THE EFFECTS OF SENSORY DENERVATION ON THE RESPONSES OF THE RABBIT EYE TO PROSTAGLANDIN E₁, BRADYKININ AND SUBSTANCE P

Abstract

Six to eight days after diathermic destruction of the fifth cranial nerve in the rabbit, the ocular hypertensive and miotic responses to intracameral administration of capsaicin, bradykinin, and prostaglandin E1 were greatly reduced or completely abolished. The response to substance P was not abolished. A response could still be obtained to chemical irritants 36 h after coagulation of the nerve and it is deduced that manifestation of the response is dependent upon functional sensory nerve terminals, and is independent of central connections. It is suggested that prostaglandin E1 and bradykinin act directly upon the sensory nerve endings and that propagation of the response is augmented by axon reflex. In view of the ability of substance P to induce miosis in the denervated eyes, it is presumed that its actions are not mediated via sensory nerves. It is considered possible that the mediator(s) released from sensory nerve endings after chemical irritation or antidromic stimulation may act in the same way as substance P with regard to the miotic effect. Synthetic substance P will only produce ocular hypertension in doses which induce a maximal miotic response. This may either be a question of access or a partial resemblance to the endogenous mediator.

Tachykinin receptors mediating responses to sensory nerve stimulation and exogenous tachykinins and analogues in the rabbit isolated iris sphincter

“…Functional studies suggest these responses are caused by nerve-released tachykinins (Butler & Hammond, 1980;Muramatsu et al, 1987), although the identity of the tachykinins released by each of the sensory nerve stimulants remains unclear. Our previous work with selective tachykinin receptor agonists (Hall et al, 1991) and antagonists (Hall et al, 1992b) indicated that activation of NK, and NK3 postjunctional receptors results in contraction in this preparation; while radioligand binding studies have demonstrated specific binding sites for substance P in iris sphincter muscle membrane preparations (Too et al, 1988;Denis et al, 1991).…”

Identification of a B2 bradykinin receptor expressed by PC12 pheochromocytoma cells.

“…Bradykinin excites nociceptive sensory endings (1)(2)(3)(4)(5), producing a sensation of pain (6,7). Chemical mediators released by bradykinin from sensory endings (8)(9)(10) and from sympathetic nerve terminals (11) contribute to vasodilatation and plasma leakage at the site of inflammation. Further, as part of its inflammatory effect, bradykinin triggers the production of prostaglandin E or other arachidonic acid metabolites in some tissues, and these mediators secondarily cause a sensitization of sensory endings to bradykinin and other stimuli (12,13).…”

Adenosine‐modulation of cholinergic and non‐adrenergic non‐cholinergic neurotransmission in the rabbit iris sphincter

“…Application of susbtance P can induce miosis and other inflammatory responses (Bill et al, 1979;Butler & Hammond, 1980;Mandahl & Bill, 1981), and it can also be released into the aqueous humor (Bill et al, 1979). Furthermore, substance P antagonists may suppress inflammation in the eye (Holmdahl et al, 1981).…”

“…It has been suggested that the non-adrenergic non-cholinergic component is mediated by substance P or a similar substance (Ueda et al, 1981;Tornqvist et al, 1982;Bjorkroth, 1983;Zhang et al, 1984), and also that substance P is the neurogenic factor responsible for the miosis of the nerve-mediated response of 'Author for correspondence. the eye to irritation (Bill et al, 1979;Butler & Hammond, 1980;Soloway et al, 1981;Mandahl & Bill, 1981).…”