Biomedical subjects

R R Socci

Publications and source records attributed to R R Socci.

25 records · Page 2Linked to original sources

PubMed1992

Adrenergic receptor-mediated increase of intracellular Ca2+ concentration in isolated bovine corneal epithelial cells.

1. We determined if Ca2+ is a second messenger for adrenergic receptor-effector coupling in bovine corneal epithelial cells. 2. Methoxamine (10(-5) M) selectively increased intracellular Ca2+ concentration (Cai) by 65%. This increase was only partially suppressed through the removal of extracellular Ca2+ or pretreatment with 10(-6) M verapamil. 3. The beta-adrenergic-mediated increases in Cai were entirely dependent on extracellular Ca2+. These increases were directly elicited through stimulation of adenylate cyclase because 10(-6) M isoproterenol and the active analogues of forskolin (10(-5) M) all elevated Cai. 4. Therefore, increases in Cai serve a second messenger function for alpha-1 and beta-adrenergic receptor-effector coupling.

Adenylyl Cyclases↗

PubMed1992

Comparative studies of furosemide effects on membrane potential and intracellular chloride activity in human and rabbit ciliary epithelium.

Furosemide (1 mM), a potent loop diuretic, caused a 10-mV (n = 14) depolarization of the intracellular potential difference (PDI) of isolated rabbit ciliary epithelium (CE), but produced a 9-mV (n = 5) hyperpolarization of PDI of isolated human CE. In rabbit CE, furosemide consistently depolarized PDI by 13, 7 and 8 mV in HCO3(-)-free Ringer, Na(+)-free Ringer and after BaCl2 treatment, respectively. The depolarization of PDI was reduced to 2 mV (n = 11) in Cl(-)-free conditions. A hyperpolarization of PDI caused by furosemide that was quantitatively similar to that seen in normal Ringer also occurred in human CE during immersion in HCO3(-)-free Ringer, Na(+)-free Ringer and after BaCl2 treatment. There was a small hyperpolarization (3 mV) of PDI in Cl(-)-free conditions. Human or rabbit tissue-cultured nonpigmented ciliary epithelial cells were loaded with the Cl(-)-sensitive fluorophore 6-methoxy-N-(3-sulfopropyl) quinolinium (SPQ) in hypotonic solution (145 mosm) for 4 min at 37 degrees C. Furosemide decreased intracellular Cl- fluorescence activity of both human and rabbit ciliary epithelial cells by 30 +/- 5 (n = 8) and 25 +/- 7% (n = 13), respectively, when the cells were immersed in Cl(-)-rich solution. It is suggested that a furosemide-sensitive Cl- movement exists in both rabbit and human CE, although the mode of Cl- movement to the aqueous across CE may differ between these species.

Animals↗

PubMed1991

The influence of 12(R)-hydroxyeicosatetraenoic acid on ciliary epithelial sodium, potassium-adenosine triphosphatase activity and intraocular pressure in the rabbit.

Ciliary epithelium was isolated from the rabbit eye and used as a source of plasma membrane material for sodium, potassium-adenosine triphosphatase (Na,K-ATPase) measurements. In the presence of 12(R)-hydroxyeicosatetraenoic acid [12(R)HETE], Na,K-ATPase (ouabain-sensitive ATPase) activity was reduced from 22.5 to 16.3 microM phosphate released/mg protein/hr. Ouabain-insensitive ATPase activity was not altered by 12(R)HETE. No changes in ciliary epithelium ATPase activity were observed in the presence of 12(S)HETE. In parallel studies with conscious rabbits, 12(R)HETE applied topically to the eye was found to lower intraocular pressure (IOP). It is possible that the IOP-lowering effect of 12(R)HETE may be, in part, associated with its ability to suppress the Na,K-ATPase activity of the ciliary epithelium.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1990

Alteration of sodium, potassium-adenosine triphosphatase activity in rabbit ciliary processes by cyclic adenosine monophosphate-dependent protein kinase.

The response of sodium, potassium-adenosine triphosphatase (Na,K-ATPase) to cyclic adenosine monophosphate (cAMP)-dependent protein kinase was examined in membranes obtained from rabbit iris-ciliary body. In the presence of the protein kinase together with 10(-5) M cAMP, Na,K-ATPase activity was reduced. No change in Na,K-ATPase activity was detected in response to the protein kinase without added cAMP. Likewise cAMP alone did not alter Na,K-ATPase activity. Reduction of Na,K-ATPase activity was also observed in the presence of the cAMP-dependent protein kinase catalytic subunit. The response of the enzyme to the kinase catalytic subunit was also examined in membranes obtained from rabbit ciliary processes. In the presence of 8 micrograms/ml of the catalytic subunit, ciliary process Na,K-ATPase activity was reduced by more than 50%. To examine whether other ATPases were suppressed by the protein kinase, calcium-stimulated ATPase activity was examined; its activity was stimulated by the catalytic subunit. To test whether the response of the ciliary process Na,K-ATPase is unique, experiments were also performed using membrane preparations from rabbit lens epithelium or rabbit kidney; the catalytic subunit significantly reduced the activity of Na,K-ATPase from the kidney but not the lens. These Na,K-ATPase studies suggest that in the iris-ciliary body, cAMP may alter sodium pump activity. In parallel 86Rb uptake studies, we observed that ouabain-inhibitable potassium uptake by intact pieces of iris-ciliary body was reduced by exogenous dibutryl cAMP or by forskolin.

