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

Myocardial contractility of normotensive and spontaneously hypertensive rabbits was determined following an iv bolus injection of propranolol HCl. Left ventricular pressure and dimension were used to calculate the contractility parameters of (dP/dt)max, maximum fiber shortening velocity (Vcf), and the slope of the end systolic pressure-end systolic volume line (ESP-ESV line). Hypertension was induced by a methoxamine HCl iv infusion which mimicked the cardiac effects seen in essential hypertension. Propranolol caused a significant decrease in all contractility parameters (p less than 0.05) within 15 min after administration, with a peak effect occurring after 30-35 mins. The pharmacokinetics and pharmacodynamics of propranolol were fit using Hill's equation in conjunction with the concentration of drug in the theoretical effect compartment. The normotensive group of rabbits had a calculated EC(50) of 12.7 ng/ml, while the hypertensive group had an EC(50) of 6.9 ng/ml, indicating that the hypertensive rabbits were much more sensitive to the propranolol than the normotensive group. In addition, the normotensive group of rabbits demonstrated a much different pharmacokinetic-pharmacodynamic relationship than that of the hypertensive group, indicating that the hypertensive state of the animal has a significant effect upon the concentration-effect relationship.
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PMID:Effect of propranolol on the myocardial contractility of normotensive and spontaneously hypertensive rabbits: relationship of pharmacokinetics and pharmacodynamics. 261 85

The effects of one month's treatment with each of nifedipine, verapamil, diltiazem, propranolol and placebo, given in random order, on fasting plasma glucose, haemoglobin Alc, serum fructosamine, immunoreactive insulin, cholesterol, and triglyceride were studied in a group of 19 patients with hypertension and non-insulin dependent diabetes mellitus. The metabolic effects of the active drugs were generally small but fasting plasma glucose was increased by propranolol from 9.3 +/- 3.0 to 10.4 +/- 3.4 mmol/l (P less than 0.01) (mean +/- SD) and to 10.1 +/- 3.2 mmol/l (P less than 0.05) by nifedipine. Serum fructosamine was increased from 2.75 +/- 0.53 to 2.89 +/- 0.62 mmol/l (P less than 0.05) by diltiazem and to 2.91 +/- 0.65 (P less than 0.05) by propranolol. Verapamil increased fasting serum immunoreactive insulin: diltiazem and propranolol tended to reduce it. Propranolol but not the other drugs significantly increased serum triglyceride. Calcium antagonists may be preferable to beta adrenoceptor blockers for the treatment of hypertensive diabetics. Of the three calcium antagonists we studied, verapamil may have advantages over nifedipine and diltiazem.
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PMID:The effects of verapamil, diltiazem, nifedipine and propranolol on metabolic control in hypertensives with non-insulin dependent diabetes mellitus. 265 57

Quality of life was evaluated in a four-month randomised double-blind trial of verapamil compared with propranolol in the treatment of hypertension in 94 patients in the UK. Scores on a health status index, measuring activity and perceived health, increased in verapamil patients compared to a decrease in propranolol patients (P = 0.01). Measures of psychiatric morbidity also tended to improve with verapamil and deteriorate with propranolol. Propranolol patients reported more symptoms overall compared with verapamil (P less than 0.05). The prevalence of certain symptoms--headaches, weak limbs and slower walking pace, increased significantly with propranolol compared with verapamil, but constipation was more common in verapamil patients (P less than 0.05). After four months, diastolic blood pressure averaged 86.2 mmHg with verapamil and 90.3 mmHg with propranolol (P = 0.02). However, this difference in final blood pressure did not explain the more favourable quality of life scores with verapamil, and the data suggest that health-related well-being is higher with this drug.
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PMID:The effects of verapamil and propranolol on quality of life in hypertension. 266 24

On the basis of echocardiographic investigations changes were analysed of certain haemodynamic parameters in 40 patients aged 21-50 years, mean 44 years, with primary arterial hypertension in stage II according to WHO classification. All patients were randomly chosen to receive for 6-9 weeks propranolol 120-480 mg daily, mean dose 280 mg, or pindolol 10-35 mg daily, mean dose 22 mg daily. The changes developing during the treatment with both drugs in relation to the initial values included the mean arterial blood pressure, the heart rate, the index of cardiac output and the systolic left-ventricular tension. In the studied patients treated with propranolol the heart rate and the ejection volume were decreased more than during pindolol treatment. Propranolol increased evidently the total peripheral vascular resistance and decreased the ejection fraction and the mean velocity of shortening of the circumferential fibres. Pindolol decreased slightly the peripheral vascular resistance and increased the ejection fraction and the mean velocity of shortening of the circumferential fibres. Pindolol, in relation to propranolol, had a more favourable effect on haemodynamics in patients with primary hypertension.
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PMID:[Effect of the treatment with propranolol and pindolol on selected hemodynamic parameters in patients with primary arterial hypertension]. 270 Oct 39

