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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of prazosin and atenolol monotherapy on plasma lipid concentrations were compared in 51 patients with mild to moderate essential hypertension. Prazosin monotherapy (mean dose 5.4 +/- 5.3 mg per day) resulted in a significant decrease in total and low-density lipoprotein cholesterol concentrations; these changes were evident at three months and at six to 12 months. Atenolol monotherapy (mean dose 66 +/- 23 mg per day) resulted in a significant increase in plasma triglyceride concentration that persisted during one year of treatment. The deletion of thiazide from the regimen of prazosin plus thiazide resulted in a small stepwise decrease in plasma triglyceride concentration over 12 months of observation. The addition of polythiazide (0.5 mg two to three times weekly) to the regimen of patients in whom acceptable blood pressure was not attained with prazosin or atenolol monotherapy resulted in a decrease in blood pressure, averaging 18.8 mm Hg for systolic and 10.3 mm Hg for diastolic, and a small, though significant, increase in the concentration of low-density lipoprotein cholesterol. It is suggested that the effects of prazosin on plasma lipid composition may be mediated, at least in part, by blocking an action of either the sympathetic nervous system or circulating catecholamines that normally modulate lipoprotein metabolism and might mediate the lipid alterations induced by thiazide diuretics.
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PMID:Effects of prazosin, atenolol, and thiazide diuretic on plasma lipids in patients with essential hypertension. 351 94

Short-term treatment with 1-(p-carbamoyl-methylphenoxy)-3-isopropylamino)-2-propanol (atenolol, Tenormin) (100 mg/d for 5 days) was conducted in 12 patients with labile essential hypertension. Before and at the end of the treatment, cardiohemodynamics, renal hemodynamic and excretory function, and renal pressor (renin-angiotensin-aldosterone) and depressor (renal kallikrein-kinin and prostaglandin) systems were examined. Atenolol decreased cardiac output (CO) without affecting total peripheral resistance. Atenolol also decreased plasma renin activity, plasma aldosterone concentration, urinary excretion of kallikrein-kinin, and urinary excretion of potassium whereas it increased plasma potassium concentration. Urinary excretion of prostaglandin E and sodium was not affected by atenolol. Glomerular filtration rate decreased, but renal plasma flow remained unchanged during the treatment by atenolol. A significant positive correlation was found between the changes in CO and in systolic blood pressure (SBP) while negative correlation was observed between the changes in total peripheral resistance and in SBP. A significant positive correlation was also noted between urinary kallikrein excretion and renal plasma flow. The change in urinary kinin excretion was conversely correlated to that in SBP. This study demonstrates that the hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.
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PMID:Mechanism of antihypertensive effect of atenolol in patients with borderline hypertension during short-term treatment. A comprehensive study. 373 23

The interaction of inhibition of prostaglandin (PG) synthesis by indomethacin (75 mg/day) with the antihypertensive effect of atenolol (50 mg b.i.d.) was studied in 11 untreated otherwise healthy men 35 to 45 years old with essential hypertension. Atenolol for 3 weeks decreased supine blood pressure (BP) from 157/109 mm Hg during placebo to 148/97 mm Hg. Indomethacin alone for 1 week slightly increased BP and antagonized the antihypertensive action of atenolol. Atenolol reduced plasma renin activity (PRA) to 40% but did not modify either the urinary excretion of vasodilatory PGs (PGE2 and prostacyclin measured as 6-keto-PGF1 alpha) or plasma kininogen and urine kallikrein. Indomethacin suppressed PRA to 27% and PG excretion to approximately 70% but did not markedly change plasma kininogen and urine kallikrein excretion. The decreased excretion of 6-keto-PGF1 alpha, the metabolite of the main vasodilatory prostanoid prostacyclin, correlated with the increased BP measured in standing subjects. The effects of indomethacin were practically the same when given with atenolol as when given alone. We conclude that the slight increase in BP by indomethacin in essential hypertension is associated with the reduced production of vasodilatory PGs but not with alterations in activities of the renin-angiotensin or kallikrein-kinin systems.
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PMID:Inhibition of prostaglandin synthesis by indomethacin interacts with the antihypertensive effect of atenolol. 389 59

Twenty-five patients with moderate essential hypertension (standing diastolic blood pressure 100-125 mmHg, phase 5) completed a single-blind placebo-controlled cross-over study comparing four week periods of treatment with atenolol 100 mg, metoprolol 100 mg, metoprolol durules 200 mg, slow-release oxprenolol 160 mg, and slow-release oxprenolol 320 mg respectively. All the drugs were significantly better than placebo at reducing resting blood pressure at 24 hours. Atenolol produced the greatest mean reduction of pressure and was the most effective drug for most patients, though the differences between atenolol and metoprolol durules were not statistically significant. These two drugs, however, were significantly more effective than the remainder. A similar ranking was seen with respect to the reduction of the blood pressure and heart rate response to exercise. None of the treatments had any significant effect on the patients' rating of perceived exertion during the exercise test.
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PMID:Comparative study of atenolol, metoprolol, metoprolol durules, and slow-release oxprenolol in essential hypertension. 611 3

Hemodynamic (systemic and regional), metabolic and cardiovascular reflexive variables were measured before and after 4 weeks of beta blockade with atenolol in 10 patients with mild essential hypertension. Atenolol reduced mean arterial pressure, heart rate, cardiac index (all p less than 0.005) and renal vascular resistance (p less than 0.01) and increased total peripheral resistance (p less than 0.005). Glomerular filtration rate and renal blood flow were unchanged; plasma renin activity fell 43%. Reflexive cardioacceleration during the Valsalva maneuver and upright passive tilt was blunted. No changes were observed in circulating fluid volumes. In six patients followed for 1 year, blood pressure and heart rate were maintained at levels similar to those during the first 4 weeks. Atenolol was shown to be an effective oral antihypertensive that has no apparent deleterious hemodynamic effects on the renal and splanchnic circulations.
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PMID:Hemodynamics, biochemical and reflexive changes produced by atenolol in hypertension. 612 14

