Key result
Prazosin infusion in anesthetized dogs greatly inhibited venous constrictor responses to norepinephrine, demonstrating marked in vivo alpha-adrenergic receptor inhibiting action.
Why the study?
Does prazosin infusion inhibit norepinephrine venoconstriction in the veins of anesthetized dogs?
Does prazosin infusion inhibit norepinephrine venoconstriction in the veins of anesthetized dogs?
Prazosin has a marked in vivo α‐adrenergic receptor inhibiting action in dog veins, which may be preceded by a transient agonistic effect.
Prazosin may modulate venous tone; leaves open translation to human alpha-blockade.
A dose–response curve was established based on increases in venous infusion pressure evoked by injection of a series of small doses of norepinephrine, before and after slow infusion of a prazosin solution into the accessory cephalic vein of anesthetized dogs. During the prazosin infusion, there was an increase in venous infusion pressure, which returned to control levels by the end of the infusion period. The reduction in arterial pressure that occurred during the infusion persisted throughout the experiment. Immediately following the prazosin infusion, venous constrictor responses to norepinephrine were greatly inhibited, an effect that was still present 1 hr later. Prazosin has a marked in vivo α‐adrenergic receptor inhibiting action in the accessory cephalic vein of the dog. This effect may be preceded by an agonistic action on these receptors at this site, as suggested by the increase in venous infusion pressure during the period of prazosin administration.
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Sticht et al. (1983) studied this question. Prazosin vs. Baseline (before prazosin infusion) was evaluated on Venous infusion pressure in response to norepinephrine. Prazosin infusion in anesthetized dogs greatly inhibited venous constrictor responses to norepinephrine, demonstrating marked in vivo alpha-adrenergic receptor inhibiting action.
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