1. C. Structural modification by placing the hydroxy groups at positions 3 and 5 of the phenyl ring has resulted in compounds that are not substrates for COMT, resulting in lower rates of metabolism and enhanced oral bioavailability compared to catecholamines.

2. C. a-Adrenoceptors mediate contraction of the radial muscle of the iris. The shortening of the radial muscle cells opens the pupil. Phentolamine blocks a-adrenoceptors, allowing parasympathetic nerves innervating the sphincter muscle to take over. This leads to a less opposed contraction of the sphincter muscle induced by transmitter acetylcholine and a constriction of the pupil or miosis.

3. D. A small dose of epinephrine (0.1 ^g/kg) given by intravenous route may cause the blood pressure to fall, decreasing peripheral resistance. The depressor effect of small doses is due to greater sensitivity to epinephrine of vasodilator ^-adrenoceptors than of constrictor a-adrenoceptors and a dominant action on ^-adrenoceptors of vessels in skeletal muscle. Consequently, diastolic blood pressure usually falls. The mean blood pressure in general, however, is not greatly elevated. The compensatory barore-ceptor reflexes do not appreciably antagonize the direct cardiac actions.

4. C. Amphetamine is an indirectly acting adreno-mimetic amine that depends on the release of nor-epinephrine from noradrenergic nerves for its action. Thus, its effect depends on neuronal uptake (blocked by cocaine) to displace norepinephrine from the vesicles and the availability of norepineph-rine (depleted by reserpine). The substitution on the a-carbon atom blocks oxidation by monoamine oxidase. With no substitution on its benzene ring, amphetamine resists metabolism by COMT.

5. B. Phenylephrine is an ^-selective agonist. It causes an increase in peripheral vascular resistance. The major cardiovascular response to this drug is a rise in blood pressure associated with reflex bradycardia. The slowing of the heart rate is blocked by atropine.

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