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)

The clinical manifestations of primary aldosteronism are not distinctive, but additional studies are warranted in certain hypertensive patients, including patients with either spontaneous or diuretic-induced hypokalemia and those with refractory hypertension without an obvious secondary cause. The best test for identifying patients with primary aldosteronism is measuring the aldosterone excretion rate during salt loading. A rate exceeding 14 micrograms/24 hour provides the highest sensitivity and specificity. The presence of hypokalemia and suppressed plasma renin activity provides corroborative evidence but their absence does not preclude the diagnosis. An adenoma is likely in the presence of significant spontaneous hypokalemia (serum potassium concentration < or = 3 mEq/L), a paradoxic decrease in ambulatory plasma aldosterone concentration, and plasma 18-hydroxycorticosterone values equal to or greater than 100 ng/dL. The adrenal CT scan should be considered the initial step in localization. Primary aldosteronism can be associated with severe and drug-resistant hypertension, and maintained hypervolemia is the reason for resistance to therapy. Sustained volume depletion is the most important therapeutic goal for these patients. Medical therapy is indicated for patients with hyperplasia and for patients with bilateral adenomas that may require total bilateral adrenalectomy. Whenever feasible, surgical excision is recommended for unilateral tumors, and cure can be achieved despite prolonged and severe hypertension.
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PMID:Primary aldosteronism. Issues in diagnosis and management. 807 Apr 22

Patients with peripheral arterial occlusive disease (PAOD) and marked atherosclerosis often present concomitant diseases like coronary heart disease, cerebral circulatory disorders or arterial hypertension. Thus, the extent of hypervolemia is limited in case of an infusion treatment without venesection. Therefore, it was tested whether a hypervolemic hemodilution without venesection is superior to a dilution with venesection in multimorbid patients suffering from PAOD stage II. The colloidal iso-molar solution used was Haes 200/0.5 6%. Both forms of hemodilution were significantly superior compared to a control group well hydrated with cristalloid saline solution; all groups practised walking exercise twice a week over a period of one hour. However, hypervolemic hemodilution without venesection was only slightly better than the dilution with venesection. The walking distance in the group without venesection increased by 68.6 m (36.7%) in the group without venesection, by 59.0 (30.4%) in the group with venesection and by 33.6 m (20.1%) in the control group. The results show that the decision to perform a hyperor isovolemic hemodilution should depend on the volume tolerance of each patient.
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PMID:Hypervolemic hemodilution with or without venesection in peripheral arterial occlusive disease stage II. 807 90

If patients are treated within the first 3 days after rupture, early definitive clipping associated with mechanical clot removal to the extent practical and instillation of fibrinolytic agents seems likely to become standard therapy. Patients should also receive calcium antagonists and be maintained in normal fluid and electrolyte balance. At the first sign of delayed ischemic deficits, therapy with hypervolemia and hypertension should be instituted. If clinical deterioration is progressive despite this, consideration should be given to intra-arterial vasodilators or balloon angioplasty. If patients are referred more than 3 days after hemorrhage, we still advocate the same course of action unless the patient presents with established severe diffuse vasospasm and is unconscious. Operation in such a setting is likely to be associated with prohibitive mortality and morbidity. In such cases, it might be worth the risk of using intra-arterial vasodilators or balloon angioplasty despite the presence of an unclipped aneurysm. The last decade has witnessed substantial advances in our knowledge of the pathogenesis of vasospasm and we now have a reasonable chance at effective prophylaxis and treatment.
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PMID:Cerebral vasospasm. 811 92

Many epidemiological and clinical studies show a strong association between arterial hypertension and obesity. The underlying pathophysiological mechanism is unknown. It is thought that the etiopathogenesis of obesity hypertension is exceptional and in that view hormonal, neural, volume and hemodynamic properties of obesity, as well as salt and/or caloric consumption, are outlined. In this article all these factors are discussed. According to the current hypothesis, hyperinsulinemia which is probably a physiologic adaptation to obesity, plays a key role in the pathogenesis of arterial hypertension. Insulin increases the reabsorption of sodium by means of an immediate effect on the kidney tubules. An increase of sodium in the body leads to hypervolemia and to the elevated blood pressure. Chronic hyperinsulinemia perhaps increases the blood pressure indirectly also by means of the central nervous system, namely, by stimulating the activity of the sympathetics.
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PMID:[Arterial hypertension in the obese--aspects of etiopathogenesis]. 823 16

