Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because the secretion of endolymph has been localized in the ampullar part of the frog semicircular canal, we attempted to determine by cytochemical methods the ultrastructural localization of two enzymes that are assumed to play a role in endolymph secretion: carbonic anhydrase and adenylate cyclase. Functionally, the epithelium of the frog semicircular canal can be schematically divided into three areas: sensory (crista ampullaris), secretory (dark cells), and non-sensory and nonsecretory (transitional and undifferentiated cells) areas. Carbonic anhydrase activity was widely distributed in dark cells. Dark cell labeling disappeared in the presence of acetazolamide. The other cells of the canal did not show any carbonic anhydrase labeling except for the supporting cells of the sensory cells. Adenylate cyclase activity was found on the basolateral and apical membranes of dark cells, and on the apical membrane of sensory cells; weak labeling was also observed in the other epithelial cells. In the apical membrane of the dark cells, adenylate cyclase labeling was dependent on the presence of vasotocin, the frog antidiuretic hormone. The dark cells of the frog semicircular canal thus possess the enzyme equipment needed for the secretion of endolymph and its possible hormonal regulation.
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PMID:Adenylate cyclase and carbonic anhydrase in the semicircular canal epithelium of the frog Rana esculenta. An ultrastructural cytochemical localization. 212 34

Turtle urinary bladder possesses four ion transport processes: Na+ absorption, H+ secretion, and HCO3- secretion-Cl- absorption. Each transport process is performed by a specific epithelial cell type. Granular cells absorb Na+ but they are not sensitive to antidiuretic hormone (ADH), unlike toad bladder granular cells. alpha-Carbonic anhydrase-rich (CA) cells secrete H+ via an apical H+-adenosinetriphosphatase (ATPase). Under conditions of low CO2 tension, this active pump is contained in the limiting membranes of certain cytoplasmic vesicles. The vesicles fuse with the apical membrane, and H+ pumps are incorporated into that membrane, as physiological conditions demand increased H+ secretion. The stimulus for fusion of these vesicles with the apical membrane appears to be intracellular acidification. beta-CA cells secrete HCO3- and reabsorb Cl-, both processes driven by H+-ATPase in the basolateral membrane in series with an apical Cl- -HCO3- exchanger. Increased intracellular adenosine 3',5'-cyclic monophosphate concentration in beta-cells stimulates net HCO3- secretion and induces an electrogenic component of this flux by activating an apical Cl- channel. This activation accompanies the fusion of an intracellular tubulovesicular network with the apical membrane. The membrane of this network may contain Cl- channels.
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PMID:Turtle urinary bladder: regulation of ion transport by dynamic changes in plasma membrane area. 251 70

Carbonic anhydrase (CA) is a zinc enzyme that catalyses the reversible hydration reaction of CO2 and plays a major role in the acid-base balance. We have previously shown that certain vasoconstrictive therapeutic agents increase CA I activity whereas vasodilating drugs reduce the activity of this isozyme by a direct mechanism of action. In this paper we studied the effect of other vasoconstrictive and vasodilating agents on CA I activity in order to elucidate the involvement of vascular smooth muscle CA I in vasoconstrictive and vasodilating processes. We studied the in vitro effects of noradrenaline, prostaglandin F2 alpha, thromboxane A2, leukotriene B4, angiotensin II, vasopressin, indomethacin, prazosin, hydralazine, clonidine, reserpine, prostaglandin I2, indapamide, furosemide, amlodipine, verapamil and irbesartan on purified human red blood cell CA I and vascular smooth muscle CA I isolated from rabbits. In vivo, we selected six groups of five rabbits each, which were administered the following substances in acute experiments: orciprenaline (group 1), desmopressin (group 2), verapamil (group 3), irbesartan (group 4), acetazolamide (group 5) and placebo (control group). Vascular smooth muscle CA I activity and systolic blood pressure were determined and compared with those of the control group. In vitro results showed that all the vasoconstrictive agents studied increased purified and human erythrocyte CA I activity as well as vascular smooth muscle CA I, while vasodilating substances reduced the activity of isozyme by a direct mechanism of action. The same results obtained in vivo showed that activation of vascular smooth muscle CA I increased blood pressure while its inhibition reduced blood pressure. The results of this study suggest that pHi changes, induced by activating or inhibiting CA I in vascular smooth muscle, might be responsible for changes in vascular tonus.
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PMID:Vasoconstrictive drugs increase carbonic anhydrase I in vascular smooth muscle while vasodilating drugs reduce the activity of this isozyme by a direct mechanism of action. 1139 54