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)

Ethanol (3%) decreases the potential difference and short-circuit current across the isolated frog skin in chloride Ringer's solution. Unidirectional fluxes of Na and Cl indicate that the drop in short-circuit current is due to an inhibition of the sodium influx. However, ethanol had no effect on the electrical parameters or sodium fluxes, when the frog skin was bathed in chloride-free solutions on both sides or the outside alone. The ethanol response is anion-dependent. In addition, chloride-free media in the inside bathing solution reduced the short-circuit current, indicating a sodium transport pathway which is dependent on chloride and confirming previous data in the literature. Other anions such as sulfate and nitrate could not substitute for chloride. The vasopressin-induced natriferic response and the ethanol effect were found to work independently of each other and different pathways of action are suggested for these agents. The intracellular sodium content of the isolated frog skin epithelium increased and potassium decreased in the presence of the Na-K adenosine triphosphatase inhibitor, ouabain, whereas ethanol or amiloride had no effect. The oxygen consumption of the isolated frog skin was unaffected by up to 10% ethanol. A general metabolic action is probably thus not mediating the response. Urea, in iso-osmotic concentrations to the ethanol, did not mimic its effect. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. It is suggested that ethanol may impede the flow of water across frog skin by a physicochemical interaction with membrane pores and the water molecules. The permeability coefficient (Ktrans) for ethanol was found to be 10 times smaller than the Ktrans for water.
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PMID:Effects of ethanol on the permeability of frog skin. 108 5

The available evidence suggests that hormones and neurophysins are associated exclusively with the neurosecretory granules, each of which contains approximately 6 times 10-4 molecules of each. Hormones and carrier proteins are complexed within the granules and the complexes are densely packed. The processes that keep the intragranular space in osmotic equilibrium with the axoplasm require further study. Freeze-fracture data, as well as studies in which histochemical methods for the detection of glycoproteins were used, suggest that the intragranular aspect of the granule membrane mostly resembles the extracellular half of the plasma membrane; on the other hand, the cytoplasmic aspects of plasma and granule membrane have similar characteristics, which may be important in permitting membrane fusion to take place prior to secretion. Little is known about the molecular species involved in this interaction between granule and plasma membrane, except that calcium is a cofactor in this process. Release is triggered in vivo by propagated action potentials which cause an influx of calcium into the secretory endings. Newly formed granules, and other granules located at the periphery of the endings are preferentially released. Irrespective of the type of stimulation of secretion, release involves the diffusion into the extracellular space of granule core constituents. The best evidence so far in support of this view comes from ultrastructural studies showing images of exocytosis, as well as from biochemical studies demonstrating that hormones and carrier proteins are secreted concomitantly in a great variety of experimental or clinical conditions, without an associated release of granule membrane constituents or of enzymes of cytoplasmic origin. Recovery mechanisms following secretion require new synthesis of granule constituents and restoration of the resting internal concentrations of potassium, sodium, and calcium. Membrane surface area is restored following exocytosis by compensatory endocytosis which involves indiscriminate uptake of extracellular medium into the secretory axon terminals. While much progress has been made in research on the cellular and subcellular processes that take place in neurons which produce, store, and secrete neurohypophyseal hormones and their carrier proteins, neurophysins, many pressing questions remain to be answered. New developments, such as organ culture of supraoptic nuclei94-96 and the recent isolation of a clone of mouse hypothalamic cells capable of synthesizing vasopressin and neurophysin,97 will hopefully allow some of these problems to be solved in the future.
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PMID:A review on neurosecretory granules: their contents and mechanisms of release. 109 Nov 94

