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)

The effect of propranolol therapy on plasma renin activity and blood pressure control was evaluated in 35 uremic patients receiving intermittent center-based outpatient hemodialysis. Patients were determined to be either compliant or noncompliant with therapy based on the steady-state predialysis plasma propranolol concentration. Noncompliance occurred with remarkable frequency and was associated with persistent hyperreninemia and poorly controlled hypertension. Blood pressure control was significantly better in compliant patients, in whom plasma renin activity was generally, but not universally, suppressed. Propranolol can be effectively used in the management of hypertensive dialysis patients, but steady-state plasma propranolol levels should be measured to assess compliance in patients apparently refractory to treatment.
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PMID:Propranolol in hypertensive dialysis patients: efficacy and compliance. 118 40

In a health examination survey of 2322 middle-aged men the prevalence of hypertension, defined as supine DBP greater than or equal to 105 mmHg and including those on treatment, was 7.5%. All untreated and those inadequately treated were invited to a hypertension clinic. One year's treatment in 86 men achieved a BP reduction of 29/17 mmHg in supine and 27/16 mmHg in erect position. This reduction was maintained for a three-year period and considered satisfactory in 80% of subjects. Propranolol, alone or in combination with other agents, was used in more than 80% of the cases. Special considerations in treating asymptomatic individuals are discussed.
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PMID:Treatment of hypertension in middle-aged men. A feasibility study in a community. 126 65

An adequate propranolol dose to reduce 25% the initial heart rate was searched in 19 children with portal hypertension. 13 were pre-hepatic and 6 hepatic hypertension, mean age: 6.96 +/- 3.48 years, range: 2-14 years. Treatment was started with 0.5 mg/kg/day increasing 0.25 mg/kg/day every third day, needing an average of 26 +/- 13 days (range: 6-54 days) to obtain the response. Daily dose ranged from 1 to 5.25 mg/kg/day (mean: 2.69 +/- 1.16). The highest daily dose was 175 mg, the lowest 23.4 mg (mean: 58.27 +/- 36.6 mg/day). Some parameters were evaluated before and after achieving the dose. There was a significant reduction of mean blood pressure (p < 0.01) and peripheral venous pressure (p < 0.05) in 68.4% of patients. A significant elevation (p < 0.001) of 24 hour urinary catecholamine levels occurred in 94.7%. Side effects were minimal. Propranolol could be considered a safe pharmacological option in these patients.
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PMID:[Propranolol in children and adolescents with portal hypertension: its dosage and the clinical, cardiovascular and biochemical effects]. 134 Aug 25

To determine whether the release of endothelium-derived relaxing factor (EDRF) is sympathetically mediated, we studied the effects of beta-blockade by propranolol, ganglionic blockade with hexamethonium, or mechanical pithing on the blood pressure response to EDRF inhibition in anesthetized rats. We inhibited EDRF with 10 mg/kg of either NG-monomethyl-L-arginine (L-NMMA) or N omega-nitro-L-arginine-methyl ester (L-NAME). In controls, L-NMMA and L-NAME increased blood pressure by 14 +/- 1 (p less than 0.01) and 22 +/- 2 mm Hg (p less than 0.01), respectively. Propranolol lowered blood pressure from 98 +/- 3 to 72 +/- 4 mm Hg without altering the response to L-NAME (delta 26 +/- 3). This response correlated with the resting blood pressure (r = 0.87; p less than 0.001). Hexamethonium (25 mg/kg) lowered blood pressure from 118 +/- 6 to 85 +/- 4 mm Hg but did not change the response to L-NMMA (delta 15 +/- 1). In pithed rats, blood pressure was lowered, but the pressor response to L-NAME was unchanged. When blood pressure was returned to normotensive levels by angiotensin II, norepinephrine, or phenylephrine, L-NAME increased blood pressure by 50 +/- 2, 68 +/- 8, and 109 +/- 7 mm Hg, respectively (p less than 0.001). We conclude that an intact autonomic nervous system is not needed for the pressor response to EDRF inhibition. The enhanced response in pithed rats treated with vasoconstrictors may be due to removal of the buffering effect of the baroreceptors and the absence of EDRF, which would oppose vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Sympathetic modulation of endothelium-derived relaxing factor. 135 May 73

