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

The forearm arterial effects of enalapril and propranolol were compared by means of pulsed Doppler velocimetry in 28 patients with hypertension after treatment for 3-6 months. Enalapril decreased blood pressure, increased both brachial artery diameter and blood flow, decreased vascular resistance, and increased the arterial compliance of the forearm. Propranolol also decreased blood pressure but did not produce any other changes. It may be concluded that the treatment of hypertension with enalapril, but not propranolol, is associated with dilatation effects on the arterial circulation of the forearm.
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PMID:Effects of chronic administration of enalapril and propranolol on the large arteries in essential hypertension. 241 92

The present study examined the actions of dilevalol, an antihypertensive beta-adrenoceptor blocker with arterial vasodilator actions, upon aortic compliance (AC) in anesthetized dogs. AC was determined via sonomicrometric determination of the ratio of aortic systolic-diastolic diameters (mm) and arterial pulse pressure (mm Hg). One AC unit (ACU) equals 10(-3) mm/mm Hg. Dilevalol (0.032, 0.1, and 3.2 mg/kg i.v.) significantly (p less than 0.05) increased AC by 1.4 +/- 0.3, 3.7 +/- 1.4, and 4.5 +/- 1.2 ACU, respectively, from basal values of 4.7 +/- 0.4-5.6 +/- 0.4 ACU, while reducing blood pressure by 20 +/- 2, 31 +/- 9, and 41 +/- 10 mm Hg, respectively (p less than 0.05). Increases in AC were not the passive result of altered blood pressure. Proximal mechanical aortic occlusion dropped systolic blood pressure as much as 70 mm Hg without altering AC. Propranolol (0.32 and 1.0 mg/kg) did not significantly change AC, but propranolol pretreatment attentuated dilevalol-induced increases in AC. Pindolol (0.1-1.0 mg/kg i.v.) lowered blood pressure 17 +/- 3 (p less than 0.05) to 34 +/- 7 mm Hg (p less than 0.05), while significantly increasing AC by 1.2 +/- .2 to 2.7 +/- .7 ACU. The data show that dilevalol, unlike propranolol, increases AC substantially at antihypertensive doses. The inhibition of dilevalol-induced AC increases by propranolol illustrates a beta-adrenoceptor agonist activity in large arteries. Since large artery compliance is impaired in hypertension, dilevalol may afford a vasular protective action for known risk factors for evolving systemic arterial disease.
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PMID:Effects of the antihypertensive dilevalol on large artery compliance in anesthetized dogs. 245 69

A multicenter, randomized, double-blind, comparative study was conducted in 274 patients with mild to moderate hypertension to assess the impact of nitrendipine and propranolol on quality of life. After placebo baseline, 136 patients were given nitrendipine (5-20 mg b.i.d.) and 138 were given propranolol (40-120 mg b.i.d.). Quality of life was evaluated at baseline, weeks 6-10, and weeks 14-18 of the maintenance period. At weeks 6-10, the nitrendipine group became significantly more vigorous (p less than 0.01) and less fatigued (p less than 0.05) than the propranolol group. Propranolol subjects noted decreased problems of trembling hands (p less than 0.01) and alcohol use (p less than 0.05) than the nitrendipine subjects. No other significant differences between groups in mood states, troublesome conditions (insomnia, headaches, and loss of appetite), or sexual satisfaction were noted at this visit, and patient willingness to continue study medication was marginally significantly higher (p less than 0.1) in the nitrendipine group than in the propranolol group. At weeks 14-18, the propranolol subjects perceived significantly decreased problems with the "felt worried, tense, and drank alcohol to cope" factor (p less than 0.05); however, there were no differences between groups at this visit for Profile of Mood States (POMS) scores, sex life variables, or medication preference. Based on within-group analysis, the propranolol group perceived a reduction in partner sexual satisfaction (p less than 0.05). Overall, nitrendipine seemed to be better tolerated than propranolol.
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PMID:Comparison of quality of life on nitrendipine and propranolol. 246 71