The relationship between the oral dosage and plasma concentration of the long-acting cardioselective beta-adrenoceptor blocker atenolol and the antihypertensive response to the the degree of beta-adrenoceptor blockade and change in plasma renin activity (PRA) was evaluated in patients with mild-to-moderate essential hypertension in a double-blind, randomized, between-patient, dose-ranging (25, 50 or 100 mg once daily for 4 weeks) study. The optimum, or minimum, daily dose of atenolol to treat patients with mild-to-moderate hypertension was not clearly identified in this study. A between-treatment comparison did not demonstrate that all blood pressure falls were always less in the 25 mg group than in the other two groups. Calculation of beta-error or the power for the negative results between doses suggested that a large sample size is required to draw a conclusion that no dose-antihypertensive relationship of atenolol exists in the treatment of mild-to-moderate hypertension. A relatively flat plasma concentration-antihypertensive response relationship was observed. Steady-state plasma concentrations of atenolol were dose-related and renal drug clearance was well correlated with individual creatinine clearance. beta-adrenoceptor blockade was better correlated with plasma atenolol concentration. Correlations which were less strong were between plasma drug concentration and change in various blood pressures and between blood pressure falls and beta-adrenoceptor blockade. There was no relationship between the fall in blood pressure and change in PRA. Atenolol appeared to suppress PRA in an all-or-none fashion.
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PMID:A dose ranging study of atenolol in hypertension: fall in blood pressure and plasma renin activity, beta-blockade and steady-state pharmacokinetics. 634 68

Twenty-five patients with essential hypertension were randomly assigned to treatment with either captopril or atenolol. There were 15 males and 10 females and their mean age was 53 years, range 32-66 years. Systolic and diastolic blood pressures were significantly reduced by atenolol 50-100 mg once daily. Captopril 25-50 mg 3 times daily caused a significant decrease in supine diastolic but not in systolic blood pressure. After the addition of hydrochlorothiazide (25-50 mg) to those who did not become normotensive (supine diastolic blood pressure less than 95 mm Hg) on captopril or atenolol alone, blood pressure was further reduced. Captopril combined with hydrochlorothiazide significantly reduced both supine and standing blood pressure by 31/17 mm Hg (p less than 0.01) and 33/18 mm Hg (p less than 0.001) respectively. Atenolol combined with hydrochlorothiazide caused a significant decrease of both recumbent and standing blood pressure by 21/10 mm Hg (p less than 0.01) and 23/13 mm Hg (p less than 0.05 systolic, p less than 0.001 diastolic). The reduction of systolic blood pressure was significantly better with the captopril/hydrochlorothiazide combination, while there was no difference between the groups as regards diastolic blood pressure reduction. Thus, hydrochlorothiazide potentiates the blood pressure lowering effect of captopril more than of atenolol. This could be due to a synergistic interaction between captopril and hydrochlorothiazide.
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PMID:Captopril or atenolol in essential hypertension. 636 71

A new beta-blocking agent, atenolol was studied on the supposition that it was a beta-blocker without any action on central nervous system. Atenolol was orally given to 10 patients with essential hypertension once a day and changes in various parameters were observed through 24 hours. As the results, hypotensive effect was accompanied by marked reduction of heart rate, systemic vascular resistance, plasma renin activity and blood aldosterone level over 24 hours. It was a decrease in systemic vascular resistance that showed best correlation with hypotensive effect.
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PMID:Acute effect of atenolol on hemodynamic, plasma renin activity and plasma aldosterone concentration in the once daily oral administration. 638 68

The effects of once daily dosage of the two cardioselective beta-adrenoceptor blocking agents, atenolol and metoprolol, were studied in 26 patients with primary hypertension. The study was a randomized double-blind cross-over trial with placebo run-in and wash-out. Assessment of effect was performed about 1 and 25 hours after dosing. At rest, both atenolol and metoprolol lowered the blood pressure (BP) and heart rate (HR) compared to placebo. Atenolol induced a more effective BP reduction than metoprolol, especially 25 hours after drug intake. During exercise 1 hour after dosing both drugs reduced BP and HR to a similar extent, whereas 25 hours after dosing atenolol gave a more efficient BP and HR reduction than metoprolol. Our data show that both 100 mg atenolol and 100 mg metoprolol are effective antihypertensive beta-blockers at rest and during exercise, 1 hour after intake. Metoprolol was less effective than atenolol 25 hours after dosing probably due to its shorter plasma half-life, thus implying a twice daily regimen for metoprolol in standard preparation.
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PMID:A comparison of 100 mg atenolol and 100 mg metoprolol once a day at rest and during exercise in hypertensives. 638 53

Fourteen patients with uncomplicated essential hypertension and mild asthma were treated with Atenolol 50-125 mg/day for up to 8 months. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), rate pressure index (RPI), stress testing time (STT) and peak expiratory flow rate (PEFR) were measured before, during and after stress testing (ST) before and during treatment. Atenolol significantly lowered HR, SBP, DBP and RPI. It prolonged STT and had no effect on PEFR. Furthermore, Atenolol did not worsen the patient's asthma except for one patient. The drug did not interfere with the bronchodilatation effect of salbutamol. Atenolol can be used cautiously to treat hypertension in asthmatic patients under certain conditions.
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PMID:Treatment of hypertension in mild asthmatic patients with atenolol. 650 43


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