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)

We investigated the effect of atrial natriuretic factor (ANF) on aldosterone receptors in the kidney cytosol, because the binding of aldosterone to aldosterone receptors in the cytosol is considered a critical step of its action. Rat atriopeptin III was injected into male Sprague-Dawley rats (200-250 g) via the femoral vein while under pentobarbital anesthesia, and aldosterone receptors in the kidney cytosol were determined. The maximum binding capacity and dissociation constant were calculated by the Scatchard analysis. Maximum binding capacity of both types of aldosterone receptor (Type I, high affinity and low binding capacity and Type II, low affinity and high binding capacity) gradually decreased after ANF injection, reached the lowest level after 2 hours, and then slightly recovered. When more than 2.5 micrograms/kg of rat atriopeptin III was injected, the density of aldosterone receptors significantly decreased. Injection of 12.5 micrograms/kg of rat atriopeptin III decreased maximum binding capacity of Type I receptor from 42.3 +/- 2.4 (mean +/- SD, n = 6) to 22.8 +/- 3.2 femtomole/mg protein (n = 6) (p less than 0.01), and that of Type II receptor decreased from 388 +/- 46 to 285 +/- 30 fmol/mg protein (p less than 0.01). Dissociation constant of both types of receptors did not change significantly after ANF injection. Plasma aldosterone concentration showed no significant change after ANF injection, and a significant change was noted after ANF administration on aldosterone receptors in the experiments on adrenalectomized rats 7 days after operation. Furosemide had no significant effect on aldosterone receptors in both normal and adrenalectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Apr
PMID:Regulation of aldosterone receptor in rat kidney cytosol by atrial natriuretic factor. 252 15

The effect of 30 mg/day slow-release frusemide given orally for 12 months was studied in 64 patients previously treated with thiazides for mild to moderate essential hypertension. Frusemide had a significant antihypertensive effect (P less than 0.001), and compared to thiazides significantly reduced fasting serum glucose (P less than 0.015), haemoglobin A1c (P less than 0.025), albumin (P less than 0.025) and serum calcium (P less than 0.025), and significantly increased serum sodium and chloride concentrations (P less than 0.0001). There was also a non-significant trend for frusemide to reduce serum total cholesterol, triglycerides and urate, and to increase serum potassium. Frusemide was well tolerated in all but three patients. It is concluded that slow-release frusemide has a comparable antihypertensive effect to that of thiazide diuretics, but has fewer metabolic side-effects, and should be used in-preference to thiazides for the treatment of arterial hypertension when a diuretic is indicated.
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PMID:Long-term treatment with slow-release frusemide compared with thiazide treatment in arterial hypertension. 262 32

Thirty patients with moderate to severe, uncontrolled hypertension were treated with a captopril/frusemide combination. The initial dose of captopril (6.25 mg or 12.5 mg) produced an acute fall in BP from 162 +/- 6/102 +/- 3 to 132 +/- 6/85 +/- 3 mmHg but at a dose of 12.5 mg three times daily outpatient BPs were not controlled. Frusemide (40 mg/day) was added and increased as necessary at two week intervals until BP was satisfactorily controlled or a total daily dose of 160 mg was reached. During long-term follow-up over a mean period of two years good BPs were achieved with an average daily dose of frusemide of 95 mg and captopril 52 mg (148 +/- 3/90 +/- 2 mmHg). There was no overall change in renal function or plasma potassium although small rises in blood urea were seen in some patients. In a group of 28 patients controlled on this regimen a change to a twice daily schedule without alteration of the dose of captopril or frusemide did not affect clinic BPs. In addition, BP remained controlled throughout the day as measured at home with an electronic sphygmomanometer. No case of glucose interolence was observed despite high doses of frusemide (HbA1 = 7.1 +/- 0.12%) and in 12 patients, where prospective measurements of HbA1 were measured, there was a fall from 7.6 +/- 0.21% to 6.9 +/- 0.16% suggesting an effect of captopril on insulin sensitivity. We conclude that low dose captopril with a variable frusemide dosage represents a simple and effective treatment for moderate to severe hypertension.
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PMID:Low dose, twice daily captopril and frusemide: a safe, effective and flexible third line treatment regimen for hypertension. 267 68

