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 alpha1-adrenoceptor antagonists, prazosin and naftopidil, and less sensitive to the alpha1A/D antagonist, WB4101 and alpha2 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 (2 x 10(-6) M) and cyclopiazonic acid (3 x 10(-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 alpha-adrenoceptors on the smooth muscle cells. Early responses involved both alpha1- and alpha2-adrenoceptors, while later responses were due to alpha1-adrenoceptors only. Irrespective of these changes in adrenoceptor subtypes, smooth muscle contraction resulted from the mobilization of intracellular calcium suggesting that both alpha1- and alpha2-adrenoceptors were coupled to pathways which accessed this source of calcium.
Sandow
S L
SL
Autonomic Synapse Group, Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT. shaun.sandow@anu.edu.au
Hill
C E
CE
D000221:Adaptation, Ocular / Q000187:drug effects / Q000502:physiology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000375:Aging; D000818:Animals; D000831:Animals, Newborn; D001160:Arterioles / Q000166:cytology / Q000294:innervation* / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004338:Drug Combinations; D004558:Electric Stimulation; D005260:Female; D006651:Histocytochemistry; D066298:In Vitro Techniques; D007498:Iris / Q000098:blood supply* / Q000502:physiology; D008297:Male; D008856:Microscopy, Fluorescence; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D058914:Purinergic Antagonists; D051381:Rats; D011921:Rats, Inbred WKY; D017476:Receptors, Neuropeptide Y / Q000037:antagonists & inhibitors; D013564:Sympathetic Nervous System / Q000166:cytology / Q000187:drug effects / Q000254:growth & development* / Q000502:physiology; D013997:Time Factors
D000317:Adrenergic alpha-Antagonists; D002121:Calcium Channel Blockers; D004338:Drug Combinations; D058914:Purinergic Antagonists; D017476:Receptors, Neuropeptide Y; C097212:neuropeptide Y-Y1 receptor