The aim of this study was to compare the effects of long-term monotherapy with five different beta-blockers on plasma lipids in patients with essential hypertension. We studied 99 male patients, aged 35-55 years, with mild to moderate hypertension, who worked in the same community. After a 1-month placebo period, patients were assigned to receive propranolol (160 mg/day), atenolol (100 mg/day), bisoprolol (10 mg/day), mepindolol (10 mg/day), or celiprolol (400 mg/day). Therapy was continued for 2 years. Blood pressure (BP), heart rate, and blood samples for evaluation of total cholesterol (TC), LDL-cholesterol (LDL-C), triglycerides (TG) and HDL-cholesterol (HDL-C) were taken before and after the initial placebo period, and subsequently every 6 months from the beginning of active treatment. All beta-blockers caused similar reductions in BP that were maintained throughout the study. None of the beta-blockers significantly affected TC or LDL-C. Propranolol, a nonselective beta-blocker, caused the most pronounced changes in TG (+33 to 43%) and in HDL-C (-30 to -32%). Atenolol, a beta 1-selective agent, had the same quantitative effects, but to a lesser extent (TG + 23 to 30%; HDL-C -15 to -19%). Bisoprolol, more beta 1-selective than atenolol, and mepindolol, nonselective with ISA, increased TG (+20 to 28% and +14 to 25%, respectively) but did not significantly affect HDL-C. In contrast, celiprolol, a highly cardioselective beta-blocker with beta 2-partial agonism, improved lipid risk factors by significantly reducing TG (-14 to -21%) and increasing HDL-C (+8 to 14%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma lipids during chronic antihypertensive therapy with different beta-blockers. 248 87

1. Six healthy subjects received cilazapril (2.5 mg once daily), propranolol (120 mg once daily), the combination of both and placebo for a period of 1 week each (wash-out phase 1 week). 2. Propranolol and cilazapril reduced systolic and diastolic blood pressure (BP) by 7 mm Hg at peak when compared with placebo. However after the combination, this reduction was more than doubled (18 mm Hg) and lasted longer. 3. There was a trend to lower and later peak concentrations for both drugs after administration of the combination. No clinically relevant pharmacokinetic interactions between cilazapril and propranolol were found. 4. The effects on blood pressure were confirmed in hypertensive patients (BP diastolic greater than 95 mm Hg). Thirteen patients were randomly allocated cilazapril (2.5 mg day-1) or propranolol (120 mg day-1] as part of a cross-over design. This was then followed by the combination. All treatment periods were of 3 weeks duration and all measurements were done 2 h after drug administration. 5. Cilazapril lowered the median sitting diastolic BP by 8 mm Hg, and propranolol by 9 mm Hg, whereas the combination reduced the diastolic BP by 19 mm Hg. 6. The results of these studies, attempting to elucidate drug-drug interactions, showed that combined use of propranolol and cilazapril resulted in a more pronounced and longer lasting blood pressure reduction, in healthy subjects and in patients with hypertension.
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PMID:Pharmacokinetic and pharmacodynamic interactions between the ACE inhibitor cilazapril and beta-adrenoceptor antagonist propranolol in healthy subjects and in hypertensive patients. 252 45

While there is general agreement on the natural history, pathology, and pathophysiology of hypertension, there continues to be controversy over the selection of specific antihypertensive agents. All antihypertensive agents will, by definition, lower blood pressure, and factors beyond side effects and other difficulties associated with therapy form the basis of selecting specific agents. One of these factors is the effect of a given drug on core organ function. Propranolol was the first beta-adrenoceptor-blocking agent introduced for the treatment of hypertension. Initiation of therapy with propranolol may result in a decline in blood pressure more at the expense of cardiac function due to a concomitant rise in total peripheral resistance. Furthermore, propranolol may result in a decline in both glomerular filtration rate (GFR) and renal blood flow (RBF). In contrast, cardioselective beta-blockers or those with intrinsic sympathomimetic activity may not adversely affect renal function. It had been predicted that nadolol, a noncardioselective beta-blocker without intrinsic sympathomimetic activity, should result in decreased renal function. In contrast, observations demonstrated a preservation or improvement in both RBF and GFR, suggesting the presence of an alternative effective mechanism. Recent additions to the beta-adrenolytic group of antihypertensive agents include drugs with concurrent beta-blockade and vasodilation. This vasodilatation may be achieved through agonist properties resulting in lesser increases in vasomotor tone and smaller, if any, decreases in cardiac output. Alternatively, vasodilation may be achieved by concomitant alpha-adrenoceptor blockade, such as with labetalol. This agent preserves GFR and RBF during therapy of hypertension, in patients with normal as well as diminished renal function and hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-blockers and hypertension. 256 44

