Neurogenic vasoconstriction as affected by cholinergic and nitroxidergic nerves in dog ciliary and ophthalmic arteries.

PURPOSE: To determine the involvement of noradrenergic and other vasoconstrictor nerves in the contraction of ocular arteries and the modification by cholinergic and nitroxidergic nerves of vasoconstrictor nerve function. METHODS: Changes in isometric tension were recorded in helical strips of the canine posterior ciliary and external ophthalmic arteries denuded of the endothelium, which were stimulated by transmurally applied electrical pulses (5 Hz). Vasoconstrictor mediators were analyzed by pharmacological antagonists, such as prazosin, alpha,beta-methylene ATP, a P2alpha-purinoceptor antagonist, and BIBP3226, a neuropeptide Y receptor antagonist. RESULTS: Transmural electrical stimulation produced contractions that were potentiated by N(G)-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor. The contraction was partially inhibited by prazosin and abolished by combined treatment with alpha,beta-methylene ATP but was not influenced by BIBP3226. Stimulation-induced contraction was attenuated by physostigmine and potentiated by atropine. Contractions induced by exogenous ATP were reversed to relaxations by alpha,beta-methylene ATP. In the strips treated with L-NA, prazosin, and alpha,beta-methylene ATP, the addition of L-arginine elicited relaxations by nerve stimulation. The ATP-induced relaxation was attenuated by aminophylline, whereas neurogenic relaxation was unaffected. CONCLUSIONS: Ciliary and ophthalmic arterial contractions by nerve stimulation are mediated by norepinephrine and ATP, which stimulate alpha1-adrenoceptor and P2X purinoceptor, respectively. ATP from the nerve is unlikely involved in vasodilatation. Acetylcholine derived from the nerve impairs the neurogenic contraction, possibly by interfering with the release of vasoconstrictor transmitters, and neurogenic NO also inhibits the contraction postjunctionally by physiological antagonism.     

Experimental study of the efficiency of use of sodium hypochlorite in the complex treatment of purulent keratitis

The experiment has provided evidence for the safe use of 0.1% aqueous sodium hypochlorite for ocular tissues and for its therapeutic efficacy in purulent keratitis. The therapeutic effect is achieved by accelerating the lysis of neurotic tissues, by suppressing the pathogenic microflora, by alleviating an inflammatory reaction, by stimulating epithelization and reparative regeneration, by activating the phagocytic properties of neutrophilic leukocytes by 1.8-times, by increasing their functional reserves by 1.3 times as compared to the similar parameters observed in the use of conventional treatments.     

Neural serotonin stimulates chloride transport in the rabbit corneal epithelium

Evidence is presented that serotonin acts as a neurotransmitter in the cornea of the adult rabbit. Serotonin was localized to granules in a sparse population of subepithelial corneal nerves by an electron microscopic histochemical procedure. Significant endogenous levels of serotonin and its principal metabolite, 5-hydroxyindoleacetic acid, were detected in the central cornea by a fluorometric assay. Exogenous serotonin stimulated ion transport by corneal epithelium. This effect was potentiated by monoamine oxidase inhibition and was unaffected by an alpha-adrenergic receptor antagonist. Serotonin-stimulated ion transport was inhibited by the specific antagonist, methysergide, and by the replacement of Cl- with an impermeable anion. In tracer experiments, the serotonin-stimulated ion transport was shown to be caused by increased epithelial Cl- secretion. The serotonin response was partially inhibited by the beta-adrenergic antagonist, timolol. In a companion article, assay of corneal cyclic AMP showed stimulation of cyclic AMP synthesis by serotonin, inhibition by the specific antagonist, lysergic acid diethylamide, and potentiation by monoamine oxidase inhibition. We postulate that specific serotonergic receptors are present in the corneal epithelium and that activation of these receptors by serotonin released from serotonergic neurons increases the level of cyclic AMP, which stimulates active Cl- secretion by the corneal epithelium.     