To assess the influence of long-term hemodialysis on arterial compliance, the elastic vessel wall properties of the common carotid artery were determined in 20 normotensive renal transplant recipients (age 44.7 +/- 4.1 years) 8-12 weeks after first transplantation and in 10 healthy controls (age 45.9 +/- 5.2 years). Arterial distension was measured by using a multigate pulsed Doppler system, blood pressure curve was recorded by finger-plethysmography. 10 patients with a prior long-term hemodialysis of 51 +/- 11 months were compared to 10 patients with a prior short hemodialysis of 18 +/- 7 months. The patients and controls had been matched in respect of age, sex and blood pressure. In the long and short-term hemodialysis group, the proportion of patients (n = 10) with a history of mild hypertension was similar--mild hypertension for 25 +/- 10 months (n = 5) and for 27 +/- 9 months (n = 5). In the group with long-term hemodialysis, the cross-sectional compliance and the distensibility coefficient was significantly reduced in comparison to the group with short-term hemodialysis (p < 0.005) and to the control group (p < 0.001). A significant inverse correlation between the hemodialysis period and the distensibility coefficient (r = -0.59; p < 0.005) showed a decrease in arterial compliance with the length of hemodialysis treatment. The results demonstrate that vessel wall elasticity decreases with the length of hemodialysis treatment and is reduced by hemodialysis-dependent factors, which are detached from sustained arterial hypertension. As cause of reduced arterial compliance in long-term hemodialysis hypervolemia, hypercirculation and disturbed calcium-phosphate metabolism is suggested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of long-term hemodialysis on arterial compliance in end-stage renal failure. 824 88

Thirty per cent of patients who started maintenance haemodialysis at our institution between January 1989 and December 1991 had been referred at a very late stage of their renal disease. To assess the causes and consequences of such late referral we retrospectively compared clinical and laboratory features of 65 patients who had been referred less than 1 month prior to first dialysis (late referral, or LR group) and of 153 patients who had been previously followed-up by us for more than 6 months (early referral, or ER group). Age, sex ratio, and socioeconomic status were similar in the two groups. In the LR group, 38 patients had never been referred to a nephrology unit, whereas 27 had discontinued nephrological surveillance. Fluid overload, severe hypertension, and/or pulmonary oedema was present in 57% of LR versus 15% of ER patients (P < 0.001). Mean (+/- 1 SD) systolic and diastolic blood pressure was greater in the LR than the ER group (173 +/- 19/99 +/- 12 versus 147 +/- 15/84 +/- 8 mmHg, P < 0.001). Mean plasma concentration of creatinine, urea and phosphate was significantly greater, whereas bicarbonate, calcium, haematocrit and albumin were less in the LR than the ER group. Most (88%) LR patients started dialysis in emergency conditions through central vein catheterization. Total hospital stay lasted 34.5 +/- 16.3 days in LR versus 5.8 +/- 3.0 days in ER patients (P < 0.0001), resulting in an excess cost of 0.2 million French francs per LR patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late referral to maintenance dialysis: detrimental consequences. 827 21

Bumetanide is a loop diuretic that is used for the treatment of edema and hypertension. The rapidly developing syndrome of extracellular fluid overload in some malnourished children has been successfully treated with furosemide, another loop diuretic, and digoxin; however, similar studies with bumetanide have not been conducted to date. Therefore, in the present study, the influence of dietary protein deficiency on the pharmacokinetics and pharmacodynamics of bumetanide was investigated after intravenous (i.v.) bolus and oral administration of bumetanide to male Sprague-Dawley rats fed on 23% (control rats) or 5% [protein and calorie malnutrition (PCM) rats] protein diet ad libitum for 4 weeks. After an i.v. dose of bumetanide, 1 mg/100 g body weight, the mean values of renal clearance and percentages of dose excreted as unchanged bumetanide in an 8-h urine sample were 166 and 154% higher, respectively, in PCM than control rats; however, nonrenal clearance (CLNR) was 28% lower. The decrease in nonrenal clearance in PCM rats might be because of the decrease in nonrenal metabolism of bumetanide in PCM rats. The urine output per 100 g of body weight was not significantly different between the two groups of rats after i.v. administration, although the amount of bumetanide excreted in the 8-h urine sample per 100 g body weight increased significantly in PCM rats. These results could be explained by the fact that the dose of bumetanide used results in urinary excretion rate of bumetanide at the plateau of the concentration-effect relationship.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of protein and calorie malnutrition on the pharmacokinetics and pharmacodynamics of bumetanide in rats. 837 24