Animals↗

PubMed1988

Characteristics of ascorbate transport in the rabbit iris-ciliary body.

The accumulation and efflux of [14C]ascorbic acid by the rabbit iris-ciliary body were examined in vitro. Accumulation of labelled ascorbate was observed to be reduced significantly by ouabain(10(-4) M), low sodium solutions, 0 degree C and dinitrophenol (10(-3) M). These findings suggest that the ascorbate uptake mechanism is linked to metabolism via the sodium gradient. In addition, labelled ascorbate uptake was diminished by both phloretin (10(-4) M) and phlorhizin-(10(-4) M), two glucose transport inhibitors. Clear differences were observed between the characteristics of [14C]ascorbic acid uptake and efflux. In contrast to the uptake, 14C-labelled, ascorbate efflux from the iris-ciliary body was not significantly altered by dinitrophenol, phloretin, or phlorhizin. The observation that the efflux of labelled ascorbate was not diminished by either dinitrophenol or ouabain supports the concept that the process of ascorbate efflux from the iris-ciliary body is passive and not sodium dependent. It was demonstrated that a vigorous rate of [14C]ascorbate efflux from the iris-ciliary body persisted even when the external ascorbate level was elevated to 1 mM, the concentration found in aqueous humor.

Animals↗

PubMed1988

The effect of vanadate upon calcium-stimulated ATPase of the rabbit iris-ciliary body.

In many tissues, the level of cytoplasmic calcium mediates cell function. Since cytoplasmic calcium is often maintained at a low level by active calcium extrusion, we examined whether calcium-stimulated ATPase is present in the rabbit ciliary epithelium. A technique was developed to measure calcium-stimulated ATPase in a partially enriched plasma membrane preparation. The enhancement of Na,K-ATPase activity was used to indicate the enrichment of plasma membrane. Marked stimulation of ATPase activity by calcium was observed over a range of calcium concentrations (10(-8) to 10(-3) M). The calcium concentration necessary to elicit half-maximal ATPase activity was 10(-6) M, which is similar to that reported for other membrane preparations. Calcium-stimulated ATPase activity was significantly inhibited in the presence of low concentrations of sodium orthovanadate. The inhibitory influence of vanadate was examined over a range of vanadate concentrations (10(-8) to 10(-3) M). The vanadate concentration needed to produce half-maximal inhibition of calcium-stimulated ATPase was 2 X 10(-6) M. These studies show that calcium-stimulated ATPase inhibition can occur, in vitro, at very low levels of vanadate; it is possible that this might contribute to the chain of events which results in the lowering of aqueous humor secretion reported in vanadate-treated rabbits.

Adenosine Triphosphatases↗

PubMedDate not supplied

Post-suspension hypotension is attenuated in Sprague-Dawley rats by prostacyclin synthase inhibition.

Cardiovascular deconditioning, sometimes manifested in astronauts during standing postflight, may be related to the impairment of autonomic function and/or excessive production of endothelium-dependent relaxing factors. In the present study, we examined the cardiovascular responses to 7-day 30 degrees tail-suspension and a subsequent 6-h post-suspension period in conscious male Sprague-Dawley rats to determine the role of prostacyclin in the observed post-suspension reduction in mean arterial pressure (MAP). The specific prostacyclin synthase inhibitor U-51605 (0.3 mg/kg), or saline, was administered intravenously prior to release from suspension and at 2 and 4 h post-suspension. During 7 days of suspension, MAP did not change, however, there was a post-suspension reduction in MAP which was associated with significant increases in plasma prostacyclin and nitric oxide. U-51605 attenuated the observed post-suspension hypotension and reduced plasma prostacyclin levels, but not nitric oxide levels. The baroreflex sensitivity for heart rate was modified by U-51605: increased MAP threshold and effective MAP range. Thus, the post-suspension reduction in mean arterial pressure may be due to overproduction of prostacyclin and/or other endothelium-dependent relaxing factors and alteration in baroreflex activity.

Animals↗