Of 1894 patients registered in a family medicine clinic, 101 (5.3%) had been taking diuretics for at least 6 months. The sex distribution was equal and the average age was 68.7 years. 60% were taking Kaluril, 30% Aquadon and 10% Frusemide. Most had hypertension or heart failure, or both. 6 patients developed hyperglycemia, 2 hyponatremia, 5 hypokalemia, 2 hyperkalemia and 10 hyperuricemia. In 19 the ECG showed arrhythmias. 5 of 56 patients had hypomagnesemia and another 12 had low borderline levels. In the light of these results and those in the literature, we conclude that diuretics are not as safe as previously thought.
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PMID:[Use of diuretics in family practice]. 273 88

Minoxidil is a potent antihypertensive which is reserved for severe cases. A 58-year-old man admitted for evaluation of progressive dyspnea and peripheral edema had been taking Minoxidil, Normiten and Lasix for severe hypertension. Echocardiography disclosed a massive pericardial effusion but there were no signs of tamponade. Discontinuation of Minoxidil resulted in complete clearance of the pericardial fluid within 3 months. Awareness of this potentially fatal side-effect of Minoxidil is mandatory.
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PMID:[Massive pericardial effusion following minoxidil]. 279 35

The antihypertensive efficacy and renal effects of enalapril maleate therapy were evaluated in 13 hypertensive patients with chronic renal failure. Enalapril was administered as follows: alone; added to furosemide, clonidine hydrochloride, or atenolol; or in combination with any of the aforementioned drugs. Three patients did not complete the study; uncontrolled hypertension was the cause in two of these patients. In the remaining ten patients, short-term (mean +/- SD, 63 +/- 9 days) enalapril maleate therapy decreased the patient's seated blood pressure from 161/98 +/- 19/8 to 130/80 +/- 13/7 mm Hg. Furosemide was administered to eight patients; the dose of concomitant sympatholytic therapy was decreased in five of five patients. Serum potassium concentration increased from 4.1 +/- 0.3 to 4.5 +/- 0.3 mmol/L. Levels of urinary total protein excretion decreased from 2.23 +/- 2.05 to 1.08 +/- 1.45 g/d. Renal function (creatinine clearance, 0.58 +/- 0.21 mL/s) did not change from baseline. During long-term therapy, the rate of progression of renal insufficiency seemed to slacken in three of four patients with diabetic nephropathy. Thus enalapril can reduce blood pressure and proteinuria in hypertensive patients with chronic renal insufficiency. The possibility that enalapril can slow the progression of diabetic nephropathy remains to be confirmed by future studies.
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PMID:Efficacy and renal effects of enalapril therapy for hypertensive patients with chronic renal insufficiency. 284 67

A randomised double blind study was performed in order to compare the cardiac effects of captopril and minoxidil in a subset of patients with severe primitive hypertension, uncontrolled (diastolic BP greater than 100 mmHg) by Metroprolol 200 mg/d and Furosemide 80 mg/d. 25 male pts completed the six month study, 33 pts having been excluded before randomisation (22 inadequate echoes) and 20 after randomisation (7 ambiguities on wall measurement). Average captopril dosage was 265 mg/d (150-300 mg), average minoxidil dosage was 19.6 mg/d (7.5-30 mg), dosages of Furosemide, Spironolactone and Metroprolol were similar in the two groups. Blood pressure decreased dramatically with both regimens (208/130 to 148/96 with captopril, 194/115 to 154/100 with minoxidil). Sokolow index was at the upper range of normal and decreased with both drugs. Cardiothoracic ratio decreased only with captopril. Echocardiograms were performed and read blindly at the end of the study. LV mass was measured according to Devereux, method. All patients had severe LVH. After 6 months posterior wall thickness decreased from 14.8 to 13.8 mm with captopril, remained stable from 14.1 to 14.9 mm with minoxidil, septal thickness decreased from 17.2 to 15.7 mm with captopril and remained stable (14.8 to 15.2 mm) with minoxidil. LV mass and mass index respectively decreased from 456 g and 232 g/m2 to 372 g and 190 g/m2 with captopril, and remained unchanged from 413 g and 215 g/m2 to 420 g and 218 g/m2 with minoxidil. Fractional shortening remained normal in both groups. Intra patients reproducibility was suboptimal because of difficulties in precise delineation of the endocardium in the severely hypertrophied ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of the effect of captopril and minoxidil on left ventricular mass. Results of a 6-month comparative double-blind test]. 295 36

