Aspects of aqueous humor dynamics : Studies in vivo and in vitro

Författare: Maria Samuelsson-almén; Uppsala Universitet; []

Nyckelord: MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Physiology and anatomy; Aqneous humor flow; intraocular pressure; adenylate cyclase; nonpigmented ciliary epithelium; pituitary adenylate cyclase-activating polypeptide; vasoactive intestinal polypeptide; dopamine; prostaglandin; Fysiologi och anatomi; Physiology and pharmacology; Fysiologi och farmakologi; Physiology; fysiologi;

Sammanfattning: The purpose of the present investigation was to study the effects of PGF2α-l-isopropylester, some neuropeptides, and pharmacological agents on aqueous humor dynamics and intraocular pressure (IOP) in vivo and on adenylate cyclase activity in the nonpigmented ciliary epithelium (NPE) in vitro.Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) caused a dose-dependent increase in cAMP formation, indicating that the NPE contains receptors for PACAP and VIP coupled to adenylate cyclase activation. The increase in cAMP formation caused by dopamine and the D1-receptor agonist fenoldopam was blocked by the D1-receptor antagonist SCH23390, indicating coupling to receptors belonging to the D1-receptor subfamily. Intracameral (i.c.) administration of terbutaline, VIP, and atrial natriuretic peptide (ANF) caused an increase in aqueous humor flow (AHF) by 100%, 50%, and 50%, respectively. Dopamine and fenoldopam i.c., however, had no clear-cut effect on AHF, probably because of the complex pharmacology, which involves both stimulatory andinhibitory effects.The effect on AHF by terbutaline (i.v. and i.c.) and by VIP (i.v.) was abolished by the β-receptor antagonist timolol, indicating involvement of β-receptor activation. However, the effect of VIP i.c. was unaffected by timolol i.v., suggesting that VIP i.c. stimulates AHF through local effects on the ciliary epithelium, probably via VIPreceptors. ANF given i.v. increased both basal and terbutaline-stimulated AHF, but the mechanism involved in the stimulation of AHF remains unclear.PGF2α-1 -isopropylester decreased IOP and increased uveoscleral outflow in the treated eye. Pilocarpine simultaneously prevented the drop in IOP and abolished the increase in uveoscleral outflow. There was no difference between eyes threated with PGF2α and control eyes after systemic pretreatment with atropine. Taken together, these results indicate that PGF2α decreases IOP by increasing uveoscleral outflow.

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