Drugs online research references
Circ Res. 1987 May;60(5):738-46.
Mechanism of beneficial effect of beta-adrenergic blockade on exercise-induced myocardial ischemia in conscious dogs.
Guth BD, Heusch G, Seitelberger R, Ross J Jr.
We examined the importance of decreased heart rate in the beneficial effect of beta-adrenergic blockade on exercise-induced regional myocardial ischemia and contractile dysfunction in conscious dogs with single vessel coronary stenosis (ameroid constrictor). Studies were performed during control treadmill exercise, which produced regional myocardial ischemia (blood flow measured with microspheres) and wall dysfunction (measured using sonomicrometers). A second run was performed after the administration of atenolol (0.3-1.0 mg/kg i.v.), and the reduced heart rate caused by atenolol during early steady-state running was then prevented by atrial pacing during the latter portion of the run. Atenolol reduced the exercise heart rate from 217 +/- 25 beats per minute (SD, n = 9) to 166 +/- 15, and ischemic zone wall thickening during systole improved from 27 +/- 22% of the resting value in the control run to 50 +/- 25% of the resting value in the atenolol run (p less than 0.01). Atrial pacing then increased heart rate to 217 +/- 23 beats per minute, and regional wall thickening deteriorated to 15 +/- 25% of the resting value. Regional subendocardial blood flow in the ischemic zone during atrial pacing with atenolol was slightly less than that observed in the control run, in both ischemic and control zones, indicating no remaining beneficial effect of atenolol when heart rate reduction was eliminated. We conclude that the only significant mechanism for the improvement in exercise-induced ischemia and wall motion produced by atenolol is a reduction in the exercise heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3594748&dopt=Abstract
J Pharmacol Exp Ther. 1981 Jan;216(1):95-100.
The effects of adrenergic agonists and antagonists on vesicourethral smooth muscle of rabbits.
Khanna OP, Barbieri EJ, McMichael RF.
The effects of alpha and beta adrenergic agonists and antagonists on isolated smooth muscle preparations from the rabbit bladder body, bladder base and proximal urethra have been studied. The predominance of alpha receptors in the proximal urethra and the bladder base was observed via contraction of these areas by norepinephrine and blockade by phentolamine. Alpha receptor-mediated contractile activity could be unmasked in the bladder body when beta receptors were blocked with propranolol. Isoproterenol, 1 X 10(-10) to 3 X 10(-7) M, had a strong, dose-related relaxant effect on the bladder body, but little effect on the bladder base or proximal urethra. Selective beta-2 agonists such as terbutaline, salbutamol and ritodrine elicited tissue responses similar to those of isoproterenol. The pD2 values for isoproterenol, terbutaline, salbutamol and ritodrine were 8.59, 7.87, 7.34, and 6.52, respectively. Dobutamine, a selective beta-1 agonist, failed to cause significant relaxation of these tissues. The nonselective beta receptor blocker, propranolol, and the selective beta-2 receptor blocker, butoxamine, competitively antagonized the relaxant effects of the four active beta agonists; however, atenolol, a selective beta-1 receptor blocker, was inactive. On the basis of the selective action of these agonists and antagonists, we concluded that beta-2 receptors mediate relaxation of the vesicourethral smooth muscles of the rabbit and the participation of beta-1 receptors in the areas is insignificant.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7452512&dopt=Abstract
Methods Find Exp Clin Pharmacol. 1996 Nov;18(9):559-67.
Comparative antioxidant effects of beta-adrenoceptor blockers, calcium antagonists and U-74500A against iron-dependent lipid peroxidation in murine ventricular microsomal membranes.
Reddy DS, Singh M, Chopra K.
Department of Pharmacology, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India.
Recently we have shown that ACE inhibitors and platelet activating factor antagonists inhibit iron-dependent lipid peroxidation in murine ventricular membranes and possess beneficial effects on ischemia and ischemia reperfusion-induced myocardial injury, which has been ascribed to their capacity to scavenge or impair oxygen free radical generation. In the present study we investigated the effects of beta-adrenoceptor blockers and calcium antagonists on iron-dependent lipid peroxidation (LPO) in murine ventricular membranes and compared them with the lazaroid U-74500A, a potent antioxidant. Fe(2+)-vitamin C induced LPO in a concentration- and time-dependent manner, measured as thiobarbituric acid reactive substances (TBARS) formation. Pretreatment of ventricular membranes with gallopamil, verapamil, propranolol and metaprolol at concentrations of 5 microM and higher inhibited Fe(2+)-vitamin C-induced LPO in a concentration-dependent manner with IC50 values of 192.8-208.3 microM; however, they were less potent than U-74500A (IC50 6.8 microM). In contrast, atenolol, timolol, diltiazem and nifedipine inhibited LPO at very high concentrations with IC50 values of 864.5-971.5 microM. Inhibition of LPO may not be due to the drugs' classical pharmacological actions, but rather to their characteristic chemical structures or physicochemical interactions with biological membranes. In view of the pathological importance of LPO in cardiac ischemic injury, inhibition of LPO by gallopamil, verapamil, propranolol and metaprolol may provide additional cardioprotective activity and thus reinforces their beneficial effects in the treatment of ischemic heart disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9010829&dopt=Abstract
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