Dissection of antigen-specific humoral and cellular immune responses for the development of experimental immune-mediated blepharoconjunctivitis in C57BL/6 mice

PURPOSE: Allergic conjunctivitis is characterized by allergen-specific IgE in the serum and infiltration of eosinophils into the conjunctiva. However, it remains unclear whether early-phase reaction (EPR) mediated by Ag-specific IgE links to late-phase reaction (LPR) in the conjunctiva. We aimed to investigate whether LPR is mediated by either cellular or humoral immune responses. METHODS: Experimental immune-mediated blepharoconjunctivitis (EC) was induced in C57BL/6 mice by either active immunization or passive immunization by transfer of ragweed (RW)-primed lymphocytes and RW-specific IgE, followed by RW challenge onto the conjunctiva. Transferring RW-primed lymphocytes were prepared from RW-primed splenocytes which were stimulated in vitro with RW for 3 days. Fifteen minutes after RW challenge, clinical findings were evaluated and 24 hr after challenge, the conjunctivas and sera were harvested for histologic analysis and measurement of IgE, respectively. RESULTS: EPR was most prominent when EC was induced by transfer of RW-specific IgE. EPR was hardly detectable if EC was induced by transfer of RW-primed lymphocytes. Mild EPR was noted when EC was induced by active immunization. LPR, evaluated by infiltration of eosinophils into the conjunctiva, was most severe when EC was induced by transfer of RW-primed lymphocytes. Minimal, but definite LPR was induced when EC was induced by transfer of RW-specific IgE. Intermediate severity of LPR was induced when EC was induced by active immunization. CONCLUSIONS: LPR in the conjunctiva is dominantly mediated by cellular immune responses, whereas EPR in the conjunctiva is putatively mediated by humoral immune responses. Importantly, LPR in the conjunctiva is inducible by Ag-specific IgE alone, although minute.     

The accuracy of clinical applanation tonometry

The differences between two careful applanation tonometries performed by one and by two observers, respectively, were compared. Two measurements by one observer differed by 2 mmHg or more in 8% of the pairs of measurements and by 3 mmHg or more in 2% of the pairs. One tonometry each by two observers differed by 2 mmHg or more 40% of the pairs of measurement and by 3 mmHg or more in 17% of the pairs. There was no dependence on the intraocular pressure. Possible reasons for the increase in variance are discussed.     

增生早期糖尿病视网膜病变患者视网膜及视盘新生血管的超广角OCTA与FFA检测结果对比分析

目的 对比分析超广角OCT血管成像(OCTA)与荧光素眼底血管造影(FFA)对增生早期糖尿病视网膜病变(DR)患眼视网膜及视盘新生血管的检测结果。方法 选取2021年11月至2022年5月在四川省人民医院眼科经FFA确诊为增生早期DR的患者62例(98眼)为研究对象,所有患者均行FFA和超广角OCTA检查。超广角OCTA检查选择以黄斑为中心的24 mm×20 mm扫描模式进行。所有图像均由同一位技术员采集,图像分析由同一位医师进行。以FFA的检查结果为标准,分析超广角OCTA对增生早期DR患眼视网膜及视盘新生血管的检出率。结果 共93眼(94.9%)FFA显示出视网膜新生血管,超广角OCTA显示出其中82眼,检出率88.2%,遗漏的患眼均是由于超广角OCTA检测范围受限所致;在FFA未显示出视网膜新生血管的5眼中,超广角OCTA显示出1眼存在新生血管,该新生血管在FFA检查中被误诊为视网膜内微血管异常。共17眼(17.3%)FFA显示出视盘新生血管,超广角OCTA显示出全部17眼,检出率100.0%;在余下的81眼中,超广角OCTA更灵敏地显示出10眼存在视盘新生血管。在FFA检查中,...     

眼前段光学相干断层扫描仪与A超测量中央前房深度的比较

目的前房深度是晶状体性屈光手术和青光眼手术的重要依据之一。为此探讨眼前段光学相干断层扫描仪测量中央前房深度与A型超声测量结果的一致性。方法对白内障30例（45眼）分别使用眼前段光学相干断层扫描仪及A超测量中央前房深度。采用配对t检验对之进行比较;用相关分析方法分析两种仪器测量值之间的相关性;随机选择1眼分别用两种仪器依次重复测量中央前房深度10次,采用变异系数作为评判标准,比较测量的可重复性。结果眼前段光学相干断层扫描仪测量中央前房深度的平均值为（2.63±0.48）mm,A超测量结果为（2.98±0.48）mm;眼前段光学相干断层扫描仪测量的中央前房深度比A超的测量值小（0.35±0.04）mm,眼前段光学相干断层扫描仪与A超测量中央前房深度各值有较好的相关性（r=0.894,P〈0.001）。眼前段光学相干断层扫描仪测量中央前房深度10次变异系数为0.78%,A超测量中央前房深度10次的变异系数为1.49%。结论眼前段光学相干断层扫描仪测量前房深度值比A超测量中央前房深度的各值小;两种仪器检测中央前房深度的测量值相关性较好;眼前段光学相干断层扫描仪测量结果的重复性稍好于A超。临床工作中应把二者结合起来,综合分析。     

