The influence of vanadate upon the adrenergic response of the rabbit iris (dilation) was examined in vivo, while the effects of vanadate upon adrenergic responses of the rabbit ileum and guinea pig vas deferens were investigated in vitro. Intravenously administered vanadate (2 mg/Kg) sensitized the iris to topically administered epinephrine; a small quantity of epinephrine, that elicited no change of pupil size following topical administration to the eye in the normal rabbit, produced a marked pupillary dilation in animals treated systemically with vanadate. The response of the isolated ileum to vanadate (1-10 micrograms) was identical to that elicited by norepinephrine or epinephrine. Brief exposure of the ileum to vanadate, norepinephrine, or epinephrine resulted in a transient cessation of rhythmic activity and reduction of mean tension. When the ileum was superfused continuously with solutions containing vanadate (10 micrograms/ml; 5.4 X 10(-5) M), the rhythmic activity and mean tension returned to control values within several minutes, suggesting tachyphylaxis. Exposure of the guinea pig vas deferens to vanadate did not elicit a contractile response. However, when the vas deferens was superfused continuously (greater than 60 min) with vanadate (5.4 X 10(-5) M), both the amplitude and duration of the contraction elicited by epinephrine were increased. Consistent with the above findings is the hypothesis that vanadate might inhibit the mechanisms responsible for the removal of epinephrine or norepinephrine from the site of action within a tissue.
Elevated intraocular pressure is associated with glaucomatous optic nerve damage. Other investigators have shown functional changes in optic nerve head astrocytes subjected to elevated hydrostatic pressure (HP) for 1 to 5 days. Recently, the authors reported ERK1/2, p90(RSK) and NHE1 phosphorylation after 2 hours. Here they examine calcium responses at the onset of HP to determine what precedes ERK1/2 phosphorylation.
In an earlier study it was reported that thrombin significantly reduces the rate of Na,K-adenosine triphosphatase (ATPase)-mediated ion transport by porcine lens. Because thrombin stimulates the release of endogenous endothelin (ET)-1 stores from some tissues, and because ET-1 can cause Na,K-ATPase inhibition, this study was designed to determine whether thrombin causes release of ET-1 from the lens.
