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

1. A thermistor probe designed for determination of renal blood flow in rabbits, consisted of a fast-responding bead thermistor and an injection port which was also used to measure renal venous pressure between injections. 2. By an in vitro calibration system, actual measured flow (Qa) correlates well with the thermodilution calculated flow (Qc), where Qc = 0.99 Qa + 4.9 (r = 0.97, n = 42). 3. The renal blood flow (RBF) as determined by the thermodilution technique in 3 control groups was 53 +/- 3 (8), 60 +/- 6 (8), and 62 +/- 3 (3) ml/min/kidney or about 9% of the cardiac output. 4. Hypovolemia (-10%) reduced RBF by 19% from the control value, whereas, hypervolemia (+10%) did not alter RBF. 5. Smoke-induced apnea resulted in hypertension (+30%) and bradycardia (-39%), and was associated with changes in RBF (-55%) and renal vascular resistance (+183%). 6. We conclude that the local thermodilution technique is a relatively easy and reliable method for estimating RBF in rabbits.
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PMID:Local thermodilution: a reliable technique for estimating renal blood flow in the rabbit. 612 54

Using the load independent contractility index, end-systolic pressure-volume ratio (Emax), contractility of the hypertrophied left ventricle (LV) from three different models was evaluated in conscious, resting dogs. The experimental animals included 12 dogs with perinephritic hypertension (HYP) (aortic diastolic pressure 130 +/- 5 mm Hg), 12 dogs who underwent aortic banding (AOB) at 6 to 8 weeks of age (resting aortic gradient 110 +/- 15 mm Hg), and 12 dogs with chronic fluid overload from aortocaval fistula (ACF). These were compared with 12 normal dogs (CTL). LV dimension and pressure were measured with ultrasonic tranducers and micromanometers. All three models resulted in hypertrophy with significant (P less than 0.01) increase in LV weight-to-body weight ratio (6.3 +/- 0.4, 8.4 +/- 0.5, 6.3 +/- 0.4, respectively, vs 4.4 +/- 0.1 g/kg). Cardiac output (6908 +/- 740 vs 2424 +/- 276 ml/min) and end-diastolic volume (118 +/- 11 vs 50 +/- 4 ml) were significantly (P less than 0.01) increased in AOB (18 +/- 1 vs 9 +/- 2 mm Hg). dp/dtmax was not significantly different among all groups. Emax (CTL = 5.3 +/- 0.4 mm Hg/ml) was not significantly changed in HYP (9.5 +/- 2.1) but was significantly (P less than 0.01) increased in AOB (14.1 +/- 2.6), and significantly (P less than 0.01) depressed in ACF (2.4 +/- .03). Thus, LV hypertrophy from systemic hypertension (HYP) or proximal aortic hypertension (AOB) is, at least initially, associated with preservation of contractility and normal hemodynamic performance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Global left ventricular contractility in three models of hypertrophy evaluated with Emax. 623 33

Liddle's syndrome was diagnosed in a 23-yr-old Chinese girl with hypertension and hypokalemia by the presence of suppressed renin and negligible plasma and urinary aldosterone secretion. Adrenal corticosteroids, including aldosterone, were suppressed by dexamethasone and stimulated by ACTH. While spironolactone was ineffective, triamterene (2,4,7-triamino-6-phenyl-pteridine) treatment corrected the hypertension and hypokalemia and restored PRA to normal provided that sodium intake was not excessive. During long term treatment with triamterene, blood pressure was extremely sensitive to salt intake, increasing promptly with high intake and decreasing with low salt intake. As a result of the chronic hypervolemia and sodium retention consequent upon the patient's persistent high salt intake and increased renal tubular sodium reabsorption, plasma renin and aldosterone remained low. Erythrocyte sodium concentration and membrane permeability were increased. Triamterene with salt restriction was able to lower the intracellular sodium concentration but did not correct the increased sodium permeability. This suggests that there is an abnormality of sodium transport in Liddle's syndrome which affects the erythrocytes as well as the renal tubular cells.
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PMID:The effect of triamterene and sodium intake on renin, aldosterone, and erythrocyte sodium transport in Liddle's syndrome. 626 54

