygen delivery, and oxygen utilization but not with vascular resistance or pulmonary shunt. The magnitude of the hyperdynamic state did not correlate with intracranial pressure, Glasgow Coma Score, or findings on CT scan. The metabolic response to head injury was studied by measurement of resting metabolic expenditure (RME) in 14 comatose head-injured patients in the first nine days after injury. During this period patients were fed with a continuous parenteral infusion of a formula containing 2 Kcal/cc and 10 mg nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated, nonparalyzed patients was 138 +/- 37% of that expected for a non-injured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 109 patient-days. The mean excretion was 20.2 +/- 6.4 mg/day. The mean protein caloric contribution was 23.9 +/- 6.7% and was greater than 25% for six patients, compared to normal values of 10-15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with the parenterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20-40% of the body surface.
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PMID:Cardiovascular and metabolic responses to severe head injury. 281 17

The effect of clonidine, on alpha 2-agonist and antihypertensive, on the progression of chronic renal disease was studied in rats subjected to partial nephrectomy. Treatments began four weeks after the removal of approximately 70% of renal mass. Clonidine was given once daily by gavage on an increasing dose schedule of 50 micrograms/kg for 4 weeks, followed by 100 micrograms/kg for 8 weeks and finally 200 micrograms/kg for 6 weeks. Measurements of renal functions were made at 4 week-intervals during treatment. After 18 weeks, clonidine-treated rats had lower levels of plasma urea nitrogen (P less than 0.05) and plasma creatinine (P less than 0.05). Urinary protein excretion rates were lower in clonidine-treated rats while receiving 100 micrograms/kg at 8 weeks (P less than 0.05) and 200 micrograms/kg at 18 weeks (P less than 0.05). At the end of the treatment period, anesthetized clonidine-treated rats had a numerically lower mean arterial pressure (p = 0.08), but no difference in the histological ranking of light microscopic lesions (P greater than 0.10). Based on the functional data, we conclude that clonidine retards the deterioration of renal function in this model of chronic renal disease. The lack of a consistent effect of clonidine on proteinuria and no reduction in the severity of morphological damage indicates that clonidine is less effective than previously reported treatment in this model with angiotensin converting enzyme inhibition. These differences in efficacy may be related to differences in intraglomerular hemodynamic alterations and could be an important consideration in the selection of therapies for individuals with hypertension and renal insufficiency.
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PMID:Effect of clonidine on the progression of chronic renal disease in partially nephrectomized rats. 282 94

Severe hypertension may be a difficult management issue, and it often requires therapy with multiple drugs at frequent dosing intervals. We report on the antihypertensive effects of the alpha-beta adrenergic blocking agent, labetalol, in combination with enalapril, a long-acting angiotensin-converting enzyme inhibitor, administered to 14 patients with severe hypertension (nine of whom had nephrosclerosis or renal artery stenosis) on other antihypertensive drug therapies. Blood pressure (BP), heart rate (HR), hematologic and blood chemistry values, and adverse side effects were monitored at 24 hours, 1 week, and 4 weeks of therapy. Rapid titration of the drugs was performed in the hospital in 10 patients; four were managed closely as outpatients. Following one month of combination therapy blood pressure decreased from 212 +/- 31/120 +/- 16 mm Hg at baseline to 155 +/- 19/86 +/- 12 mm Hg, and heart rate declined from 86 +/- 18 bpm to 70 +/- 16 bpm. Ten of the 14 patients (71%) maintained good BP control (BP less than 140/90 mm Hg) with no additional treatment. Serum potassium, creatinine, blood urea nitrogen concentrations, and hematologic parameters did not significantly change in 13 of 14 patients. Three patients developed symptomatic postural hypotension; in one patient this side effect resulted in discontinuation from the study. These data suggest that combination therapy with labetalol and enalapril is effective in lowering BP in patients with severe essential or renovascular hypertension. An additional advantage of this regimen is the twice-daily dosing interval, which may promote better long-term compliance.
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PMID:Clinical experience with labetalol and enalapril in combination in patients with severe essential and renovascular hypertension. 284 81

The relation between blood pressure and urinary electrolytes, including sodium, potassium, calcium, and magnesium were examined in male farmers of the Yi nationality who live in three separate communities in Sichuan and Yunnan provinces in China, where the lifestyles, habits, and living conditions are very different. One of these three communities was unacculturated and had the lowest average blood pressure as well as the lowest prevalence rate of hypertension in China; one was acculturated and had the highest average blood pressure; and the third was moderately acculturated with its average blood pressure between the other two. Blood pressure was taken on each of 3 days and corresponding 24-hour urine specimens were collected to measure potassium, sodium, calcium, magnesium, urea nitrogen, and creatinine. Ecological and individual-based data correlation analyses were employed to study the relations among age, body mass index, some related indexes of electrolyte derivatives, and blood pressure. Multiple regression analyses were used to explore the relation of blood pressure to the above indexes, adjusted for age, body mass index, urea nitrogen and creatinine, and geographical differences. Statistically significant correlation analyses showed that systolic blood pressure was positively associated with sodium-creatinine, calcium-creatinine, sodium-potassium, calcium-magnesium, and urea nitrogen and creatinine ratios; negatively associated with potassium-creatinine and magnesium-creatinine ratios. The ridge regression analysis selected only calcium-magnesium ratio as a predictor of systolic blood pressure.
Hypertension 1989 Jan
PMID:Urinary electrolytes and blood pressure in three Yi farmer populations, China. 291 Aug 11