Modulation of corneal lipoxygenase by ascorbic acid

We have examined the influence of ascorbic acid on the generation of lipoxygenase products by the rabbit cornea, an avascular tissue which is continuously bathed by high concentrations of ascorbic acid present within the aqueous humor of the eye. Corneal homogenates were incubated with [14C]arachidonic acid and the resulting metabolites separated by thin-layer chromatography. The metabolites were then quantified by liquid scintillation counting techniques. The biosynthesis of the major lipoxygenase product formed by the cornea, 12-HETE, was significantly inhibited by physiological concentrations of ascorbic acid; PGE2 formation by the cornea was not altered in the presence of ascorbic acid. Furthermore, ascorbic acid inhibited the formation of 12-HETE in the presence of catalase, indicating that hydrogen peroxide generated by ascorbate was not responsible for diminishing the lipoxygenase activity of the cornea. However, high concentrations of hydrogen peroxide (10(-4) M) did inhibit the formation of 12-HETE by the corneal homogenates. Another antioxidant, 2,6-dichlorophenol-indophenol (10 micrograms ml-1), also inhibited the formation of 12-HETE by the cornea. Therefore, it appears that the inhibition of corneal lipoxygenase by ascorbic acid could be related to the antioxidant properties of this vitamin. These studies suggest that ascorbic acid within the aqueous humor might modulate lipoxygenase activity within the cornea.     

Properties of the pupillary dilation produced by the humoral factor in the pupillary reflex dilation: an experimental study in the cat

Physiopharmacological properties of the pupillary dilation produced by the humoral factor in the reflex pupillary dilation were studied in cats anesthetized with ketamine-HC1. Pupillary dilation produced by the humoral factor was separated from that produced by the neural mechanism, ie, sympathetic activation and parasympathetic inhibition, by atropinization of acutely sympathectomized pupil. To evoke the pupillary reflex dilation, the sciatic nerve was stimulated by using a bipolar electrode. The stimulus consisted of trains of 0.5 milliseconds duration rectangular pulses and was given for 5 seconds. The stimulus frequency was usually 50 Hz; high frequency stimuli were more effective to evoke pupillary dilation produced by the humoral factor. The pupillary dilation was recorded with an infrared pupillo-analyzing system. A long latency (about 6 seconds) and long peak latency (about 10 seconds) pupillary dilation was produced by the humoral factor. The threshold of pupillary dilation produced by the humoral factor was always higher than that produced by parasympathetic inhibition. The pupillary dilation produced by the humoral factor was not affected by local application and intravitreal injection of 10(-2) M propranolol-HC1 and 10(-2) M yohimbine-HC1. However, the dilation was markedly inhibited by intravitreal injection of 10(-2) M phenoxybenzamine-HC1 or local application of 10(-2) M bunazosin-HC1.     

Effects of antibiotics on the in vitro ERG of the albino rabbit

This study describes the effects of penicillin G (PC-G) potassium, PC-G sodium, cloxacillin sodium (MCIPC), disodium sulbenicillin (SBPC), cefazolin sodium (CEZ) and cefsulodin sodium (CFS) on the in-vitro electroretinogram (ERG) of the albino rabbit.The b-wave and oscillatory potentials (OPs) were unchanged by 0.1 mM PC-G potassium or PC-G sodium. The OPs were slightly suppressed by 0.3 mM of either drug. While the a- and b-waves were not deteriorated, the OPs were greatly suppressed by 1.0 mM concentration. The effect of PC-G on the ERG was characterized by a selective suppression of the OPs. The b-wave and OPs were not suppressed by 0.03 mM MCIPC. They were slightly suppressed by 0.05 mM MCIPC. The a-wave, b-wave and OPs were not deteriorated by 1.0 mM SBPC. The b-wave and OPs were suppressed by 3.0 mM or 6.0 mM SBPC respectively. These changes appeared to be dose-dependent. Since the b-wave and OPs were concomitantly suppressed by both MCIPC and SBPC, these antibiotics, unlike PC-G, did not selectively suppress the OPs. The b-wave and OPs were unchanged by 0.1 mM CEZ or CFS. The OPs were slightly suppressed by 0.3mM CEZ or CFS. CEZ or CFS of 1.0 mM did not deteriorate the a- and b-waves, but selectively suppressed the OPs. The effects of CEZ and CFS on the ERG were characterized by a selective suppression of the OPs. The above-described changes in the ERG were reversible.     