Experiments on rat mesenteric arterioles, metarterioles, and aortae demonstrate that although alpha-methylnorepinephrine is much less potent in inducing contraction than epinephrine on all three blood vessel types, it is either equivalent or only one and a half to two times less potent than the natural postganglionic neurotransmitter, norepinephrine, on these blood vessels. Furthermore, alpha-methylnorepinephrine is equivalent to norepinephrine in its ability to induce maximal contractile responses on rat arterioles, metarterioles, and aortae. Systemic administration of alpha-methyldopa to rats for 15 days shifted the log dose-response curves for all three catecholamines, but not vasopressin or potassium chloride, to the right of all three blood vessel types; the maximal contractile responses to these amines were, however, not affected by chronic treatment with alpha-methyldopa. In addition, acute, intra-arterial administration of 500 mg/kg of alpha-methyldopa was found not only to induce mesenteric arteriolar vasodilatation gradually but also to depress arteriolar reponsiveness to catecholamines. In view of these direct findings, it is difficult to accept the hypothesis that alpha-methyldopa induces hypotension via formation of a "false" postganglionic neurotransmitter substance, namely, alpha-methylnorepinephrine. The present findings suggest that alpha-methyldopa may exert some of its anti-hypertensive action, at least in the rat, by (1) depressing arteriolar responsiveness to circulating and released catecholamines and (2) some unknown direct action on peripheral vascular muscle. In addition, the present study indicates that octopamine is (1) between 60 and 15,000 times less potent than norepinephrine on rat arterioles and metarterioles and (2) incapable of eliciting more than a 40% occlusion of these terminal vessels. It is suggested that such data support the concept that octopamine, in contrast to alpha-methylnorepinephrine, could serve as a false adrenergic neurotransmitter agent and thus account for part or all of the hypotensive action of monoamine oxidase inhibitors like pargyline. The use of complete dose-response curves, several different adrenergic compounds (i.e., epinephrine, norepinephrine, alpha-methylnorepinephrine, octopamine, phenylephrine, and dopamine), and different rat blood vessels supports the concept that adrenergic molecules containing a catecholamine nucleus and a beta-hydroxyl group elicit the most potent constrictor responses from peripheral blood vessels. In addition, the data suggest that the structure-activity relationships for catecholamines and their analogs on terminal vascular smooth muscle are probably different from those for arterial smooth muscle.
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PMID:Pharmacological effects of alpha-methyldopa, alpha-methylnorepinephrine, and octopamine on rat arteriolar, arterial, and terminal vascular smooth. 109 55

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

The influence of administration of ovine prolactin in vivo on intestinal fluid and ion transport in vitro was investigated using intact and hypophysectomized male rats. Prolactin administration significantly stimulated fluid, sodium,potassium, calcium, magnesium and chloride transport across everted jejunal sacs. The last two ions were affected less than the others. Hypophysectomy caused a significant decrease in fluid and sodium absorption, but prolactin treatment for 2 days restored normal absorption rates but not uniformly in all sacs. Prolactin action on fluid and sodium absorption showed a dose-dependent tendency, maximal stimulation resulting from administration of 1.0 to 2.0 mg prolactin daily; higher doses failed to elicit significant response. The stimulatory action of prolactin was inhibited by a simultaneous administration of vasopressin which when given alone had no effect on intestinal absorption. In the absence of glucose or in the presence of phlorizin, fluid transport was inhibited, the reduction being more dramatic in the presence of phlorizin. Similarly, either application of ouabain or partial replacement of sodium with isotonic choline chloride reduced fluid transport. Although these in vitro treatments nullified the stimulatory effects of prolactin, only phlorizin and ouabain significantly decreased sodium transport. These results suggest that the effects of prolactin on intestinal transport may be dependent on increased movement of sodium.
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PMID:Further studies on the action of prolactin on fluid and ion absorption by the rat jejunum. 112 80

In preparation for the conduct of biochemical experiments in the Skylab Orbital Workshop a study was performed on the stability of various chemical constituents in urine in 2 different techniques for preservation and storage. Urine samples were either vacuum dried or frozen and maintained in storage at minus 20 degrees for periods of up to 10 weeks. The urinary constituents studied included aldosterone, antidiuretic hormone, epinephrine, norepinephrine, urea, nitrogen, creatine, hydroxyproline, 17-hydroxycorticosteroids, calcium, sodium potassium, chloride, magnesium and phosphate. Some degradation of urinary compounds was observed after both treatments. The rate and variability of destruction following the vacuum drying treatment, however, was greater than for freezing. It was concluded that only the freezing treatment could be used to preserve with predictable loss the urinary samples which would be returned to earth following the conclusion of each Skylab flight.
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PMID:Acomparative study of two methods of urine preservation. 112 11