The density of beta 2-receptors in intact lymphocytes was studied by binding with 125iodo-cyanopindolol in 18 male patients with mild or moderate hypertension before and after monotherapy with propranolol. The density of these receptors was also determined in 5 patients before and after dynamic exercise. We found that propranolol therapy evoked different changes in the density of beta-receptors in patients with essential hypertension. Based on these results, all patients were divided into two groups: (a) patients who responded to the administration of propranolol by an increase in receptor density and (b) patients who responded with a decrease in receptor density. Propranolol therapy had a pronounced hypotensive effect in the second group and no hypotensive effect in the first group. In the second group, heart rate was significantly higher initially and showed a significantly greater decrease after treatment. The initial values for beta 2-receptor density were also significantly higher in this group than in the first group. Mean values of baseline plasma renin activity (PRA) were higher in the second group, but this difference was nonsignificant. The 5 patients who participated in dynamic exercise exhibited different changes in beta-receptor density, which correlated with the changes observed with propranolol treatment. There was no correlation between PRA and the density of beta 2-receptors in lymphocytes. Positive correlations were found between the density of these receptors and left-ventricular myocardial mass and interventricular septal thickness. The data indicate that the density of these receptors in lymphocytes is regulated in a qualitatively different manner in the two groups of patients with essential hypertension; this difference appears to be related to baseline renin levels or, perhaps, catecholamine levels. Additional studies are needed to clarify the regulation of beta 2-receptors in essential hypertension.
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PMID:Characteristics of lymphocyte beta-adrenoceptors in essential hypertension: effects of propranolol treatment and dynamic exercise. 285 50

The autonomic and antihypertensive activities of amosulalol (YM-09538) were studied in conscious rats. Single oral administration of amosulalol antagonized the phenylephrine-induced pressor and isoproterenol-induced positive chronotropic responses with DR10 values of 11.5 and 13.6 mg/kg in pithed rats, respectively, indicating that the compound inhibits both alpha 1- and beta 1-adrenoceptors to almost the same extent in agreement with previously reported results in vitro. Amosulalol was approximately 50 times less potent than prazosin and 12 times more potent than labetalol at alpha 1-adrenoceptors, and it was approximately as effective as labetalol and 2 times more potent than propranolol at beta 1-adrenoceptors. In spontaneously hypertensive rats (SHR), renal hypertensive rats and DOCA/salt hypertensive rats, a single oral administration of amosulalol (3-30 mg/kg) lowered acutely systolic blood pressure with a duration of over 6 hr and was found to be approximately 50 times less potent than prazosin and 3 times more potent than labetalol in lowering blood pressure. Propranolol did not cause such an immediate hypotensive effect. Amosulalol and labetalol did not increase heart rate, whereas prazosin induced a tachycardia in the hypertensive rats. Repeated oral administrations of amosulalol and labetalol (50 mg/kg/day, b.i.d., for 12 weeks) produced not only an antihypertensive effect without evidence of tolerance, but also reductions in plasma renin activity (PRA) and heart rate in SHR with established hypertension. We conclude that alpha-adrenoceptor blockade by amosulalol might account for its antihypertensive activity and that its beta-adrenoceptor blockade might inhibit reflexogenic increases in heart rate and PRA due to the reduction in blood pressure.
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PMID:Autonomic and antihypertensive activity of oral amosulalol (YM-09538), a combined alpha- and beta-adrenoceptor blocking agent in conscious rats. 286 2

Esmolol is a beta 1-selective adrenoceptor blocker that is rapidly metabolized by blood and liver esterases. The beta-receptor and hemodynamic effects of esmolol were determined in a group of 12 healthy men and were compared with those induced by both oral and intravenous propranolol. Esmolol was rapidly effective in inducing at least 90% of steady-state beta-blockade within 5 minutes of either initiating or changing the esmolol infusion rate. More importantly, when esmolol infusion was discontinued the beta-blockade had totally disappeared by 18 minutes after esmolol, 300 micrograms/kg/min, and had been reduced by 50% after 750 micrograms/kg/min. In contrast, 30 minutes after discontinuation of a propranolol infusion, there was no change in the level of beta-blockade. Propranolol was much more potent at blocking isoproterenol-induced tachycardia (dose ratio 33.5 +/- 2.5) than was even the highest dose (750 micrograms/kg/min) of esmolol (dose ratio 13.1 +/- 1.0). The same dose of intravenous propranolol was approximately equipotent to oral propranolol, 40 mg every 8 hours (dose ratio 33.5 +/- 2.5 and 34.5 +/- 3.6, respectively). In contrast, propranolol, 40 mg every 8 hours, and esmolol, 300 micrograms/kg/min, were equipotent in antagonizing exercise-induced tachycardia (40.1% +/- 2.3% and 42.7% +/- 3.2%, respectively). Esmolol had striking hypotensive effects. Systolic blood pressure fell by 20 mm Hg during esmolol infusions of 750 micrograms/kg/min. Esmolol appears to be a potent beta 1-selective adrenoceptor antagonist with a particularly strong hypotensive effect. It is likely to be very useful in the treatment of hemodynamically unstable patients and may be useful in the emergency treatment of hypertension.
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PMID:Ultra-short-acting beta-blockade: a comparison with conventional beta-blockade. 286 29