Optical problems of anterior chamber depth biometry by scheimpflug photography.

For the first time, the Scheimpflug camera was used in the comparative investigation of the anterior chamber depth. Comparative measurements were carried out by a device developed by Jaeger, a clinically and scientifically proved method in anterior chamber depth determination. The physical problems of measuring the anterior chamber depth by using optical methods can be shown by the examination demonstrated here. The apparent change of the cornea profile depending on the cornea radius, which you can see in optical investigations, schematically described by Collignon-Brach, can be represented photographically by the Scheimpflug image.     

Comparison of standard and computerized tonography instruments on human eyes

We compared the outflow facility coefficient results after indentation tonography obtained with a standard tonography unit and with a new computerized tonography machine. Goldmann applanation tonometry was followed by standard tonography on one eye and computerized tonography on the other. After a one-hour equilibration period, tonometry was repeated and followed by tonography with the testing units used on the opposite eyes. In nine of 60 eyes the results were discarded because of poor tracings or high error. Results of initial indentation intraocular pressure measured by the two units were not statistically different from those measured by Goldmann applanation tonometry. Mean outflow facilities determined by the standard unit and by the computerized machine with the average scleral rigidity program showed no statistically significant difference by the paired t-test.     

Potentiation of acetylcholine action by huperzine-A and physostigmine on some vertebrate effectors, including human iris sphincter muscle.

The main objective of this investigation was to compare the acetylcholine potentiating action of huperzine-A with acetylcholinesterase inhibitor physostigmine on the frog rectus abdominus muscle, rat phrenic nerve diaphragm preparation, guinea pig ileum and human iris sphincter muscle. In vitro on the frog rectus abdominus muscle, microM of each alkaloid, incubated for 10 min, shifted the acetylcholine concentration response curve to the left. At EC(50) level, physostigmine potentiated acetylcholine response by 4-fold. The potentiation by huperzine-A was 40-fold. The acetylcholine maximum effect, relative to the control, increased to approximately 130% by each alkaloid. Neurally mediated twitch contraction of the rat diaphragm, a skeletal muscle at 1 microM was also potentiated more by huperzine-A than that by physostigmine. Neuromuscular block by (+)-tubocurarine was reversed more easily by huperzine-A than that by physostigmine. On guinea pig ileum, a 30 nM concentration of each alkaloid incubated for 5 min potentiated acetylcholine (10 nM) by 42%, and 33% for huperzine-A and physostigmine respectively. The difference in potentiation between the alkaloids was not significant. At 300 nM of each alkaloid, intrinsic indirect contractions were observed on the ileum, where the rate of contraction by huperzine-A was faster than that by physostigmine. On the iris sphincter, huperzine-A and physostigmine produced a concentration-dependent effect. Maximum effect after each alkaloid was achieved at 30 microM. Potentiation of acetylcholine response by 0.3 microM huperzine-A after a 10-min incubation was greater than that achieved by physostigmine at an equivalent concentration on the contralateral iris sphincter. In summary, huperzine-A exhibits greater acetylcholine potentiating activity on vertebrate muscles than that produced by physostigmine. The results are discussed in relation to the potential therapeutic value of huperzine-A.     

Corneal thickness measurement by confocal microscopy, ultrasound, and scanning slit methods

PURPOSE: To measure corneal thickness by using a calibrated confocal microscope and to compare this measurement to thickness determined by ultrasonic and noncontact scanning slit pachymetry. DESIGN: Comparison of corneal thickness measured by using four instruments in normal subjects. METHODS: Thickness measured by a clinical confocal microscope (Tandem Scanning) was calibrated from measurements of polymethylmethacrylate contact lenses with known thickness. Corneal thickness was measured in one eye of 24 normal subjects by using this instrument, two ultrasonic pachymeters (DHG-1000 and Sonogage), and a noncontact optical scanning slit pachymeter (Orbscan II). RESULTS: Mean corneal thickness measured by confocal microscopy was 516 +/- 30 microm (+/-SD). This was less than the mean thickness measured by both ultrasonic pachymeters, 554 +/- 28 microm by the DGH, and 555 +/- 28 microm by the Sonogage (P <.001). Thickness measured by the Orbscan II pachymeter was 540 +/- 35 microm (P <.001, compared with either confocal or ultrasound) after applying an "acoustic factor" of 0.92, a default correction of the software. CONCLUSION: Corneal thickness measured by calibrated confocal microscopy is approximately 39 microm (7.0%) less than thickness measured by two commonly used ultrasonic pachymeters and approximately 24 microm (4.4%) less than thickness measured by the corrected Orbscan II pachymeter. These differences are important for planning and measuring the effects of refractive and other surgical procedures. The precision of confocal microscopy is limited by corneal motion in an anterior-posterior direction. The difference between instruments suggests that verification of clinical ultrasonic pachymeters should be revisited.     