We examined clinical and laboratory features retrospectively in 402 patients at the start of chronic hemodialysis in order to define better the "uremic syndrome" in the dialysis era. The information gathered included demographic data, renal diagnoses, uremic symptoms, biochemical values, and prevalences of hypertension (69%), diabetes mellitus (23%) and ischemic heart disease (16%). Unexpected findings were the wide ranges of serum creatinine levels (3.5 to 35 mg/dl) and blood urea nitrogen levels (35 to 345 mg/dl), and the frequency of hyponatremia (27%), hypoalbuminemia (52%), and anion gaps above 25 mg/dl (5%). There were higher hematocrits in males and diabetics, lower serum creatinine levels in females, diabetics and older patients, and lower blood urea nitrogen levels in blacks. The time interval from diagnosis of diabetes mellitus to initiation of dialysis in patients with diabetic nephropathy due to juvenile-onset diabetes mellitus (20.6 +/- 6.8 years) was twice that in adult onset diabetes mellitus (10.3 +/- 8.3 years).
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PMID:Clinical and laboratory features of patients with chronic renal disease at the start of dialysis. 292 Apr 71

The mechanisms by which variations in blood ionized calcium (Ca2+) influence systemic arterial pressures independent of changes in extracellular fluid volume, pH, and electrolytes are unknown. To study this issue, we dialyzed eight stable hemodialysis patients on three separate occasions during 1 week with dialysates differing only in calcium concentration. Ultrafiltration was adjusted to achieve the patient's estimated dry weight. Postdialysis Ca2+ was measured, as were arterial blood gases, electrolytes, magnesium, blood urea nitrogen, creatinine, and hematocrit. Blood pressures and two-dimensional, targeted M-mode echocardiograms were recorded with the patient in the supine position after 15 minutes of rest. Postdialysis, three different levels of Ca2+ were achieved. Other measured biochemical variables and body weight did not differ among the three study periods. Changes in Ca2+ correlated directly with changes in systolic, diastolic, and mean blood pressures, left ventricular stroke volume, and cardiac output. In contrast, heart rate, left ventricular end-diastolic dimension, and total systemic vascular resistance were not altered significantly by changes in Ca2+. Thus, alterations in Ca2+ within the physiological range affect systemic blood pressure primarily through changes in left ventricular output rather than in peripheral vascular tone in stable dialysis patients.
Hypertension 1989 Mar
PMID:Physiological mechanisms for calcium-induced changes in systemic arterial pressure in stable dialysis patients. 292 Oct 76

To study the effects of volume overload and renal failure on plasma levels of immunoreactive atrial natriuretic hormone (IR-ANH), we measured levels of this hormone in normal subjects, in patients with advanced chronic renal failure (CRF) with and without clinically evident volume overload, and in patients with end-stage renal disease (ESRD) treated with chronic hemodialysis. The levels were 13 +/- 2 pmol/l in normal volunteers, 77 +/- 24 pmol/l in patients with CRF without volume overload, and 219 +/- 50 pmol/l in patients with CRF and clinically evident volume overload (analysis of variance, p less than 0.001, alpha = 0.05 compared to normals). In patients with ESRD, the levels of IR-ANH were 145 +/- 46 pmol/l before dialysis and decreased to 87 +/- 31 after dialysis (p less than 0.025). No correlation was found between the decrease in IR-ANH levels and the decrease in weight during dialysis. A significant positive correlation was found between the IR-ANH levels and blood urea nitrogen in patients with CRF (r = 0.658, p less than 0.01). Volume overload appears to be the most important stimulatory factor for ANH secretion in renal failure patients but other mechanisms, especially a decrease in metabolic clearance, may also contribute to elevated plasma levels. The increased secretion of ANH in patients with renal failure may be an important adaptive response to volume overload and hypertension.
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PMID:Atrial natriuretic hormone secretion in patients with renal failure. 295 60

The present study was made to clarify the mechanisms of the antinephritic action of SA-446, an angiotensin I converting enzyme inhibitor, on crescentic-type anti-GBM nephritis in rats as compared to the actions of spironolactone (an antialdosterone agent), kallidinogenase (a kallikrein agent) and saralasin (an angiotensin II antagonist). SA-446 (25 mg/kg/day, p.o.) had a tendency to reduce the urinary protein excretion and plasma urea nitrogen content. In addition, this drug remarkably inhibited not only glomerular histopathological changes (i.e., crescent formation, the adhesion of capillary walls to Bowman's capsule and fibrinoid necrosis) but also the elevation of blood pressure. Spironolactone (25 mg/kg/day, p.o.) and kallidinogenase (25 KU/day, i.m.) also showed beneficial effects on glomerular histopathological changes and hypertension, although both drugs were not as effective as SA-446. However, saralasin (72 micrograms/day, s.c.) caused a marked aggravating action on this nephritis. This nephritic model showed a marked low activity of plasma renin all through the 40 day experimental period. In this model, the urinary aldosterone excretion was increased, in spite of the decrease in plasma renin activity. SA-446 and kallidinogenase significantly inhibited the decrease in plasma renin activity and the increase in urinary aldosterone excretion. Spironolactone inhibited only the increase in the aldosterone excretion. However, saralasin decreased the plasma renin activity under the control level and strongly increased the urinary aldosterone excretion (about 1.8 times the control level on the 20th day). These results suggest that the antinephritic effect of SA-446 may be related to the antihypertensive action and the increase in renal blood flow through activation of the kallikrein-kinin and prostaglandins systems.
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PMID:Studies on mechanisms of antinephritic action of SA-446 an angiotensin I converting enzyme inhibitor (1). A comparison with actions of spironolactone, kallidinogenase and saralasin. 302 37


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