The metabolic effects of celiprolol, a new beta-adrenoceptor blocking agent with intrinsic sympathomimetic activity and alpha 2-blocking properties, were evaluated in a series of patients with hypertension, both with and without hyperlipidemia. Propranolol was tested as the reference drug in a randomized double-blind trial. Of the 35 patients of both sexes who completed the study, 17 were hyperlipidemic (low-density lipoprotein cholesterol greater than or equal to 170 mg/dl) and 18 were normolipidemic. Both drugs exerted a similar hypotensive effect after gradual dose adjustment; however, propranolol reduced heart rate to a higher extent (-20.5%) than celiprolol (-7.7%). Propranolol determined a significant rise of total and very low-density lipoprotein (VLDL) associated triglyceridemia, whereas high-density lipoprotein cholesterol (HDL cholesterol) levels and the total cholesterol/HDL cholesterol ratios were significantly depressed, particularly in hyperlipidemic patients. Celiprolol, in contrast, slightly decreased triglyceridemia (significantly in the hyperlipidemic group at week 12) and caused a 5% increase of the HDL cholesterol levels. The total cholesterol/HDL cholesterol ratio was reduced by celiprolol at week 16 in both hyperlipidemic and normolipidemic patients. The effects of the two beta-adrenoceptor blockers on HDL cholesterol and triglyceride levels differed significantly after 12 and 16 weeks of treatment, which confirm the divergent metabolic effects of the two agents.
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PMID:Lipid effects of celiprolol, a new cardioselective beta-blocker, versus propranolol. 256 18

The effects of rilmenidine [(N-dicyclopropylmethyl) amino-2-oxazoline; S 3341], an alpha 2 agonist, on the hypertensive rat heart have been compared with those of propranolol, using a model of deoxycorticosterone acetate (DOCA)-salt hypertension. One week after nephrectomy and initial treatment with DOCA-salt, which was continued for an additional 7 weeks, the two drugs were added to the rats drinking water at a concentration of 10 mg/kg per day for rilmenidine and 15 mg/kg per day for propranolol. Both drugs had a slight and similarly significant antihypertensive effect at their respective concentrations [systolic blood pressure in controls, 141 +/- 15 mmHg (n = 20); after DOCA-salt, 209 +/- 22 mmHg (n = 24); after propranolol, 182 +/- 19 mmHg (n = 20, P less than 0.01); after rilmenidine, 192 +/- 15 mmHg (n = 19, P less than 0.05)]. They also lowered the systolic blood pressure x frequency product (P less than 0.001). Propranolol, but not rilmenidine, significantly reduced the left ventricular weight: body weight ratio [in controls, 2.00 +/- 0.2 mg/g; after DOCA-salt, 3.04 +/- 0.5 mg/g; after propranolol, 2.67 +/- 0.4 mg/g (P less than 0.05); after rilmenidine, 3.13 +/- 0.6 mg/g (P = NS)]. However, both propranolol and rilmenidine reduced left ventricular weight [in controls, 676 +/- 57 mg; after DOCA-salt, 827 +/- 114 mg; after propranolol, 732 +/- 108 mg (P less than 0.01); after rilmenidine, 760 +/- 100 mg (P less than 0.05)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Remodelling of the heart in DOCA-salt hypertensive rats by propranolol and by an alpha-2 agonist, rilmenidine. 257 30

