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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated rat paraventricular (PVN) and supraoptic (SON) nuclei were perifused in vitro and oxytocin and vasopressin releases were measured by radioimmunoassay during rest and during electrical stimulation. Stimulations at a frequency of 10 Hz (10-s bursts, every 10 s for 5 min) and an intensity of 4 mA, induced significant hormone release only with long duration pulses (10 ms). Short pulses (1 ms) applied at various frequencies (10, 20, 40 or 80 Hz) and intensities (4, 5, 10 or 20 mA) had no effect. The electrically evoked release of both hormones was not affected by tetrodotoxin (TTX), a sodium channel blocker, but was blocked in low-calcium medium or in the presence of gallopamil hydrochloride (D-600), a calcium channel blocker. These results suggest that, following electrical stimulation, oxytocin and vasopressin are released locally within the magnocellular nuclei even when blocking action potentials. The possibility of dendritic release is discussed.
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PMID:Electrical stimulations of perifused magnocellular nuclei in vitro elicit Ca2+-dependent, tetrodotoxin-insensitive release of oxytocin and vasopressin. 243 5

The effects of the organic calcium antagonists verapamil and methoxyverapamil (D-600) on vasopressin-stimulated water flow in response to an osmotic gradient were investigated. When toad bladders were exposed to either verapamil or D-600 for 60 min, vasopressin-stimulated water flow was inhibited. In the presence of verapamil (100 microM), water flow decreased from 38 +/- 3 to 26 +/- 3 mg/min/hemibladder (P less than .05, n = 5) and in the presence of D-600 (100 microM) from 48 +/- 3 to 32 +/- 4 mg/min/hemibladder (P less than .02, n = 5). When preincubated with hemibladders for 90 min they also inhibited basal 45Ca uptake into isolated toad bladder epithelial cells (from 1.58 +/- 0.20 to 1.02 +/- 0.14 nmol/mg of protein per 5 min, P less than .05, n = 6). Addition of verapamil to the bathing media during recovery from a vasopressin stimulus to block reuptake of calcium into the epithelial cells inhibited water flow in response to a subsequent incubation with vasopressin to a greater extent than the inhibition of water flow when verapamil was present only before exposure to vasopressin. Inhibition was also greater in the presence of lower extracellular calcium concentrations. The results are consistent with the notion that the calcium antagonists inhibit vasopressin-stimulated water flow by virtue of depleting a critical pool of intracellular calcium rather than preventing the simultaneous entry of calcium from extracellular sites during the exposure to vasopressin.
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PMID:Verapamil inhibition of vasopressin-stimulated water flow: possible role of intracellular calcium. 641 96

1. Synthetic arginine-vasopressin (ADH or antidiuretic hormone) inhibited renin secretory rate of rat renal cortical slices. The response was concentration-dependent and was maximal at 0.1 U . ml.-1. 2. Ca depletion (incubation of slices in medium containing Na2EGTA and no added CaCl2) stimulated renin secretion and eventually abolished the inhibitory effect of ADH. Both these effects were reversible. 3. The Ca antagonist D-600, at 0.5 microM, reversed the inhibitory effect of K depolarization on secretory rate but had no effect on secretory rate on on-depolarized slices. In the presence of 0.5 microM-D-600, ADH inhibited the secretory rate of either depolarized or non-depolarized slices. 4. These results confirm and extend previous observations suggesting that Ca plays an inhibitory coupling role in the control of renin secretion. Moreover they suggest that although Ca influx through voltage-sensitive Ca channels influences the secretory activity of juxtaglomerular cells, ADH activates an independent pathway for Ca mobilization.
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PMID:Calcium dependency of the inhibitory effect of antidiuretic hormone on in vitro renin secretion in rats. 703 Dec 29