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

The effect of propranolol on renal haemodynamics was studied in nine patients with arterial hypertension and moderate to severe chronic renal failure. A reduction of the renal function in this type of patient might have clinical consequence. The patients, whose glomerular filtration rate (GFR) ranged between 17 ml/min/1.73 m2 and 71 ml/min/1.73 m2, were studied during three 4-week periods with alternately placebo, propranolol (40 mg b.i.d.) and placebo treatment. The GFR and the effective renal plasma flow (ERPF) were determined as the plasma clearance of 51Cr-EDTA and 125I-hippurane. The GFR fell on the average 7% (95% confidence limits: 1-12%) during propranolol treatment, and the fall was reversible. No changes were found in ERPF. In conclusion, propranolol treatment in this type of patient causes a modest and reversible fall of GFR.
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PMID:Renal haemodynamics during propranolol treatment in patients with arterial hypertension and chronic renal failure. 371 80

The present study is a proton NMR investigation of the influence of Ca2+ on the interaction between the intact sialic acid residues on HBP (Hepatic Binding Protein) and methyl-beta-D-galactoses. The proton NMR spectra of HBP and methyl-beta-D-galactose mixing solution at different Ca2+ concentration have been measured. The analysis of the experimental results indicates that Ca2+ participates in the binding of sialic acid residues on HBP with methyl-beta-D-galactoses and this enables the galactose molecules to be in stable bound state. The proton NMR spectra of the samples containing EDTA have confirmed this conclusion.
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PMID:1H NMR investigation of the binding of methyl-beta-D-galactoses with sialic acid residues on hepatic binding protein--the effect of divalent calcium ions. 374 68

The new calcium antagonist felodipine with a pronounced arteriolar dilating capacity was used to treat 11 patients with severe hypertension resistant to treatment (4 with essential hypertension, 5 with renoparechymatous hypertension, 2 with renovascular hypertension). Mean glomerular filtration rate for 10 patients was 34 +/- 27 ml/min/1.73 m2 body surface area (51Cr-EDTA clearance) before felodipine. One patient was on haemodialysis treatment. Mean arterial blood pressure in the outpatient clinic was 206 +/- 39/119 +/- 18 mm Hg in spite of treatment with 3 or more antihypertensive drugs. All but 2 patients had been given an angiotensin converting-enzyme inhibitor without success. All vasodilating agents were discontinued and the following morning 5 to 10 mg felodipine was given orally. This resulted in a reduction of average supine blood pressure from 190/110 mm Hg to 150/90 mm Hg during the first hour. The antihypertensive effect was unchanged during 6 hours and the drug was subsequently administered twice or three times a day. Mean systolic and diastolic blood pressure after 1 month was 155 +/- 19/91 +/- 12 mm Hg. Eight patients showed a favourable long term response with a mean systolic and diastolic blood pressure of 154 +/- 17/89 +/- 6mm Hg after 6 months. One patient died from his underlying disease after 2 months and 1 patient discontinued treatment because of ankle oedema after 6 weeks. In the long term treated patients with glomerular filtration rates greater than 15 ml/min/1.73m2 all but 1 showed an improved renal function by 26 +/- 19% (n = 5) after initiation of felodipine therapy. In 2 cases with very low glomerular filtration rate (6 to 7 ml/min/1.73m2) the deterioration of renal function continued after felodipine, but at a slower rate. It is concluded that felodipine decreased blood pressure dramatically in patients with severe hypertension where a majority of the cases had been resistant to a previous therapy. The drug appeared safe also in advanced renal insufficiency.
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PMID:Renal effects of felodipine in hypertensive patients with reduced renal function. 398 48

