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

To evaluate the role of dietary sodium and antihypertensive drugs in the modulation of myocardial structure, especially myosin isozymic pattern, renal hypertensive rats (two-kidney, one clip) were treated with a sodium-deficient diet (7 mEq/kg), captopril, or atenolol. Native myosin was extracted under nondissociating conditions and separated by polyacrylamide gel electrophoresis. The percentage of myosin isozyme V1 was significantly decreased from 71.5 +/- 7.5 (Wistar controls) to 52.4 +/- 1.7% (p less than 0.05) in renal hypertensive rats and was associated with an increase in V3 component from 12.7 +/- 5.1 (Wistar controls) to 23.1 +/- 1.4% (renal hypertensive rats; p less than 0.05). There was a dramatic change in the myosin isozyme distribution pattern after treatment with low sodium and captopril. Six weeks of low sodium therapy in renal hypertensive rats resulted in an increase in V1 from 52.4 +/- 1.7 to 74.8 +/- 4.8% and a reduction in V3 from 23.1 +/- 1.4 to 9.5 +/- 2.4%. Normal rats treated with low sodium showed similar results. The percentage distribution of isozymes after low sodium therapy in the captopril-treated rats was not different from that in normal Wistar controls. Captopril therapy also caused an increase in V1 and a decrease in V3. Atenolol therapy, on the other hand, caused a significant increase in V3 and decrease in V1 with no change in blood pressure or heart weight. These data suggest that dietary sodium may play an important role in the modulation of myocardial mass and may modulate signals for synthesis of V1 or V3 myosin phenotypes.
Hypertension 1986 Oct
PMID:Role of sodium in modulation of myocardial hypertrophy in renal hypertensive rats. 294 27

Twenty-one patients with mild or moderate hypertension were randomised to receive either Atenolol 100 mg (N = 10) or Pindolol 15 mg (N = 11) in a once daily dosage over a two month period. The effects of these two betablockers on the blood pressure and plasma lipid profile were studied. Special attention was paid to the methodology: obese patients (30% over theoretical weight derived from the Lorenz formula) and those with pre-treatment triglyceride levels higher than 1.82 mmol/l were excluded because of the well documented biological instability of such patients. The selected patients were given placebo for two weeks. At the end of the placebo period those subjects whose body weight, total cholesterol, apolipoproteins or triglycerides had varied by more than 10%, 15% and 30% respectively, were also excluded from the study. At the end of the 60 days active treatment period, a comparable fall in the blood pressure was observed in both groups and there was no significant difference in the biological parameters as compared with pre-treatment values. In addition, the cardiovascular risk, evaluated by the B/A1 apolipoprotein ratio, increased in only one patient in the group receiving Atenolol and one patient receiving Pindolol.
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PMID:[Comparative effects of pindolol and atenolol on blood pressure and lipids in mild to moderate arterial hypertension]. 307 94

Dynamic response of arterial blood pressure during exercise has been studied in 40 normotensive young subjects and 20 mild hypertensive young patients (20-40 years of age). Hypertensive patients were treated with atenolol (beta blocker) and prazosin (vasodilator). Both groups underwent maximal exercise stress test. A double-blind nonrandomized study was practiced in hypertensive patients with placebo, prazosin (3 mg/12 h), and atenolol (100 mg/24 h). Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and exercise duration (ED) were analyzed. All parameters remained stable in both groups. The hypertensive patients showed an increase in maximum SBP more than 230 mmHg during the placebo phase. This same group showed a significant increase in HR at rest two hours after administration of prazosin. Atenolol produced a significant reduction in HR both during rest and exercise. Both drugs produced a significant decrease in SBP and DBP (at rest and exercise). We conclude that exercise test is a noninvasive procedure that could distinguish mild arterial hypertension. The dynamic changes of arterial blood pressure can be controlled with prazosin (3 mg/12 h) or 1 daily intake of 100 mg atenolol.
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PMID:Exercise stress test in young hypertensive patients. Response to vasodilators (prazosin) vs. beta-blocker (atenolol) agents. 328 Jan 91

Hypertension and diabetes mellitus frequently coexist and are independent risk factors for reduced peripheral perfusion. Antihypertensive medications that reduce blood pressure and improve peripheral perfusion would have advantages in diabetic patients with hypertension. In a randomized, two-placebo period, single-blind, two-way crossover study, we determined finger and forearm blood flow, lipid levels, and blood pressure control in 19 diabetic patients with hypertension, with each atenolol or prazosin and placebo period of 4 weeks' duration. Both drugs reduced blood pressure (sitting: 157/95 to 142/84 mm Hg, atenolol; 155/95 to 138/82 mm Hg, prazosin; standing: 154/94 to 144/84 mm Hg, atenolol; 154/94 to 133/81 mm Hg, prazosin). Lipid levels did not change except that low-density lipoprotein levels fell from 148 to 127 mg/dl with prazosin. Atenolol did not change forearm or finger blood flow or vascular resistance. Prazosin increased blood flow and reduced vascular resistance in both finger and forearm. In conclusion, prazosin has a potentially more appropriate hemodynamic profile than has atenolol in diabetic patients with hypertension.
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PMID:Forearm and finger hemodynamics, blood pressure control, and lipid changes in patients with diabetic hypertension treated with atenolol and prazosin. 329 75