The aim of this work was an evaluation of the effect of the acute hypervolemia induced by 90 min intravenous infusion of 1500 ml 0.9% NaCl (16.7 ml/min) on blood pressure, plasma concentration of the atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), aldosterone (ALDO), plasma renin activity (PRA) in patients with essential hypertension on the normal, low and high sodium intake. Twelve patients with noncomplicated essential sodium-sensitive arterial hypertension participated in the study. Sodium chloride infusions were performed three times: first--on the fifth day of normal daily sodium u intake (110-120 mmol/day), second--on the fifth day of low sodium intake (10-20 mmol/day), third--on the fifth day of high sodium intake (200-220 mmol/day). Acute intravenous sodium chloride load induced a significant increase of the mean arterial pressure (MBP) only when the patients were on the high sodium diet. This increase of the MBP was associated with a significantly lower increment of plasma ANP, cGMP, lower decrement of ALDO and PRA when compared to normal- or low- sodium intake. The results suggest an impairment of the adaptive homeostatic mechanisms induced by an acute intravenous sodium load in patients with noncomplicated salt-sensitive essential hypertension ingesting high-sodium diet.
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PMID:[Effect of intravenous sodium chloride load on levels of atrial natriuretic peptide (ANP) and 3'5' guanosine monophosphate (cGMP) in plasma of patients with uncomplicated sodium-sensitive arterial hypertension maintained on different dietary sodium intake]. 838 45

To evaluate the actual role of extracellular fluid volume (ECFV) expansion per se in modulating the rate of urinary calcium excretion, a thermoneutral water immersion (WI) study was conducted in 10 normal subjects and 30 patients with essential hypertension. Central hypervolemia by 2 hours of WI caused a significant diuretic and natriuretic response (P < .005) in normal subjects; no significant changes were detected in urinary calcium and magnesium excretion. WI provoked either an appropriate or exaggerated natriuresis (P < .001) in 21 hypertensive patients; these subjects also exhibited a highly positive correlation between urinary sodium and calcium excretion during WI (P < .001). In the remaining nine hypertensive patients, WI produced a significant diuretic response, but a barely discernible (P = NS) natriuresis (inappropriate response). These subjects also exhibited a significant reduction of urinary calcium (P < .001) and magnesium (P < .01) excretion. The data indicate that (1) volume expansion per se may have a role in regulating calcium excretion in hypertensive subjects; (2) a calcium leak may be attributable to a close relationship between urinary sodium and calcium metabolism, and causally related to a disturbance of sodium and volume homeostasis in hypertension.
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PMID:Calcium and sodium handling during volume expansion in essential hypertension. 841 47

The atrial natriuretic peptide (ANP) is part of a new family of cardiac hormones regulating water and salt homeostasis. Besides acting as a blood pressure-lowering agent, it also exerts potent natriuretic and diuretic effects. ANP can be considered an endogenous antagonist of the reninangiotensin-aldosterone system and the antidiuretic hormone. One of the roles of ANP is to protect the body against fluid overload: it decreases intravascular fluid volume, which in turn diminishes cardiac secretion of ANP. The pharmacokinetic parameters of ANP reported in the literature vary widely. In general, ANP rapidly disappears from plasma with a high total body clearance. This is in agreement with the short-lived effects of the hormone. The actions of ANP have led to efforts to use this peptide hormone in the treatment of various cardiovascular disorders such as hypertension and congestive heart failure. Intravenous ANP administration indeed resulted in beneficial effects in these disorders. However, the peptide nature of ANP and its rapid elimination from the circulation limit its suitability as a drug. More promising is the development of long-acting ANP analogues and inhibitors of ANP degradation. Proper understanding of ANP pharmacokinetics is essential for the clinical use of these pharmacological agents.
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PMID:Atrial natriuretic peptide. An overview of clinical pharmacology and pharmacokinetics. 844 71


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