[TREATING VASOMOTOR RHINITIS WITH PSYCHOPHARMACEUTICAL DRUGS].
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The effects of cholinomimetic drugs such as mecholyl (methacholine) and pilocarpine on autonomic functions (including sudomotor, metabolic, respiratory, vasomotor, and temperature responses) were assessed at room temperature (24 degrees C) in three groups of individuals, including normal, hyperhidrotic, and denervated subjects. The normal group had no palmar hyperhidrosis, with intact T2-3 ganglia, the hyperhidrotic group had palmar hyperhidrosis with intact T2-3 ganglia, and the denervated group had palmar hyperhidrosis treated with T2-3 ganglionectomy. Subcutaneous administration of mecholyl and pilocarpine each produced a fall in oral temperature in the normal group. The hypothermia was brought about by a decrease in metabolic rate, an increase in local sweating rate (mainly of the upper limb and trunk), and an increase in cutaneous circulation (estimated by an increase in the upper limb and trunk skin temperatures). The autonomic functions induced by these cholinomimetic drugs were antagonized by pretreatment with atropine sulfate (an antagonist of cholinergic receptors). Moreover, the hypothermia induced by mecholyl or pilocarpine was greatly reduced in the hyperhidrotic group. The reduction in the cholinomimetic-induced hypothermia in the hyperhidrotic group was due to the reduced sudomotor and metabolic responses after the injections of these cholinomimetic drugs, as compared to those of the normal group. However, neither the excessive sweating of the palms nor the reduced cholinergic responses in the hyperhidrotic group was observed after T2-3 ganglionectomy. The data indicate that the T2-3 ganglia play a role in the elaboration or modulation of the sudomotor and metabolic responses induced by activation of certain cholinergic receptors in humans.
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The involvement of nonadrenergic imidazoline specific receptors in the central control of the vasomotor tone and in the mechanism of action of drugs bearing an imidazoline structure, or analogs, is now well documented. Imidazoline-specific binding sites were found in many tissues and species. Moreover, until now, it is only in the brainstem that such binding sites are associated with a function: the hypotensive effect of imidazoline-like drugs. Rilmenidine, which is an oxazoline structurally related to the reference imidazolines, exerts a central hypotensive effect of central origin involving imidazoline receptors. The selectivity of rilmenidine for the imidazoline receptors compared to alpha 2-adrenergic receptors could explain the low incidence of sedative side effects observed with this antihypertensive drug. A specific anti-imidazoline radioimmunoassay allowed us to detect the presence of an immunoreactive imidazoline-like substance in human sera. High levels of this immunoreactive substance are associated with high blood pressure in 20-30% of the hypertensive patients. This observation indicates that high levels of this immunoreactive substance in the serum can be associated with some kinds of primary hypertension. The cause-and-effect relation between these 2 phenomena has not yet been determined. This substance is in process of purification; it could be a candidate to be an endogenous ligand of the imidazoline receptors.
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