The effects of chronic oral administration of bopindolol (twice daily for 12 weeks beginning at 5 weeks of age) on serum lipoprotein concentrations, blood pressure and heart rate, were studied in spontaneously hypertensive rats. They were compared with those of two other beta-blockers. Bopindolol and propranolol (15 mg/kg) attenuated the increase in heart rate. Pindolol produced a similar, gradual change in heart rate, but only after the 6th week of treatment. Propranolol and bopindolol attenuated the development of hypertension, whereas pindolol showed no such effect. Pindolol and bopindolol produced a significant increase in high-density lipoprotein cholesterol concentration, but did not produce an increase in serum creatine phosphokinase activity. Administration of these drugs in an acute regimen at 10 weeks of age, provoked changes in blood pressure and heart rate, reflecting partial agonist activities of varying degree, in agreement with the results obtained in chronic experiments with regard to serum lipoprotein concentrations. Pindolol (5 mg/kg) provoked a larger decrease of blood pressure without decrease of heart rate, while the decrease of blood pressure after bopindolol (5 and 15 mg/kg) was associated with a decrease of heart rate. It was concluded that bopindolol is a beta-adrenergic blocking agent with a mild partial agonist activity and devoid of adverse effects on lipid metabolism.
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PMID:Effects of chronic oral administration of a new beta-blocker, bopindolol, on serum lipoprotein concentrations and blood pressure of spontaneously hypertensive rats. 257 91

Dilevalol (SCH 19927) is a potent, long-acting, nonselective beta-blocker with marked vasodilator actions. Unlike classical beta-blockers, dilevalol promptly lowers blood pressure and vascular resistance in animal models of hypertension. The present studies address the peripheral vascular effects of dilevalol and explore the role of beta-receptor agonism in the acute vasodilator and antihypertensive effects of the compound. In the denervated dog hindlimb preparation, dilevalol (0.1, 0.3, 1.0 and 3.0 micrograms, i.a.) significantly increased femoral blood flow by 12 +/- 6, 27 +/- 6, 84 +/- 31 and 132 +/- 41 ml/min, respectively. In contrast, celiprolol, a beta-blocker with purported vasodilator activity, caused a significant increase in flow of 31 +/- 9 ml/min at a dose of 30 micrograms i.a. Systematic pretreatment with the selective beta 2-antagonist ICI 118,551 virtually abolished dilevalol's vasodilator effect in the dog hindlimb. In conscious spontaneously hypertensive rats, 3 mg/kg i.v. dilevalol reduced blood pressure by 58 +/- 8 mmHg (P less than 0.05) and vascular resistance by 171 +/- 27 dyne.sec.cm-5/100 g (P less than 0.05) but did not change cardiac output significantly. Pretreatment of spontaneously hypertensive rats with ICI 118,551 significantly reduced both dilevalol's antihypertensive and resistance-lowering effects. Oral doses of 10 and 25 mg/kg dilevalol lowered blood pressure by 19 +/- 3 (P less than 0.05) and 37 +/- 5 mmHg (P less than 0.05) in spontaneously hypertensive rats with chronically implanted Doppler flow probes. The lower dilevalol dose reduced mesenteric vascular resistance 38 +/- 6% (P less than 0.05) while the higher dose significantly lowered vascular resistance in the hindlimb, mesenteric and renal vascular beds of spontaneously hypertensive rats by 18 +/- 8, 33 +/- 2 and 43 +/- 4%, respectively. Propranolol lowered neither blood pressure nor regional vascular resistances at the above doses in spontaneously hypertensive rats. Thus, dilevalol promotes a generalized fall in vascular resistance. Furthermore, the present studies illustrate that beta 2-receptor stimulation plays an obligatory role in both the vasodilatory and antihypertensive actions of dilevalol.
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PMID:Role of beta 2-receptor stimulation in the peripheral vascular actions of the antihypertensive dilevalol. 257 92


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