Propranolol antagonism

Consroe, P. Boren, J.L. and Hsu, C.H. Propranolol antagonizes phencyclidine-induced hyperactivity and stereotypy in rats. Pharmacology 24 96-104, 1982. 

Pentel PR, AsingerRW, Benowitz, NL. Propranolol antagonism of phenylpropanolamine-induced hypertension. Clin Pharmacol Ther ( 9%5) 37,488-94. 

Jackson, E.K., and Campbell, W.D. (1981). A possible antihypertensive mechanism of propranolol Antagonism of angiotensin 11 enhancement of sympathetic nerve transmission through prostaglandins. Hypertension, 3, 23-33... 

FIGURE 1.21 Schild plots for the antagonism by propranolol of the actions of noradrenaline (open circles) and isoprenaline (closed circles) on the contractile force of the isolated atrium of the guinea pig. The x shows the value obtained with noradrenaline as agonist but in the presence of cocaine (20 pM). (From Furchgott, R. F., Handbook of Experimental Pharmacology, Vol. 23, 1972, pp. 283-335 based on the results of Blinks, J. R Ann. N.Y.Acad. Sci., 139, 673-685, 1967.)... 

In the rat, we observed a decrease of the spontaneous frequency of right atrial preparations and biphasic inotropic effects in left atrial preparations. Negative effects were not antagonized by atropine. The positive inotropic effect was modified very little by prior reserpinization or prior exposure to propranolol and phentolamine but was sensitive to Mn ions. On the other hand. 

The cardiovascular response to dopamine in humans depends on the concentration infused. Low rates of dopamine infusion can produce vasodilation in the renal, mesenteric, coronary, and intercerebral vascular beds with little effect on other blood vessels or on the heart. The vasodilation produced by dopamine is not antagonized by the p-adrenoceptor blocking agent propranolol but is antagonized by haloperidol and other dopamine receptor-blocking agents. 

Propranolol increases airway resistance by antagonizing 32-receptor-mediated bronchodilation. Although the resulting bronchoconstriction is not a great concern in patients with normal lung function, it can be quite serious in the asthmatic. The cardioselective (5-blockers produce less bronchoconstriction than do the nonselec-tive antagonists. 

Labetalol produces equilibrium-competitive antagonism at p-receptors but does not exhibit selectivity for Pi- or P2-receptors. Like certain other p-blockers (e.g., pindolol and timolol), labetalol possesses some degree of intrinsic activity. This intrinsic activity, or partial ago-nism, especially at P2-receptors in the vasculature, has been suggested to contribute to the vasodilator effect of the drug. The membrane-stabilizing effect, or local anesthetic action, of propranolol and several other p-blockers, is also possessed by labetalol, and in fact the drug is a reasonably potent local anesthetic. 

Which of the following actions of epinephrine would be antagonized by prazosin but not by propranolol ... 

The myocardial response to exercise includes an increase in heart rate and myocardial contractility. These effects are mediated in part by the sympathetic nervous system. Propranolol and other p-adrenoceptor blockers antagonize the actions of catecholamines on the heart... 

The pharmacology of drugs that antagonize catecholamines at a- and B-adrenoceptors is presented in Chapter 10 Adrenoceptor Antagonist Drugs. This chapter will concentrate on two prototypical drugs, propranolol and prazosin, primarily in relation to their use in treatment of hypertension. 

Drugs that preferentially block the [ receptors have been developed to eliminate the unwanted bronchoconstrictor effect (p2) of propranolol seen among asthmatic patients. Cardioselective p-blockers, such as acebutolol [a se BYOO toe lole], atenolol [a TEN oh lole], and metoprolol [me TOE proe lole], antagonize receptors at closes 50 to 100 times less than those required to block p2 receptors. This cardioselectivity is thus most pronounced at low doses and is lost at high drug doses. [Note Acebutolol has some intrinsic agonist activity.]... 

TNF-a and increasing IL-8 (Webster et al., 2002). Consistent with this, selective receptor antagonists such as butox-amine can antagonize the corticotrophin-releasing factor-induced reduction in natural killer (NK) cell activity (Irwdn et al., 1990). Sympathetic nerve stimulation also enhances T 2 cytokine production while inhibiting cytokine production. Thus, pj receptor agonists can suppress interferon-y (IFN-y) production by cells, an effect, which can be blocked by propranolol. Interestingly, prion presence in the brain has been linked to an interaction between splenic monocytic cells and the sympathetic nervous system (Steinman, 2004). 

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