Evidence was sought for beta-adrenergic-induced increase in femoral vascular angiotensin production in sham-operated and nephrectomized rabbits. Systemic blood pressure and right femoral blood flow were monitored in anesthetized rabbits. Arterial and femoral venous plasma angiotensin II (Ang II) and angiotensin I (Ang I) were measured by radioimmunoassay after high-performance liquid chromatography. Isoproterenol, 1 and 10 nmol/min, was infused intrafemoral arterially, reducing femoral vascular resistance by 47 +/- 5% and 60 +/- 6% in the sham-operated group, and by 50 +/- 6% and 63 +/- 4% in the nephrectomized group, respectively. The hemodynamic effect of isoproterenol was blocked by 2 mumol/kg propranolol injected intravenously plus 0.2 mumol/min infused intrafemoral arterially, indicating that the effect was beta-adrenergically mediated. In the sham-operated group, arterial Ang II and Ang I levels were increased, respectively, by 85 +/- 16% and 103 +/- 23% with the low dose of isoproterenol, and by 121 +/- 13% and 563 +/- 126% with the high dose of isoproterenol. The apparent femoral Ang II secretion rate was increased by 3.2-fold and 4.4-fold, and the apparent femoral Ang I secretion rate increased by 4.3-fold and 21.2-fold, with the low and high dose of isoproterenol, respectively. Propranolol abolished or markedly attenuated the increased arterial angiotensin levels and the increased femoral angiotensin secretion rates. Neither the low nor the high dose of isoproterenol caused any increase in plasma levels or the apparent femoral secretion rates of the angiotensins in the nephrectomized group. Low plasma levels of Ang I and Ang II remained in the nephrectomized group, representing some locally generated angiotensins.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Beta-adrenergic-induced local angiotensin generation in the rabbit hind limb is dependent on the kidney. 167 1

Feline myocardial diseases today are largely represented by disorders involving LV hypertrophy. They may be attended by arrhythmias, congestive heart failure, systemic hypertension, thromboembolic complications, and sudden death. These structural myocardial disorders and their hemodynamic and electrocardiographic derangements may cause or result in variable degrees of diastolic dysfunction. Propranolol and aspirin represent two agents commonly employed to treat feline cardiomyopathies for more than 15 years. Nevertheless, clinical data describing their effect on morbidity and mortality are lacking. It is likely that propranolol administered at moderate to high doses effects favorable responses in some cats with clinical signs attributable to severe hypertrophy, outflow obstruction, or tachyarrhythmias. It is unknown whether clinical improvements are due to direct myocardial effects or (more likely) secondary responses to a beta-adrenergic blockade reduction in heart rate or contractility. Personal experience also indicates that high numbers of cats have received the drug for many years in combination with other therapies (especially furosemide) and remain in a compensated state of heart failure without untoward drug effects. On the other hand, many cardiomyopathic cats experience heart failure, arrhythmias, and death despite treatment with beta-blocking agents. Feline thromboembolism is a devastating complication of cardiomyopathic disorders. Until or unless the primary cause(s) of current diseases is elucidated to promote disease reversal, factors responsible for thrombus formation will accompany the heart diseases, protected from effective management. It appears unlikely that aspirin as currently recommended produces any obvious benefit in treating or preventing thromboembolism. Modifications of therapeutic protocols prescribing these frequently used drugs await well-constructed clinical trials evaluating their efficacy with respect to cardiovascular morbidity and mortality.
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PMID:Evidence for or against efficacy of beta-blockers and aspirin for management of feline cardiomyopathies. 168 44