The aim of the present study was to evaluate whether beta blockade presents a risk of intermittent claudication and how it affects the walking capacity and lower limb haemodynamics in patients with intermittent claudication. The study was divided into six parts: A case-control study with 55 pairs, cases with hypertension and intermittent claudication and controls with hypertension only, matched for age, sex, place of residence, and time of examination, all without coronary heart disease, which is a known confounding factor. An open controlled study on the effect of withdrawal of beta blockade on walking capacity of 28 patients with intermittent claudication. A placebo-controlled double-blind crossover study on the effect of antihypertensive treatment on the walking capacity of 14 patients with intermittent claudication. Three placebo-controlled double-blind crossover studies on the effect of propranolol, metoprolol, pindolol, labetalol, and/or methyldopa on calf blood flow in 34 hypertensive subjects without peripheral arterial disease and in altogether 21 patients with intermittent claudication. Walking capacity was measured on a treadmill. Calf blood flow was measured with strain gauge plethysmography by the venous occlusion technique. The case-control comparison showed that beta blockers were used as often by patients with intermittent claudication as by controls. Walking capacity increased during the first month of the open controlled study irrespective of whether the beta blockade was withdrawn or continued. There was no difference in this respect between the various types of beta blockers. Antihypertensive treatment with metoprolol or methyldopa did not affect walking capacity. Resting calf blood flow was unaffected by propranolol or metoprolol, regardless of the presence or absence of peripheral arterial disease, as well as by pindolol, labetalol, or methyldopa in patients with intermittent claudication. During reactive hyperaemia, propranolol and metoprolol reduced flow in patients without peripheral arterial disease. Propranolol also reduced hyperaemic blood flow in the limb with less or no symptoms in patients with intermittent claudication. None of the active drugs decreased the hyperaemic flow consistently in the limb with the stronger symptoms. In a comparison of haemodynamic effects between the drugs, calf blood flow at rest was higher after pindolol than after propranolol and hyperaemic flow of the better limb was higher after pindolol than after propranolol and labetalol.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Beta blockade and intermittent claudication. 286 73

The finger systolic pressure of 25 healthy subjects and 23 hypertensives was studied by plethysmography at 30 degrees, 15 degrees and 10 degrees centigrade. The hypertensive group was given equipotent doses of either Metoprolol or Propranolol in accordance with a double-blind cross-over protocol including a washout period. The fall in systolic pressure between the brachial artery in the upper arm and the digital artery was significantly increased in the hypertensive group as compared to healthy controls; the rise persisted under hot and hyperemic conditions and remained constant during both betablocker treatments. In the hypertensive group digital arterial tone increased under cold conditions before any treatment; this abnormality did not vary under Metoprolol but intensified significantly under Propranolol. Finger plethysmography made it possible to show and quantify the peripheral vascular repercussions of hypertension on the digital artery and evaluate the changes induced by treatments. It also helps to clarify the physiopathology of certain side effects caused by betablockers and might to some extent help in the choice and the survey of treatment and in the subsequent follow-up.
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PMID:[Hemodynamic study, under hot and cold conditions, of the digital artery in arterial hypertension and the effects of cardioselective and non-cardioselective beta blocker treatment]. 287 43

20 patients with confirmed diagnoses of arterial hypertension and chronic obstructive pulmonary disease were studied. Groups of 10 patients each were treated with propranolol 2 X 40 mg p.o. or betaxolol (Kerlone) 20 mg p.o., respectively. Pulmonary function, blood pressure and heart rate were assessed before and at 2, 4 and 6 h after administration of the first tablet on day 1 of the study. The same parameters were recorded 2 h after ingestion of the morning dose on each of the following days. Both drugs caused comparable significant decreases in blood pressure and heart rate on the 1st day of treatment. Propranolol was associated with a documented increase in the degree of bronchial obstruction.
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PMID:[Effect of different beta-receptor blockers on the respiratory function of patients with chronic obstructive pulmonary disease and arterial hypertension]. 289 6


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