Physiological and anatomical studies of the development of the sympatheticinnervation to rat iris arterioles

The development of the sympathetic innervation to rat irideal arterioles ha s been investigated using histochemical and in vitro pharmacological and el ectrophysiological methods. A plexus of fibres and varicosities appeared ov er the surface of the vessels after the first postnatal week and increased to reach a maximum density during the fourth postnatal week Transmural nerv e stimulation produced small, consistent contractions that were first recor ded in arterioles of 7-day old rats. Contractions became larger and faster, reaching the adult form during the fourth postnatal week. Contractions bec ame more sensitive to the alpha(1)-adrenoceptor antagonists, prazosin and n aftopidil, and less sensitive to the alpha(1A/D) antagonist, WB4101 and alp ha(2) antagonist, yohimbine, during development. At both 10 and 21 days, co ntractile responses resulted from the release of intracellular calcium as t hey were abolished by caffeine (10(-3) M), thapsigargin (2 x 10(-6) M) and cyclopiazonic acid (3 x 10(-6) M), but not by nifedipine (10(-6) M). Interc ellular recordings showed that nerve stimulation produced large, slow depol arizations at all ages tested. Time to peak potential decreased during deve lopment, while the amplitude of the depolarizations did not vary significan tly. Results suggest that, throughout development, sympathetic nerves cause constriction of iris arterioles due to the release of noradrenaline and ac tivation of a-adrenoceptors on the smooth muscle cells. Early responses inv olved both alpha(1)- and alpha(2)-adrenoceptors, while later responses were due to alpha(1)-adrenoceptors only. Irrespective of these changes in adren oceptor subtypes, smooth muscle contraction resulted from the mobilization of intracellular calcium suggesting that both alpha(1)- and alpha(2)-adreno ceptors were coupled to pathways which accessed this source of calcium. (C) 1999 Elsevier Science B.V. All rights reserved.