Drugs online research references
Br J Clin Pharmacol. 1977 Apr;4(2):147-51.
Haemodynamic long-term effects of metoprolol at rest and during exercise in essential hypertension.
Lund-Johansen P, Ohm OJ.
1 Twelve men with untreated essential hypertension in WHO stage I were studied on an outpatient basis to evaluate the haemodynamic long-term effect of a new beta-adrenoceptor blocker, metoprolol. 2 Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intraarterial brachial pressure were recorded at rest in a supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. 3 The subjects were treated with metoprolol (dose 50-250 mg/day) as the sole drug for 1 year and the haemodynamic study was repeated. 4 Mean arterial blood pressure was reduced about 12% at rest and 9% during exercise. The heart rate was decreased about 22% at rest and 20% during exercise. There was no significant compensatory increase in the stroke volume and consequently the cardiac index was reduced about 22% at rest sitting and about 17% during exercise. There was no decrease in total peripheral resistance. 5 No side-effects were seen. 6 The major haemodynamic long-term effects of metoprolol in mild and moderate essential hypertension resemble those seen by other beta-adrenoceptor blockers like alprenolol, atenolol and timolol. The study has not given support to the assumption that metoprolol should cause less depression in cardiac output than other beta-adrenoceptor blockers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=861129&dopt=Abstract
Br J Clin Pharmacol. 1976 Jun;3(3):445-51.
Haemodynamic long-term effects of a new beta-adrenoceptor blocking drug, atenolol (ICI 66082), in essential hypertension.
Lund-Johansen P.
1 Thirteen men with untreated essential hypertension in WHO stage I were studied on an outpatient basis to evaluate the haemodynamic long-tern effect of a new beta-adrenoceptor blocker, atenolol. 2 Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intraarterial branchial pressure were recorded at rest in a supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. 3 The subjects were treated with atenolol (dose 100-200 mg/day) as the sole drug for 1 year and the haemodynamic study was repeated. 4 The blood pressure was reduced approximately 18% both at rest and during exercise, the heart rate approximately 25% and the cardiac output 16% at rest supine and 27% at rest sitting. During exercise the reductions in cardiac output were approximately 20%. The calculated total peripheral resistance was not decreased compared to pretreatment values. The mean arterial pressure-heart rate product was reduced almost 40%. 5 Apart from temporary muscular fatigue during the first weeks, no side-effects were seen. 6 Atenolol is an effective blood pressure lowering drug in mild and moderate hypertension, but the drop in blood pressure is associated with marked reduction in heart rate and cardiac output at rest as well as during exercise.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=973971&dopt=Abstract
Am J Physiol. 1997 Apr;272(4 Pt 2):H1672-9.
Beta-blockade reduces effects of adenosine and carbachol by transregulation of inhibitory receptors and Gi proteins.
Borst MM, Marquetant R, Kubler W, Strasser RH.
Department of Cardiology, University of Heidelberg, Germany.
Chronic blockade of stimulatory beta-adrenergic receptors may decrease inhibitory receptors of the adrenergic signal transduction system. This transregulation process might reduce the negative inotropic response of the myocardium to inhibitory receptor stimulation. Rats were treated for 6 days with the beta-blocker atenolol (2 mg/day). beta-Adrenergic receptors in cardiac plasma membranes increased from 49 +/- 6 to 75 +/- 9 fmol/mg protein (means +/- SE; P = 0.053), whereas muscarinic M2 receptors decreased (155 +/- 15 vs. 105 +/- 10 fmol/mg protein; P < or = 0.05). Moreover, inhibitory G alpha(i) proteins were reduced by 36%. The functional responses of isolated hearts to inhibitory agonists after prestimulation with isoproterenol (3 nmol/l) were significantly blunted. The Ki value for the negative inotropic response of the maximal rise in developed left ventricular pressure (dP/dt(max)) to adenosine (0.1-100 micromol/l) increased from 5.9 +/- 1.7 to 24.0 +/- 2.5 micromol/l (P < or = 0.001). A similar rightward shift of the dose-response curve was observed for the effects of adenosine on developed left ventricular pressure (LVP) and of carbachol (0.01-10 micromol/l) on LVP and dP/dt. Thus chronic beta-blockade leads to a coordinate transregulation of inhibitory receptors and Gi proteins, reducing the effects of inhibitory receptor activation of the heart. This mechanism may contribute to the beneficial effects of beta-blocker therapy in heart failure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9139950&dopt=Abstract
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