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

Endothelium-derived relaxing factor (EDRF) is a labile humoral agent released by vascular endothelium that mediates the relaxation induced by some vasodilators, including acetylcholine and bradykinin. EDRF also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to vascular endothelium. These actions of EDRF are mediated through stimulation of the soluble guanylate cyclase and the consequent elevation of cyclic guanosine 3',5'-monophosphate. EDRF has been identified as nitric oxide (NO). The pharmacology of NO and EDRF is indistinguishable; furthermore, sufficient NO is released from endothelial cells to account for the biological activities of EDRF. Organic nitrates exert their vasodilator activity following conversion to NO in vascular smooth muscle cells. Thus, NO may be considered the endogenous nitrovasodilator. NO is synthesized by vascular endothelium from the terminal guanido nitrogen atom(s) of the amino acid L-arginine. This indicates the existence of an enzymic pathway in which L-arginine is the endogenous precursor for the synthesis of NO. The discovery of the release of NO by vascular endothelial cells, the biosynthetic pathway leading to its generation, and its interaction with other vasoactive substances opens up new avenues for research into the physiology and pathophysiology of the vessel wall.
Hypertension 1988 Oct
PMID:The discovery of nitric oxide as the endogenous nitrovasodilator. 304 40

The response to angiotensin-converting enzyme inhibitors (ACEIs) can be of considerable help in the diagnosis of human renovascular hypertension (RVH) in three settings. First, a particularly dramatic antihypertensive response or a decline in glomerular filtration rate (GFR), as indexed by a rise in serum creatinine or blood urea nitrogen concentrations, are useful clues to the presence of renovascular hypertension. Second, an exaggerated rise in plasma renin activity (PRA) after short-term captopril administration is a very promising screening test for this condition. Third, ACEI-induced changes in single-kidney hemodynamics (assessed by renography) may be helpful in confirming the diagnosis and offers the prospect of localizing the ischemic kidney.
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PMID:Diagnostic uses of angiotensin-converting enzyme inhibitors in renovascular hypertension. 305 43

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25

The absorption, metabolism and excretion of ketanserin [+)-3-[2-[4-(4-fluorobenzoyl)-1-piperidinyl]ethyl]-2,4(1H,3H)- quinazolinedione, R 41 468), a novel serotonin S2-receptor antagonist used in hypertension, was studied after a single oral dose of 14C-ketanserin tartrate in three healthy subjects. Absorption from the gastrointestinal tract was rapid and almost complete. The excretion of radioactivity amounted to about 90% after 4 days and was more abundant in urine (68%) than in faeces (24%). Ketone reduction and oxidative N-dealkylation at the piperidine nitrogen were by far the two main metabolic pathways. The former pathway resulted in ketanserin-ol, the main metabolite in plasma as well as in urine (24% of dose) and faeces (5%), the latter pathway in the urinary metabolite 1,4-dihydro-2,4-dioxo-3(2H)quinazolineacetic acid (20%). Other pathways were aromatic hydroxylation at the quinazolinedione moiety and the formation of ether glucuronides. None of the metabolites substantially contributes to the overall pharmacological activity of ketanserin. The metabolic pathways of ketanserin in man were identical to those revealed previously in rats and dogs, but the mass balance of the major metabolites resembled more that in dogs than that in rats.
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PMID:Absorption, metabolism and excretion of ketanserin in man after oral administration. 317 19

Erythrocyte morphologic characteristics and serum chemistry results were studied in 10 gravid ewes during experimental ovine pregnancy-induced hypertension and subsequent administration of the thromboxane synthetase inhibitors CGS13080 and CGS12970. During the hypertensive period mean arterial blood pressure, plasma thromboxane B2 levels, and serum chemistry results, and electrolyte levels were significantly altered. Parameters returned to baseline values or were improved after drug administration. Erythrocyte morphologic features did not change significantly with the onset of the syndrome. Echinocytosis was present during baseline measurement and persisted throughout hypertension. However, after thromboxane synthetase inhibition, percentages of discocytes increased (p less than or equal to 0.005) with the same frequency that echinocyte numbers decreased (p less than or equal to 0.05). Schistocytes were present throughout the study, and changes in their numbers were not detected. Serum phosphorus, blood urea nitrogen, and bilirubin levels and anion gap rose significantly during hypertension and returned to normal levels after drug treatment. We speculate that CGS13080 or CGS12970, by decreasing thromboxane levels and blood pressure, promoted the normalization of erythrocyte membranes.
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PMID:Erythrocyte morphologic features and serum chemistry studies in ovine pregnancy-induced hypertension treated with thromboxane synthetase inhibitors. 318 58