The preventive effects of long-term treatment with arotinolol on the development of cerebral stroke were examined in SHRSP fed a high salt diet. Arotinolol (4.87 mg/kg per day for 20 weeks) prevented cerebral lesions, reduced signs of stroke and delayed early mortality but did not alter blood pressure from control SHRSP, when the administration of the drug was started before the onset of hypertension. At dosage levels similar to arotinolol, both pindolol and labetalol were less effective in preventing cerebral lesions despite lower blood pressure. Propranolol produced no detectable effect on blood pressure or frequency of cerebral lesions. Furthermore, arotinolol (4.27 mg/kg per day) markedly inhibited the development of stroke without blood pressure reduction, when the administration was started after the onset of severe hypertension. These results suggest that arotinolol is more effective in preventing cerebral stroke than pindolol, labetalol and propranolol, and that factors other than blood pressure reduction may be involved in this preventive effect.
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PMID:Prevention of cerebral stroke by arotinolol in salt-loaded SHRSP. 172 31

The pharmacokinetic and pharmacodynamic profiles of lacidipine, a 1,4-dihydropyridine calcium antagonist, and the beta-adrenoceptor blocker propranolol were determined alone and in combination in 24 healthy male volunteers. One group (I) of 12 subjects received a single oral dose of 4 mg lacidipine on two separate occasions, which was taken together with a single oral dose of either 160 mg propranolol or placebo; a second group (II) of 12 subjects received propranolol on two occasions, taken with either lacidipine or placebo. Propranolol significantly decreased the maximum plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) of lacidipine (by 38% and 42%, respectively) whereas lacidipine significantly increased the Cmax and AUC of propranolol (by 35% and 26%, respectively); neither the time to maximum plasma concentration (tmax) nor the terminal half-life (t 1/2) were affected. With regard to the pharmacodynamics, in Group I, there was a greater reduction in supine systolic blood pressure (6 mm Hg) and diastolic blood pressure (4 mm Hg) compared to the reduction produced by lacidipine alone, and pulse rate was approximately 5 beats/min less. In Group II, a significantly greater reduction (6 mm Hg) in supine systolic blood pressure compared to the reduction produced by propranolol alone occurred, but there was no marked difference in supine diastolic blood pressure and pulse rate. In conclusion, a modest pharmacokinetic and pharmacodynamic interaction is evident and should be evaluated further in patients with hypertension.
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PMID:The pharmacokinetic and pharmacodynamic interaction between lacidipine and propranolol in healthy volunteers. 172 44

Patients with mild asymptomatic primary hyperparathyroidism who do not meet currently accepted guidelines for surgery may be followed medically. General medical management of these individuals should be directed toward maintaining adequate hydration, therapy of hypertension, and avoiding immobilization. Diuretics should be used only with caution. Moderate dietary calcium intake (500-800 mg/day) should be encouraged. Propranolol and cimetidine are not useful in the therapy of primary hyperparathyroidism. Oral phosphate is efficacious in lowering serum and urinary calcium. However, because of concerns related to ectopic calcification, phosphate is usually reserved for those patients who meet surgical guidelines but who are not to undergo surgery. Bisphosphonates, potent inhibitors of osteoclast-mediated bone resorption, have been shown to lower serum and urinary calcium in patients with primary hyperparathyroidism. However, long-term data on their efficacy in this disorder are not yet available. The use of bisphosphonates at the present time is generally restricted to the research setting. More potent bisphosphonates as well as the design of newer agents that interfere with parathyroid hormone secretion may become very useful in future approaches to the medical management of primary hyperparathyroidism.
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PMID:Medical management of asymptomatic primary hyperparathyroidism. 176 64

The effects of steady-state flosequinan, a new peripheral vasodilator, and propranolol on glucose tolerance and plasma lipids in 22 non-insulin-dependent diabetics were investigated in a randomized double-blind placebo-controlled, three-way crossover trial. Flosequinan produced no impairment of glucose tolerance compared with placebo. Propranolol produced significant increases in fasting plasma glucose (P less than 0.01) and increases in the area under the glucose tolerance curve (P less than 0.05) compared to placebo. No significant effects on cholesterol levels were seen on either treatment but triglyceride levels were significantly elevated on propranolol compared with placebo (P less than 0.01). These data suggest that flosequinan, used in therapeutic dosage, has no adverse metabolic effects on the non-insulin-dependent diabetic and this may be an advantage for a drug used in the treatment of hypertension or congestive heart failure.
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PMID:A comparison of the metabolic effects of flosequinan and propranolol in patients with non-insulin-dependent diabetes mellitus. 186 95


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