The authors present a contemporary picture of the pathogenesis and clinical course of diabetic nephropathy in type I diabetics describing the stages of the disease and the possible evidence for reversibility of the kidney damage with tight metabolic control. During the so-called latency period, which is clinically non-detectable, the predominant functional abnormalities (increase in GFR with sub-clinical glomerular proteinuria) can be corrected by strict control although there is no evidence for the regression of the associated anatomical changes such as the enlarged filtration area. As for the described increase in thickness of the glomerular basement membrane, from experimental data and pancreatic transplants in man, delay in its development and to some extent regression of the glomerular lesions can be expected. The problem of how the renal lesions in experimental diabetes mirror the changes in the human kidney is discussed. During the symptomatic period, with intermittent and subsequently constant proteinuria and progressive decline in renal function, which are observed in only about 30% of type I diabetics, the role of arterial hypertension and its effective control is emphasized. Finally, the renal failure period is indicative of irreversible damage to the kidneys. The progression from its early to its late stages is variable between different patients but each individual patient shows a constant rate of deterioration. The evidence for the efficacy of medical treatment in slowing down its progression is very limited at present but much can be done to improve the quality of life by dietary measures, treatment of fluid overload and hypertension. When the end-stage diabetic kidney disease is reached, with serum creatinine above 8 mg/dl, renal transplantation from a living donor offers a good chance for a relatively acceptable quality of life for years. In conclusion, it is stressed that the morbidity of diabetic nephropathy could eventually be reduced through effective control of the metabolic abnormalities of diabetes with the methods presently available.
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PMID:The natural history of diabetic nephropathy in type I diabetes and the role of metabolic control in its prevention, reversibility and clinical course. 634 25

In acutely uremic animals, the contractile force of the heart is consistently increased; such an increase can be dissociated from changes of afterload or catecholaminergic drive. It is associated with diminished sarcolemmal Na,K-ATPase activity in the heart which, in turn, may be related to increased levels of endogenous digitalis-like substances (endigens) that have been postulated to represent a natriuretic factor. In patients with chronic uremia, myocardial contractility is usually normal, but occasionally there may be heart failure unrelated to pre-existing hypertension, coronary heart disease, anemia, fluid overload, or other recognizable factors. So far, the experimental basis for this clinical observation is uncertain. Possible causes for the clinical syndrome include an excess of parathyroid hormone or cardiodepressor substances. There is experimental evidence of impaired cardiac response to beta adrenergic agonists, e.g., decreased isoproterenol-dependent calcium uptake, diminished inotropic and chronotropic responses. In acutely uremic rats, cardiac cyclic AMP levels are high but can be reversed by beta blockers. Heart calcium content is variable and heart weight is constantly increased in acutely uremic rats, despite decreased skeletal muscle mass. The change in heart weight is not related to anemia, to an excess of parathyroid hormone, or to sympathetic activity; its cause remains unknown. Experimental studies to date have shown a variety of abnormalities, but do not provide a uniform concept of the mechanisms or an explanation for the cardiac dysfunction so often observed in patients with uremia.
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PMID:Cardiac function in experimental uremia. 636 51

The circulatory volume and exchangeable sodium were measured in 110 normal subjects and 120 patients with benign untreated essential hypertension. The two study groups did not differ in age, sodium and potassium metabolism, and plasma levels of renin, aldosterone and norepinephrine, while plasma epinephrine was slightly higher in essential hypertension. Total plasma and blood volume correlated with total exchangeable sodium (r = 0.64-0.75; p less than 0.001); these correlations were similar in normal and hypertensive subjects. Body surface area was found to be the most appropriate frame of reference for judging individual values of plasma and blood volume or exchangeable sodium; using this approach these body constituents were on average normal in the hypertensive population. Blood volume was unrelated to age or blood pressure in normal and hypertensive subjects. Exchangeable sodium tended to increase with age (r = 0.25; p less than 0.02) and correlated positively with blood pressure (r = 0.25; p less than 0.02) in essential hypertension but not in normal subjects. The latter body constituent was slightly but significantly decreased in hypertensive males aged less than 35 years as compared with appropriate normal controls (96.1 +/- 6.8% versus 99.6 +/- 6.7%; p less than 0.05). These findings confirm that blood volume and exchangeable sodium are on average normal in patients with benign essential hypertension. Body sodium may even be decreased in certain young hypertensive patients. These observations do not support the concept that hypervolemia may represent the initial event leading to high blood pressure in essential hypertension; in contrast, changes in blood volume appear to reflect variations in blood pressure.
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PMID:Circulatory volume in essential hypertension. Relationships with age, blood pressure, exchangeable sodium, renin, aldosterone and catecholamines. 638 28