Streptozotocin diabetes in rats was complicated by spontaneous hypertension (SHR) and myocardial infarction (MIC), considered as "risk groups". Renal function was assessed on the basis of blood urea nitrogen (BUN) and albuminuria. BUN increased by 36% in Wistar diabetic group, by 100% in SHR + diabetes, and by 51% in MIR + diabetes. Morphologic changes were assessed by estimation of PAS-positive glycosaminoglycans and measurement of vascular wall thickness of glomerular arterioles. The risk groups showed exaggerated tendency for development of diabetic angiopathy. A significant imbalance between TXA2 and prostacyclin was found, which was reflected by TXB2/6-keto-PGF1 alpha (the stable metabolites of TXA2 and prostacyclin, respectively) ratio, which increased by 38% in Wistar diabetic rats, by 61% in SHR + diabetes, and by 133% in MIR + diabetes. These changes correlated very well with increased platelet aggregability (r = 0.70; p less than 0.05) and with increased lipid peroxide level (r = 0.60; p less than 0.05), but neither with total plasma cholesterol (r = 0.20), nor with plasma triglycerides (r = 0.34). Lipid peroxides increased 5-fold in Wistar diabetic rats, 6-fold in SHR + diabetes, and 5.5-fold in MIR + diabetes. A causative relationship between TXA2/PGI2 imbalance and lipid peroxide changes on one hand, and diabetic angiopathy, on the other, was suggested.
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PMID:Streptozotocin-induced diabetes in rat. I. Influence of hypertension and myocardial infarction on the development of vascular complications. 322 39

The authors reviewed the effect of low dose dopamine administration (1-5 micrograms/kg/min) in neurosurgical patients with acute renal failure (5 cases) or hypernatremia (7 cases) in whom cerebral dehydration therapy for intracranial hypertension was thought to be causative of these disorders. Cases with hypernatremia (serum sodium over 155 mEq/l) were considered in the stage of impending acute renal failure as in the majority of cases serum creatinine levels were mildly elevated while urinary sodium was markedly diminished. Associated with systemic hypovolemia, in cases with acute renal failure (with serum creatinine over 3.5 mg/dl and urinary output of less than 20 ml/hr for more than 4 hour duration) the urinary sodium levels were less than 20 mEq/l. In all the cases treated by low dose dopamine, urinary output and sodium increased within 6 hours and in the following 24 hours stabilized urinary output with its elevated sodium (some 100 mEq/l) was obtained. As the result, elevated urea-nitrogen or serum sodium was rather easily washed out and the patients were kept adequately hydrated afterwards. Any complications such as aggravation of cerebral edema or convulsive disorder were not associated with this regime. The authors, therefore, would emphasize that low dose dopamine administration resulting in sodium diuresis and increase in renal blood flow is a practical way of method in treating patients with hypernatremia or acute renal failure caused by hyperosmolar agent infusion in their acute stage.
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PMID:[Renal protection in acute neurosurgical diseases--effect of a low dose dopamine with reference to acute renal failure and hypernatremia in patients with dehydration]. 322 69

The aim of the study was to evaluate risk factors for the development and progression of diabetic nephropathy. For this purpose, a reliable method of monitoring renal function is necessary. Five different methods of estimating renal function (plasma and renal clearance of 51Cr EDTA, serum creatinine, plasma beta-2-microglobulin and endogenous creatinine clearance) were compared. The risk factors studied were hyperglycaemia, smoking, diabetic cystopathy and dietary protein. All patients were treated for hypertension. The metabolic control was evaluated by assay of HbA1c and repeated estimation of blood glucose. A careful interview about previous and current smoking habits was used for evaluation of the role of smoking. Presence of residual urine, registered with an isotope technique using 131I-Hippuran, was used as the criterion of diabetic cystopathy. Dietary protein intake was studied with a dietary history interview and by measuring the urinary excretion of nitrogen. All five renal function tested evaluated have disadvantages. The most reliable information is given by the combined measurement of plasma clearance and renal clearance of 51Cr EDTA. Hypertension is the most important factor for progression but metabolic control also has an impact, which can be shown when hypertension is adequately controlled. Diabetic patients with nephropathy have smoked more and still smoke more than patients without nephropathy. Diabetic cystopathy is common but with instructions it can be kept constant for several years. Although a correlation of cystopathy to progression is likely, it could not be demonstrated. The study of protein intake does not support the theory of a harmful effect of dietary protein on the development or progression of diabetic nephropathy. By intervening against risk factors, it is possible to achieve a very low progression rate or even to arrest the progression for several years.
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PMID:Diabetic nephropathy. A clinical study of risk factors in type-I diabetes mellitus. 322 21