Protective role of heme oxygenase-1 against endotoxin-induced uveitis in rats

Endotoxin-induced uveitis (EIU) is an animal model of acute ocular inflammation. Cytokines, chemokines, and nitric oxide (NO) have been reported to play important roles. We have determined whether heme oxygenase (HO)-1, a heat shock protein, can suppress EIU. EIU was induced by a footpad injection of lipopolysaccharide (LPS) in male Lewis rats. Hemin, an inducer of HO-1, was injected intraperitoneally 1 hr prior to the LPS injection. HO-1 and HO-2 expression in the iris-ciliary body (ICB) was studied by real time PCR and Western blot analysis. The number of infiltrating cells and the protein concentration in the aqueous humor (AqH) were evaluated by microscopy and by protein assay. The expression of inducible nitric oxide synthase (iNOS), interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and IL-1beta mRNA was determined by real time PCR. The concentration of nitrate plus nitrite, and levels of IL-6 and TNF-alpha in the AqH were also evaluated by Griess reagents and by enzyme-linked immunosorbent assay, respectively. The expression of HO-1 mRNA and protein, induced by LPS, was enhanced significantly by pre-injection of hemin (P<0.001). HO-2 was constitutively present in the ICB and was not up-regulated by LPS or by hemin. The number of infiltrating cells and the concentration of protein in the AqH was significantly elevated by LPS injection, and hemin significantly reduced the number of cells and the protein concentration (P<0.0001). The expression of iNOS and IL-6 mRNA and protein were down-regulated by hemin (P<0.001). Hemin is effective in inducing HO-1 and in reducing the ocular inflammation induced by LPS probably by down-regulating NO and pro-inflammatory cytokine expression.     

Rod- and cone-mediated interactions in the fine-grain movement illusion

The sequence in which two small, spatially unresolved spots of light are flashed in the periphery of the visual field can be determined by means of a “fine-grain” movement illusion. The illusion can be produced not only by rod-rod and by cone-cone stimulation, but also by rod-cone stimulation. Dynamics of the illusion are obtained by sequence-discrimination experiments for each of these three stimulus conditions.     

Nitric oxide as a second messenger in phagocytosis by cultured retinal pigment epithelial cells

PURPOSE: To investigate a possible role of the nitric oxide (NO)-cGMP signal transduction system in phagocytosis of rod outer segments (ROS) by cultured retinal pigment epithelial (RPE) cells. METHODS: Primary cultures of RPE cells from 10-day-old Brown Norway rats were used to study the phagocytosis of ROS by these cells. Phagocytosis of ROS was evaluated with or without an inhibitor of nitric oxide synthase (NOS), N(G)-nitro-L-arginine (L-NNA), and the reverse effects of L-NNA by L-arginine and 8-bromo-cGMP on phagocytosis were also studied. NO-associated cGMP production by RPE cells was monitored during phagocytosis using L-NNA. NOS activity was assayed in RPE cells and ROS to locate the source of NO. RESULTS: Phagocytosis of ROS was inhibited by L-NNA but not by D-NNA. L-NNA inhibited the ingestion in a dose-dependent manner, but not the binding of ROS. The inhibition was reversed by L-arginine and also by an NO donor, SIN-1. RPE cells challenged with ROS showed increased cGMP activity, which was significantly reduced by L-NNA and again restored by an overdose of L-arginine. NOS activity was found in RPE cells but not in ROS. CONCLUSIONS: Our data show that cGMP plays a role in the ingestion phase of ROS phagocytosis by RPE cells via a cGMP second-messenger system.     

