Physiological and anatomical studies of the development of the sympathetic innervation to rat iris arterioles

The development of the sympathetic innervation to rat irideal arterioles has been investigated using histochemical and in vitro pharmacological and electrophysiological methods. A plexus of fibres and varicosities appeared over the surface of the vessels after the first postnatal week and increased to reach a maximum density during the fourth postnatal week. Transmural nerve stimulation produced small, consistent contractions that were first recorded in arterioles of 7-day old rats. Contractions became larger and faster, reaching the adult form during the fourth postnatal week. Contractions became more sensitive to the α₁-adrenoceptor antagonists, prazosin and naftopidil, and less sensitive to the α(1A/D) antagonist, WB4101 and α₂ antagonist, yohimbine, during development. At both 10 and 21 days, contractile responses resulted from the release of intracellular calcium as they were abolished by caffeine (10^-3 M), thapsigargin (2x10^-6 M) and cyclopiazonic acid (3x10^-6 M), but not by nifedipine (10^-6 M). Intracellular recordings showed that nerve stimulation produced large, slow depolarizations at all ages tested. Time to peak potential decreased during development, while the amplitude of the depolarizations did not vary significantly. Results suggest that, throughout development, sympathetic nerves cause constriction of iris arterioles due to the release of noradrenaline and activation of α-adrenoceptors on the smooth muscle cells. Early responses involved both α₁- and α₂-adrenoceptors, while later responses were due to α₁-adrenoceptors only. Irrespective of these changes in adrenoceptor subtypes, smooth muscle contraction resulted from the mobilization of intracellular calcium suggesting that both α₁- and α₂-adrenoceptors were coupled to pathways which accessed this source of calcium. Copyright (C) 1999 Elsevier Science B.V.