Cardiovascular effects of 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride (ST 155)

Drug‐induced changes in the release of [3H]‐noradrenaline from field stimulated rat iris

“…In line with this is the finding that a-adrenoceptor blocking drugs greatly increase [3H]-NA overflow in the field stimulated mouse atrium, while f3-adrenoceptor blocking drugs are without marked effects (unpublished results). The view that NA release can be influenced via a-adrenoceptors is further supported by the results obtained with the a-adrenoceptor stimulating agent clonidine (Hoefke & Kobinger, 1966;Boissier et al 1968) which slightly decreases the stimulation-induced NA overflow (Werner, Starke & Schiimann, 1970).…”

Lack of Correlation Between Presynaptic Inhibition of Noradrenaline Release and End Organ Responses During Nerve Stimulation

“…In some cases this has been done with little, if any, attention being paid to alterations in sensitivity of the end organ responses after drug treatment despite the early paper by Boissier, Giudicelli, Fichelle, Schmitt & Schmitt (1968) which demonstrates that clonidine modifies the blood pressure response to injected noradrenaline in anaesthetized dogs.…”

The animal pharmacology of drugs used in the treatment of migraine

“…In cats, dogs, monkeys, rabbits and rats intravenous injection of clonidine between 2 and 10 pg kg-l produces a shortacting pressor response of 1 to 2 min duration which is superceded by a sustained depressor response accompanied by bradycardia which may last up to 2 h (Boissier, Giudicelli & others, 1968;Constantine & McShane, 1968;Nayler, Price & others, 1968;Rand & Wilson, 1968;Bolme & Fuxe, 1971). The brief rise in blood pressure is the result of peripheral vasoconstriction and is discussed in section (b) below.…”