Bovine hypothalamus contains a stable, low molecular weight substance with ouabain-like properties. To further study its mechanism of action and potential physiological importance we examined its effects on purified Na+-K+-ATPase in a kinetic coupled-enzyme assay. Under optimal conditions up to 95% of Na+-K+-ATPase activity could be inhibited by the factor. Mg2+ is required for maximal inhibitory activity, but ligand requirements for optimal activity are otherwise distinct from those of both ouabain and vanadate. Inhibition is reversed by high concentrations of sodium chloride plus EDTA. Kinetic analysis yielded a Ki = 1.4 nM. The hypothalamic factor is a high-affinity reversible inhibitor of Na+-K+-ATPase, being at least as potent as the cardiac glycoside ouabain and may be a circulating inhibitor of sodium transport, which appears to be associated with experimental volume-expanded hypertension and human essential hypertension.
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PMID:Hypothalamic sodium-transport inhibitor is a high-affinity reversible inhibitor of Na+-K+-ATPase. 609 82

The present study was undertaken to quantify the circulating kinins in patients with various cardiovascular diseases using a newly developed radioimmunoassay technique and to evaluate this method in terms of its clinical application. For the determination of bradykinin (BK), this assay uses a rabbit anti-serum which has been injected with kallidin. This assay shows good specific activity, recovery and reproducibility. In order to avoid the formation of kinin as well as to block its inactivation, human blood samples were collected with a polypropylene syringe containing an inhibitor mixture (EDTA, trasylol, 1-10-phenanthroline, soybean trypsin inhibitor, polybrene). 1) The plasma BK concentration in normal human subjects, in patients with essential hypertension, effort angina and other cardiac diseases were 12.2, 9.2, 8.0 and 14.0 pg/ml, respectively. 2) Thirty min after captopril (12.5 mg, p.o.) administration, blood pressure and pulmonary wedge pressures decreased, and cardiac output increased accompanied with increases in plasma renin activity, plasma BK concentration and plasma norepinephrine concentration. 3) During the cold pressor test, both plasma BK concentration and blood pressure increased in the normal human subjects, whereas plasma BK levels decreased and blood pressure increased in the patients with hypertension. This radioimmunoassay for plasma BK determination makes it possible to measure plasma BK concentration in patients with various cardiac diseases.
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PMID:[Plasma bradykinin concentration in patients with cardiovascular diseases]. 636 31

Hypertension of unknown cause is generally termed "essential." Because hypertension has long been considered a possible complication of lead poisoning and the EDTA lead-mobilization test has proved to be a sensitive indicator of excessive body stores of lead, we used this test to evaluate cumulative past lead absorption in 48 men diagnosed as having essential hypertension. Patients who had hypertension with reduced renal function (i.e., serum creatinine level greater than 1.5 mg per deciliter [133 mumols per liter]) had significantly larger amounts of mobilizable lead than did patients who had hypertension without renal impairment. The increase in mobilizable lead was not due to the renal disease itself, since 22 control patients without a history of essential hypertension but with comparable renal impairment from known causes excreted significantly less lead chelate during the three-day test. These data suggest that lead may have an etiologic role in the renal disease of some patients usually designated as having "essential" hypertension.
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PMID:Contribution of lead to hypertension with renal impairment. 640 92

Ten patients with gout, hypertension, and mild to moderate renal insufficiency were studied for possible lead nephropathy by measuring stimulated urinary lead excretion. Seven had a history of lead exposure, 5 from illegal alcohol and 2 from industrial sources. Occult lead was assessed by 24 h urine collection measurements over a 72 h period after intramuscular administration of calcium disodium EDTA. Two patients with a history of lead exposure excreted 707 and 687 micrograms Pb/72 h, respectively, and a 3rd excreted 506 micrograms Pb/72 h. The remainder had a normal response, with mean urinary lead excretion of 251 +/- 42 micrograms Pb/72 h. Since we were unable to demonstrate that lead was important to the pathogenesis of the renal we were unable to demonstrate that lead was important to the pathogenesis of the renal failure in 7 patients despite a positive history of lead exposure in 2, we suggest that factors other than lead may be the cause of renal failure in most patients with gout and renal disease.
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PMID:Occult lead intoxication in patients with gout and kidney disease. 643 39