Three therapies were used to treat 35 patients with mild to moderate systemic hypertension: (1) the cardioselective beta-adrenoceptor blocker atenolol, (2) the calcium antagonist nifedipine and (3) combination therapy for those who failed to reach the target diastolic blood pressure (BP) of less than 90 mm Hg with monotherapy. After an initial run-in placebo period, when the mean supine diastolic BP was 102 +/- 1 mm Hg (mean +/- standard error of the mean), patients were randomized (double-blind) to atenolol, 100 mg as a single daily dose or nifedipine (slow-release form), 20 mg twice daily, then to a washout dummy placebo period before crossover. Each period lasted 4 weeks. Supine, erect and exercise BP were recorded. Atenolol and nifedipine, in the same fixed doses but in combination, were given to 20 patients in whom either supine or erect diastolic BP exceeded 90 mm Hg after the period of monotherapy. Atenolol monotherapy reduced the erect diastolic BP to less than 90 mm Hg in 14 patients (40%); of the remainder, 1 patient responded only to fixed-dose nifedipine and 11 to combination therapy, yielding a total success rate of 74%. The combination gave enhanced control, as shown by a further decrease in supine and erect BP and by better control of exercise BP; these effects were achieved without an increased incidence of adverse effects. The mean reductions in supine diastolic BP were: atenolol, 9 +/- 2 mm Hg; nifedipine, 6 +/- 2 mm Hg; and combination therapy, 16 +/- 2 mm Hg (p less than 0.05 vs atenolol or nifedipine).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atenolol plus nifedipine for mild to moderate systemic hypertension after fixed doses of either agent alone. 351 99

1. The cardiovascular responses to electrical stimulation of the central nucleus of the amygdala (c.n.) have been studied in chloralose-anaesthetized rabbits. A pattern of response involving bradycardia, hypotension and hind-limb vasodilatation, accompanied by an increase in the rate of phrenic nerve discharge, was evoked only in response to stimulation within the medial portion of the c.n. 2. The cardiovascular responses were not secondary to the changes in respiratory activity since they were unaffected by altering central respiratory drive by either hypo- or hyperventilation of the animal. 3. The bradycardia was attenuated by the administration of atropine sulphate and abolished by the subsequent administration of propranolol, which when given alone attenuated the bradycardia. Atropine or propranolol given alone also attenuated the hypotension evoked by medial c.n. stimulation but the concurrent hind-limb vasodilatation was unaffected. 4. Atenolol, which unlike propranolol does not cross the blood-brain barrier, had little effect on the bradycardia in response to medial c.n. stimulation, but the subsequent administration of atropine abolished it. The hypotension in response to medial c.n. stimulation was also unaffected by atenolol. 5. The vasodilatation in response to medial c.n. stimulation was abolished by administration of guanethidine even after restoration of hind-limb perfusion pressure to control values by the infusion of angiotensin II into the hind-limb perfusion circuit. 6. Electrical stimulation of areas within 0.5 mm of the medial c.n. also resulted in bradycardia but then it was accompanied by hypertension and hind-limb vasoconstriction. Stimulation of areas 1.0 mm distant to the medial c.n. resulted in small and inconsistent cardiovascular responses. 7. These results show that hind-limb vasodilatation, mediated by withdrawal of sympathetic tone, occurs in response to stimulation within the medial c.n. of the rabbit and is in part responsible for the observed hypotension. It has also been confirmed that the bradycardia in response to medial c.n. stimulation is mediated by the vagus nerves.
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PMID:Cardiovascular and phrenic nerve responses to stimulation of the amygdala central nucleus in the anaesthetized rabbit. 368 36