The preparation, application and clinical usage of 99mTc-mercaptoacetyltriglycine, MAG3, a tubular secreted compound, is described in the first 225 patients in a phase III study. Image quality, relative renal function, and renal transit times were compared with a 4 fold greater administered activity of 99mTc-DTPA in 11 patients. Correlation coefficients of 0.94 for relative function, 0.83 for parenchymal transit time index and 0.82 for whole kidney transit time index were found. Frusemide responses were similar. 99mTc-MAG3 is an efficacious radiopharmaceutical for routine renal radionuclide studies, giving excellent image quality in patients with hypertension, poor renal function, obstructive nephropathy or a renal transplant.
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PMID:Clinical experience with 99mTc-MAG3, mercaptoacetyltriglycine, and a comparison with 99mTc-DTPA. 297 19

To measure specifically angiotensin-(1-8)octapeptide, peptides were extracted from 2 ml of plasma by reversible adsorption to bonded-phase silica. The angiotensin-(1-8)octapeptide was then isolated by isocratic reversed-phase high-performance liquid chromatography and quantified by radioimmunoassay. The extraction recovery of 125I-angiotensin II added to 2 ml of plasma was 99 +/- 2% (mean +/- SD). The overall recovery of 5, 10, and 20 fmol unlabeled angiotensin II added to 1 ml of plasma was 80 +/- 10%. The coefficient of variation for within-assay precision was 0.06 and for between-assay precision 0.13. The detection limit was 0.4 fmol/ml. Buffer and plasma blanks were below the detection limit. Normal subjects on a free diet in supine position averaged 4.2 +/- 1.7 fmol/ml angiotensin-(1-8)octapeptide. Furosemide (40 mg p.o.) and standing increased these values to 22 +/- 7.6 fmol/ml. In four volunteers, immunoreactive "angiotensin II" (more or less angiotensin-like material) was measured serially before and after converting-enzyme inhibition (Hoe 498) with conventional Dowex extraction. At peak inhibition, plasma immunoreactive "angiotensin II" levels decreased by only 44%. In contrast, angiotensin-(1-8)-octapeptide isolated by high-performance liquid chromatography completely disappeared. In hypertensive patients receiving long-term treatment with enalapril, plasma levels of angiotensin-(1-8)octapeptide fell from 2.7 +/- 0.9 to 0.9 +/- 0.3 fmol/ml (mean +/- SEM) 2 hours after the morning dose, whereas levels of immunoreactive "angiotensin II" were not significantly changed. We found that this sensitive method specifically measured angiotensin-(1-8)octapeptide and demonstrated that true angiotensin II virtually disappears during converting-enzyme inhibition.
Hypertension
PMID:True versus immunoreactive angiotensin II in human plasma. 298 22

The inhibitory effect of high and low molecular weight native and synthetic rat atrial peptides on oxygen consumption in isolated rat kidney mitochondria and slices was measured. Oxygen consumption by mitochondria was measured in the presence of succinate and/or adenosine diphosphate, furosemide, and low and high molecular weight native and synthetic rat atrial peptides. After the addition of succinate, adenosine diphosphate limiting respiration (State 4) increased in the presence of low, but not high, molecular weight native rat atrial peptides. Furosemide caused a significant decrease in State 4 respiration (p less than 0.001). Angiotensin II and arginine vasopressin did not alter State 4 respiration. The rate of oxygen consumption after the addition of saturating adenosine diphosphate in the presence of saturating succinate (State 3 respiration) was reduced by low and high molecular weight native rat atrial peptides. Furosemide completely blocked oxygen consumption after the addition of adenosine diphosphate. Oxygen consumption was unchanged by trypsin treated (natriuretically inactive) low molecular weight rat atrial peptides and ventricular protein extracts of high and low molecular weight native rat atrial peptides. Synthetic and low molecular weight native rat atrial peptides had similar effects on mitochondrial oxygen consumption. Low molecular weight native and synthetic rat atrial peptides decreased the adenosine diphosphate to oxygen ratio, and these peptides, as well as furosemide, also induced mitochondrial swelling; none of the other rat atrial peptide combinations nor angiotensin II produced this effect. In kidney slices, basal oxygen consumption (without substrates) was stimulated by succinate.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Rat atrial natriuretic peptides inhibit oxygen consumption by rat kidney. 315 63


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