Dogs infused with 2 meq KCl/kg per h exhibit electrocardiographic evidence of prelethal cardiotoxicity in about 3 h when serum potassium reaches a level between 10.2-10.5 meq/liter. During this time, their urine output of 30 ml/h is equal to the volume of KCl infused. Studies of the potassium distribution in these animals indicate that 20 percent of the infused ion is added to the extracellular fluid and red blood cell mass, 20 percent is excreted in the urine, while the remaining 60 percent is unaccounted for and presumably transferred to intracellular fluid. Dogs treated with moderately large doses of antidiuretic hormone intramuscularly before and during KCl infusion delay development of prelethal cardiotoxicity for about 5 h, with serum potassium levels comparable to those of untreated dogs. In addition, treated animals display a considerable diuresis and kaluresis with urine volumes nearly 4 times that of the volume infused. The potassium ion distribution in animals given antidiuretic hormone is much different from that of untreated dogs, with 55 percent of the infused ion found in the urine, about 15 percent in extracellular fluid and red blood cell mass, and only 30 percent presumably transferred to intracellular fluid. Transfer of potassium to intracellular fluid was calculated to be 3.1 plus or minus 0.7 meq/kg in antidiuretic-hormone-treated animals and 3.8 plus or minus 0.7 meq/kg in untreated (control) animals. Since these values are, within experimental error, quite comparable, it is possible that antidiuretic-hormone-induced kaluresis and diuresis are involved in protecting some animals from the effects of hyperkalemia by delaying the attainment of cardiotoxic blood levels.
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PMID:Kaluresis and diuresis after administration of antidiuretic hormone to hyperkalemic dogs. 113 May 11

Electrical and permeability features of the distal convoluted tubule (DCT) and the cortical collecting tubule (CCT) were examined using the technique in which isolated segments of rabbit tubules were perfused in vitro. When rabbits were given a regular diet and tubules were perfused and bathed in artificial solutions simulating plasma ultrafiltrate, the potential difference (PD) was +3.7 plus or minus 1.9 mV in the CCT and -40.4 plus or minus 2.8 mV in the DCT. When rabbits were given a low sodium, high potassium diet plus i.m. deoxycorticosterone acetate (DOCA) (1 mg/kg per day), the PD in both the CCT (-30.8 plus or minus 3.9 mV) and the DCT (-33.8 plus or minus 5.5 mV) was negative. The PD in the CCT was quantitatively similar to that of diet plus DOCA when animals were given DOCA alone. The PD in both segments was inhibited by ouabain (10-minus 5 M) in the bath or by amiloride (10-minus 5 M) in the perfusate. Addition of vasopressin (200 muU/ml) to the bath caused a gradual decline of PD to zero in the CCT but failed to produce a potential response in the DCT. Osmotic water permeability was essentially zero in both segments in the absence of vasopressin. After addition of the vasopressin to the bath, osmotic water permeability in the DCT remained zero but increased to 71.9 plus or minus 25.5 X 10-minus 7 cm/s per atm in the CCT. We conclude that both segments are similar in that each possesses an electrogenic transport process but that these segments differ in that: (a) the CCT requires either exogenous or endogenous mineralocorticoid to maintain a maximal negative PD, whereas the PD in the DCT appears to be independent of mineralocorticoid effect; and (b) the CCT responds to vasopressin with a marked rise in water permeability, whereas the DCT is impermeable to water before and after addition of vasopressin.
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PMID:A functional comparison of the cortical collecting tubule and the distal convoluted tubule. 113 74

1. Isolated rat neurohypophyses were incubated in Locke solution at 37 degress C and the vasopressin output into the medium determined by bioassay. 2. Potassium chloride 60 mM caused a 9-fold increase in the rate of vasopressin release that was abolished when calcium chloride was omitted from the Locke solution. 3. Acetylcholine 5.5x10-4M neither alone nor in the presence of atropine 2.9x10-6M changed the "resting" release of vasopressin. 4. Neither acetylcholine 5.5x10-4M oxotremorine 10-4 and k3x10-4M altered the vasopressin release evoked by potassium chloride 60 mM. 5. In contrast to the peripheral adrenergic nerve fibres, the secretory terminal fibres of the neurohypophysis do not appear to contain muscarinic inhibitory or nicotinic excitatory receptors.
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PMID:Absence of muscarinic modulation of vasopressin release from the isolated rat neurophypophysis. 114 65

Peptide hormones are now widely used for both medicinal and veterinary purposes. It is, therefore, imminent to improve the process of peptide synthesis to meet the needs of production. This paper describes an improved method for the solid-phase synthesis of peptides. By reacting the potassium salt, instead of the triethyl ammonium salt, of the N-protected amino acid with the chloromethylated polystyrene-divinyl benzene (2%) support, esterification was found to attain higher levels, thus obviating or minimizing the formation of a quaternary anion exchanger which might cause side reactions during the subsequent steps of synthesis. The method has been applied to the syntheses of oxytocin and vasopressin and found to be quite satisfactory. A new method was introduced for the determination of free alpha-amino groups of the peptide polymer support through the formation of a Schiff's base with salicylaldehyde.
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PMID:An improved solid-phase method for peptide synthesis--the syntheses of oxytocin and vasopressin. 116 26


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