Acute animal studies were conducted to explore the effect of calcium manipulation on blood pressure and in the blood pressure response to angiotensin blockade under conditions of renovascular hypertension in anesthetized mongrel dogs. Ethylenediaminetetraacetic acid (EDTA) was used to lower serum calcium (SCa) levels, while nifedipine was infused intravenously to antagonize calcium at the cellular level. Angiotensin blockade was accomplished by infusion of the competitive inhibitor of angiotensin, saralasin. Following renal artery clamping, mean arterial pressure (MAP) increased a mean of 21 +/- 3 mm Hg from 116 +/- 5 to 137 +/- 6 mm Hg (p less than 0.001) in 23 studies. Lowering of SCa by 30 min of EDTA infusion in 9 of these animals resulted in a mean fall of -21 +/- 4 mm Hg from 127 +/- 7 to 105 +/- 7 mm Hg (p less than 0.005). A 30 min infusion of nifedipine solution in 5 animals did not significantly affect blood pressure. In 9 normocalcemic hypertensive animals, saralasin reduced MAP from 138 +/- 8 to 127 +/- 8 mm HG (p less than 0.001). In 9 animals with lowered SCa (6.9 +/- 0.2 mg/dl) due to 30 min of EDTA infusion, the same dose of saralasin resulted in a greater reduction of MAP from 127 +/- 7 to 78 +/- 9 mm Hg (p less than 0.001). Nifedipine and saralasin used together in 5 hypertensive animals resulted in the reduction of MAP from 155 +/- 14 to 131 +/- 14 mm Hg (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium chelation and calcium-channel blockade in anesthetized acute renovascular hypertensive dogs. 643 63

The CaNa2EDTA lead mobilization test permits identification of lead nephropathy in a variety of situations in which past-exposure is uncertain and acute symptoms of lead poisoning are lacking. In addition to lead workers and moonshiners, lead nephropathy has been identified in gout patients with renal failure and in hypertensives with renal failure. The presence of excessive mobilizable lead in these patients and its absence in control patients with comparable renal dysfunction suggests that unrecognized lead poisoning is sometimes responsible for renal failure in gout and hypertension. Use of the EDTA lead-mobilization test may thus permit prevention and sometimes treatment of renal failure in patients who might otherwise enter the End-Stage Renal-Disease Program. The controversies surrounding interstitial nephritis in lead poisoning, gout and hypertension may in part be explained by the surreptitious role of lead.
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PMID:The role of lead in renal failure. 675 98

The glomerular filtration rate (GFR) was determined in rats with an isogeneic kidney transplant and compared with that of unilaterally nephrectomized rats. Experiments were carried out in adult rats, 3 months of age, weighing approximately 300 g, as well as in juvenile rats, 6 to 8 weeks of age, weighing approximately 170 g. All donor kidneys were taken from adult rats. The GFR was measured regularly, using a chromium 51-EDTA clearance technique which permitted repeated measurements to be taken in the same animals, during a 15-week followup period. After unilateral nephrectomy the GFR per 100 g body weight (BW) increased compared with that of a single normal kidney. Adult transplant recipients had a GFR per 100 g BW of about 80% of that of unilaterally nephrectomized rats. There was no statistical difference in the GFR when comparing adult recipients of either a normal or a hyperfunctional kidney. When isografts were transplanted to juvenile recipients, there was an initial decrease in the absolute GFR compared with the donor value in the case of a normal adult donor kidney. This decrease was even more pronounced when a hyperfunctioning kidney was transplanted to a juvenile recipient. However, when related to BW the GFR was, as in the adult recipients, about 80% of that of unilaterally nephrectomized juvenile rats. During the followup period the systolic blood pressure was measured regularly by tail plethysmography, in order to detect any blood pressure elevations, which are a frequent complication in adult and pediatric human renal transplantation. However, no hypertension was observed after isogeneic kidney transplantation in the various groups. These results show that the GFR of isogeneically transplanted rat kidneys amounts to about 80% of the maximally attainable level. Isogeneic transplantation of an adult kidney to a juvenile recipient results in a rapid adaptation of the GFR to the smaller size of the body and does not cause an increase in blood pressure.
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PMID:The glomerular filtration rate of isogeneically transplanted rat kidneys. 704 95


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