Dimethyl sulfoxide (DMSO) has shown promise as a drug for the treatment of intracranial hypertension. In this report, we describe our experience in six patients, two who received a bolus administration of 10% DMSO and four who received a 20% solution titrated against the intracranial pressure (ICP). Five of the patients in this series suffered from severe head injury, and one had a cortical venous thrombosis associated with pregnancy. The first two patients were treated with a rapid infusion of a 10% solution of DMSO. Initially, the ICP was satisfactorily controlled using this method. Over time, however, fluid overload, severe electrolyte disturbances, and an ultimate loss of ICP control occurred. In subsequent patients, a 20% solution titrated against the ICP was used. Although ICP control was better achieved using this method of administration, problems with fluid management and electrolytes occurred again despite a high level of vigilance. In addition, because of the solvent properties of DMSO and its propensity over time to dissolve most standard intravenous infusion systems, mechanical difficulties in its administration were encountered in all six patients. The mechanism of action of DMSO is not well understood. It differs from the barbiturates, but acts too rapidly to function solely as a diuretic. The drug is extremely complex to use, and difficulties with its administration may make its risks ultimately greater than its potential benefits. Until more laboratory data are available concerning its use and better delivery systems are developed, neurosurgeons are cautioned against treating intracranial hypertension with DMSO.
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PMID:Dimethyl sulfoxide for the treatment of intracranial hypertension: a preliminary trial. 646 99

A 50-year-old man with hypertension showed hypokalemia, hyporesponsive low reninemia, and low levels of aldosterone in the plasma and urine. Plasma DOC and corticosterone level, adrenal scintigram, and phlebogram were within normal limits. Hypertension and hypokalemia were correctable by spironolactone. It was revealed that he had been ingesting Jintan granules in large doses, corresponding to 150-220 mg of glycyrrhizic acid per day for 10 years. Upon cessation of Jintan ingestion, blood pressure and serum potassium level were normalized after 40 days. Metabolic alkalosis, hypervolemia, hyporesponsive low reninemia, and the low levels of plasma and urine aldosterone were also improved. Thus, the present case of pseudoaldosteronism was attributed to Jintan, and raises a caution to excessive Jintan ingestion.
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PMID:A case of pseudoaldosteronism due to addiction of Jintan, a mouth refresher popular among Japanese. 675 76

Fifteen episodes of encephalopathy have been studied in 13 renal transplant recipients. All episodes of encephalopathy occurred during an acute rejection crisis. Clinical and biochemical features were recorded during rejection crises associated with encephalopathy and in an equal number of uncomplicated rejection episodes in the same patients. Encephalopathy was related to the severity of the rejection crisis and not to other features such as blood pressure, fever, steroid therapy or plasma electrolytes. The definition of the syndrome of rejection encephalopathy and its relation to the severity of the rejection has important therapeutic implications. Steroid therapy should not be withdrawn or reduced because of acute neurological features. Control of hypertension, fluid overload and electrolyte imbalance, in addition to treatment of the rejection episode, are necessary to reverse the encephalopathy. The prognosis of this syndrome is excellent with no long-term sequelae.
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PMID:Rejection encephalopathy. An acute neurological syndrome complicating renal transplantation. 675 75

Effective diuresis requires both sufficient glomerular filtrate and adequate delivery of the diuretic drug to the lumen of the renal tubule. Diuretics will not "force open" the kidney. Diuretics that work primarily in the proximal tubule include osmotic diuretics (e.g., mannitol), diuretics that interfere with the adenyl cyclase system (e.g., xanthines), and those which inhibit carbonic anhydrase (e.g., acetazolamide). Some thiazide and thiazide-like diuretics have a secondary site of action in the proximal tubule based on either carbonic anhydrase inhibition or other mechanisms, such as inhibition of sodium phosphate reabsorption. The diuretics that work primarily in the medullary diluting segment of the loop of Henle, furosemide and ethacrynic acid, block the active reabsorption of chloride and interfere with the tubular reabsorption of free water. The exact mechanism remains unknown. These diuretics tend to have a "high ceiling," to be potent and rapidly acting, and to have a short duration of effect. They are excellent for the treatment of severe fluid overload or pulmonary edema but are not ideal for the treatment of uncomplicated hypertension. Furosemide is a sulfonamide derivative; ethacrynic acid can be used in patients who are allergic to sulfa drugs. Diuretics that work primarily in the cortical diluting segment include the thiazides and thiazide-like drugs. They inhibit sodium transport by an undetermined mechanism. Most of them seem to reach a dose-response plateau beyond which little additional effect is gained by increasing the dose. Most of them appear to lose efficacy as the glomerular filtration rate decreases, except for metolazone and indapamide. The thiazides are most commonly used to treat hypertension. Diuretics that work primarily in the distal tubule and collecting tubule include the aldosterone inhibitor spironolactone and two drugs that impair tubular reabsorption of sodium by direct action, triamterene and amiloride. These drugs are primarily used for their potassium-sparing effect.
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PMID:Insights into intrarenal sites and mechanisms of action of diuretic agents. 686 1


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