Comparison of IOL powers by corrected method in eyes after PRK and LASIK

The purpose of this study is to compare, by statistical analysis, intraocular lens (IOL) powers by SRK/T formula using autorefractokeratometer-measured keratometric (K) values (SRK/T-ARK-mK), by SRK/T formula using refraction-derived K values (SRK/T-R-dK), and by refraction corrected method (RCM), in eyes treated with photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK) for myopia. Thirty-eight consecutive eyes of 23 patients with PRK for mild to moderate myopia and 35 consecutive eyes of 25 patients with LASIK for high myopia were followed up for more than 1 year. In the two groups, IOL powers by SRK/T-ARK-mK, by SRK/T-R-dK, and by RCM were compared by statistical analysis. In PRK group, the mean value of IOL powers by RCM was statistically higher than that obtained by the other two methods (p < 0.05), while there was no significant statistical difference between the mean values of IOL powers by SRK/T-ARK-mK and by SRK/T-R-dK (p > 0.05). However, in LASIK group, the mean values of IOL powers by RCM and by SRK/T-R-dK, which did not differ statistically (p > 0.05), were both statistically higher than that by SRK/T-ARK-mK (p < 0.05). In conclusion, there is a statistical difference in IOL powers by the methods used for IOL calculation, as there is according to the level of myopia in patients with PRK and LASIK treatment. We suggest that, in IOL power calculation in eyes with previous corneal refractive surgery, correction methods such as RCM and SRK/T-R-dK are more effective at higher levels of myopia.     

Mechanisms underlying the neurogenic relaxation of isolated porcine sphincter pupillae

Mechanisms of relaxation induced by nerve stimulation were examined in isolated porcine iris sphincter muscle in reference to norepinephrine, nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) and the functional interaction of inhibitory and excitatory nerves. Changes in isometric tension were recorded in strips of the sphincter pupillae, which were stimulated by transmurally applied electrical pulses. The presence of neurons containing acetylcholinesterase and tyrosine hydroxylase (TH) was determined histochemically. Transmural electrical stimulation (0.5-20 Hz) produced a frequency-related contraction, which was reversed to a relaxation by atropine in prostaglandin F2alpha-contracted strips. The relaxant response was abolished by timolol and suppressed by metoprolol, a beta1-adrenoceptor antagonist, but was not influenced by butoxamine, a beta2-receptor antagonist. Norepinephrine-induced relaxations were also attenuated only by timolol and metoprolol. Treatment with NG-nitro-L-arginine, a NO synthase inhibitor, and [D-p-Cl-Phe6,Leu17]VIP, a VIP receptor antagonist, did not inhibit the neurogenic relaxation. Contractions induced by nerve stimulation were potentiated by timolol and physostigmine but not by the NO synthase inhibitor. In the sphincter muscle, cholinesterase- and TH-positive nerve fibers and bundles were histologically detected. It is concluded that porcine iris sphincter is innervated by cholinergic excitatory and adrenergic inhibitory nerves. The neurogenic relaxation is associated solely with activation of beta1 adrenoceptors by norepinephrine but is not mediated by NO or VIP.     

Interaction between alpha 2- and beta 2-adrenergic receptors in rabbit ciliary processes

The interaction between the alpha 2- and beta 2-adrenergic receptors of ciliary processes has been studied by examining dose-response curves for adrenergic agonist stimulation of cyclic AMP production by intact, excised rabbit ciliary processes. Stimulation of cyclic AMP production by 1-isoproterenol is maximum from 0.1 to 1.0 microM; at higher concentrations stimulation decreases and approaches basal levels. Decreased cyclic AMP production at high concentrations of isoproterenol is blocked by the specific alpha 2-adrenergic antagonist, yohimbine, but not by the alpha 1-adrenergic antagonist, prazosin. Ciliary processes from animals after bilateral cervical ganglionectomy also show reduced cyclic AMP production at high concentrations of isoproterenol and this reduction is blocked by yohimbine, but not prazosin. This experiment suggests that the inhibition at high concentrations of isoproterenol is mediated by postsynaptic alpha 2-adrenergic receptors. Cyclic AMP production is relatively insensitive to epinephrine and norepinephrine, but their responses are potentiated by yohimbine. Catecholamines and clonidine, a specific alpha 2-adrenergic agonist, exhibit dose-dependent inhibition of forskolin-stimulated cyclic AMP production by ciliary processes. I50s from the dose-response curves are consistent with the characteristic binding affinities of these adrenergic agonists for alpha 2-adrenergic receptors: clonidine = epinephrine greater than norepinephrine greater than isoproterenol. Inhibition of forskolin-stimulated cyclic AMP production by clonidine is blocked by yohimbine but not by prazosin.(ABSTRACT TRUNCATED AT 250 WORDS)