The pharmacodynamic effects of single oral doses of atenolol (100 mg), labetalol (300 mg), and propranolol (80 mg) were compared with those of placebo in a randomized, double-blind, Latin square design in 12 patients with hypertension. Atenolol and propranolol both significantly reduced cardiac output (-0.55 vs. -0.31 L/min) and heart rate (-8.0 vs. -6.6 bpm), whereas labetalol had no effect on either parameter (-0.08 L/min; + 1.0 bpm). Labetalol significantly reduced vascular resistance (-339 dynes X cm/sec5), but atenolol and propranolol did not (147 vs. 62 dynes X cm/sec5). Only labetalol significantly reduced the systolic (-15.3 mm Hg), diastolic (-11.5 mm Hg), and mean blood pressures (-12.8 mm Hg). Atenolol significantly reduced only diastolic blood pressure (-5.20 mm Hg), whereas propranolol failed to lower these parameters significantly. These data indicate that the hemodynamic profile of labetalol differs from that of selective and nonselective beta-blockers. Labetalol lowered blood pressure primarily by reducing vascular resistance, whereas reductions in heart rate and cardiac output were the predominant effects of atenolol and propranolol.
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PMID:The effects of single-dose atenolol, labetalol, and propranolol on cardiac and vascular function. 374 33

In a 12-week double-blind randomised study the efficacy of atenolol and a new longer-acting formulation of trimazosin were compared when given once daily in patients with mild to moderate hypertension. Two parallel groups, each consisting of 18 patients, were studied. At randomisation the two groups were well matched for age and sex distribution. They were also well matched for blood pressure, pulse rate and body weight; these latter measurements were recorded at regular intervals during the 12 weeks of study. Atenolol produced substantial reduction in both systolic and diastolic blood pressure, and in heart rate, during 12 weeks of treatment. This therapeutic effect was maintained until the next dose after 24 hours. Trimazosin, by comparison, failed to reduce either systolic or diastolic pressure, or to alter heart rate. Side effects were minor with both agents and compliance with treatment was good. Atenolol caused significant elevation of plasma concentration of triglyceride, with reduction in high density lipoprotein concentration when compared with trimazosin. In conclusion, atenolol was confirmed as an effective agent for the treatment of mild to moderate hypertension. By comparison trimazosin in the longer-acting formulation was ineffective in this study. However, trimazosin may still find a place in treatment if used at higher dose.
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PMID:A comparison of atenolol and long-acting trimazosin in mild to moderate essential hypertension. 389 76

The treatments of mild hypertension with atenolol and prazosin in occupationally active men and women were compared in a double blind cross-over with placebo. The hypotensive effect of the beta-adreno-receptor blocking drug, atenolol, were striking and in accordance with current knowledge, using one daily dose of 100 mg. In contrast, the hypotensive effect of taking 2 mg prazosin twice a day was modest, averaging about 3% when compared with placebo, somewhat less but still detectable during the performance of muscular exercises. Atenolol medication significantly reduced heart rate and blood pressure responses to muscular exercises, covering a range of work loads experienced during ordinary working days. No increased feeling of muscular fatigue or other discomfort during muscular work compared to that on prazosin and placebo medication could be detected. It was therefore concluded that atenolol medication was a useful treatment of mild hypertension and did not reduce the normal working ability and exercise tolerance. Prazosin medication did not significantly change working ability and exercise tolerance.
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PMID:Working ability and exercise tolerance during treatment of mild hypertension. II. A comparison between atenolol and prazosin medication. 389 71

Episodes of depression and acute psychosis in two patients receiving propranolol hydrochloride are described, and the literature on propranolol-induced depression and psychosis is reviewed. A 42-year-old woman developed severe depression, marked apathy, social withdrawal, and anorexia after taking propranolol hydrochloride (80 mg/day) for three months to control her hypertension. Five days after the dose was reduced to 40 mg/day, there was a major improvement in her depressive symptoms, with a complete resolution in eight days. Upon rechallenge with 80 mg/day of propranolol, she again experienced depressive symptoms. Atenolol 50 mg/day was substituted for the propranolol therapy, and she exhibited a complete remission of her depression. The second patient was a 63-year-old man who had been taking propranolol hydrochloride 160 mg/day for three months without incident. Because of an increased frequency of anginal attacks, the dosage was increased to 240 mg/day. Within two days, he demonstrated such agitation, excitement, and combativeness that he had to be controlled with a 25-mg dose of methotrimeprazine. When the propranolol dose was reduced to 160 mg/day, his psychotic symptoms rapidly cleared. However, when the dose was subsequently increased to 200 mg/day, he again showed increased agitation. After substituting atenolol 100 mg/day for propranolol, the patient's mental status returned to normal. Both of these patients experienced symptoms that were temporarily associated with propranolol. Both patients were subsequently controlled without symptoms with atenolol therapy. Propranolol is a highly lipophilic beta blocker that achieves high concentrations in the brain. When continued beta-blocking therapy is necessary or beta blockade is indicated, a weakly lipophilic agent such as atenolol is indicated.
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PMID:Propranolol-induced depression and psychosis. 398 22


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