We started a special follow-up system for women who had a history of severe toxemic pregnancy in our department since 1975. All medical records from 1956 to 1975 were reviewed and 468 deliveries with such disease were registered at that time. One hundred and ninety five deliveries (186 women) also were added from the prospective point of view until 1985. Among 654 patients, 374 women were available to address. I. The latter 186 women were divided into 7 groups: A1, A2, A3, A4, B1; and B2. The definitions of each group were as follows. A1: primipara with severe toxemia; A2: multipara that had a severe toxemia at the first time and then normal pregnancy (ies); A3: multipara that had a severe toxemia in the first pregnancy and then mild one(s); A4: multipara that repeated severe diseases; A5: multipara that had a severe toxemia and then unclassified type(s) of the disease; B1: multipara that had a normal pregnancy at the first time and then severe toxemia(s); B2: multipara that had a mild toxemia in the first pregnancy and then severe one(s). The percent of each group was 25, 24, 13, 15, 4, 6, and 12% respectively. Those women who had severe toxemia(s) were found to have hypertension, high levels of blood urea nitrogen, hyperhematocritemia, and hyperlipemia from the results of clinical and laboratory data. Consequently, they are a high risk group of atherosclerosis, because hypertension and hyperlipemia are main risk factors of that disease. II. Eighty percent of 374 women who had a history of severe toxemia from 1956 to 1985 was able to be followed up by us until 1987. Those women also were divided into the same groups as described above except A5, and checked up as to hypertension, hyperlipemia, body weight, and so on. The characteristic features were that the group A2 is in a well condition, and that many of group A4 are suffering from various diseases with regard to the remote prognosis. In conclusions, it was suggested that there may be four etiologic causes as to toxemia of pregnancy. The first is a disadaptation during pregnancy, and this seems to consist mainly of pregnancy induced hypertension. The second has various underlying diseases, such as chronic hypertension or renal disease, etc.. The third has a hypertensive trait which is manifested as the pregnancy advances. The fourth is considered to be related to biologic ageing.
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PMID:[Follow-up study on women suffered from severe toxemia of pregnancy]. 325 67

Total body elemental composition was measured in 40 patients with well documented heart failure who were oedema-free on digoxin and diuretics. The results were compared with values for 20 patients with untreated essential hypertension matched for height, weight, age, and sex. Total body potassium alone was also measured in 20 normal subjects also matched for anthropomorphic measurements. Patients with hypertension had a very similar total body potassium content to that of normal subjects, but patients with heart failure had significantly reduced total body potassium. This could not be explained by muscle wasting because total body nitrogen, largely present in muscle tissue, was well maintained. When total body potassium was expressed as a ratio of potassium to nitrogen mass a consistent depletion of potassium was revealed in the group with heart failure. Potassium depletion was poorly related to diuretic dose, severity of heart failure, age, or renal function. Activation of the renin-angiotensin-aldosterone system was, however, related to hypokalaemia and potassium depletion. Such patients also had significantly lower concentrations of serum sodium and blood pressure. Serum potassium was related directly to total body potassium. Despite the absence of clinically apparent oedema total body chlorine was not consistently increased in heart failure, but the calculated extracellular fluid volume remained expanded in the heart failure group. Total body sodium was significantly increased in patients with heart failure, but less than half of this increase could be accounted for by extracellular fluid volume expansion. Potassium depletion in heart failure may account in part for the high frequency of arrhythmias and sudden death in this condition.
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PMID:Total body electrolyte composition in patients with heart failure: a comparison with normal subjects and patients with untreated hypertension. 331 Oct 97


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