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)

Neurohypophyseal blood flow was studied using radiolabelled microspheres in 13 dogs. Hypoxic hypoxia and carbon monoxide hypoxia with similar arterial oxygen contents (CaO2, approximately 8 vol %) were produced. Under conditions of hypoxic hypoxia, 100-200% increases in blood flow in caudate nucleus, white matter, neurohypophysis, and all other brain regions occurred. Similar blood flow responses were observed with carbon monoxide hypoxia in all brain regions except the neurohypophysis. The role of carotid and aortic chemoreceptors in mediating this blood flow response was studied in 6 additional dogs. Similar degrees of hypoxic hypoxia were produced in chemoreceptor-intact and completely denervated animals (CaO2 approximately 8 vol %, PaO2 approximately 33 mm Hg). Hypoxic hypoxia produced a 250% increase in neurohypophyseal blood flow and a concurrent rise in plasma arginine vasopressin from 8 +/- 3 to 52 +/- 8 pg/ml. Chemoreceptor denervation completely inhibited the increase in neurohypophyseal blood flow associated with hypoxic hypoxia. Arginine vasopressin was not increased by hypoxic hypoxia under conditions of complete denervation. A unique role for peripheral chemoreceptors in regulating neurohypophyseal blood flow is postulated.
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PMID:Influence of chemoreceptors on neurohypophyseal blood flow during hypoxic hypoxia. 366 88

We evaluated the effects of common vasoactive agents on collateral blood flow to an ischemic segment of small intestine and on the hemodynamic determinants of that flow. Two adjacent canine jejunal segments were isolated together, and the artery to each was cannulated for autoperfusion from a femoral and a carotid artery, respectively. Arterial pressure, arterial blood flow into, and venous outflow from each segment was measured separately. Venous pressure was zero. Vascular resistances were calculated. After clamping the arterial circuit to one segment, designated "ischemic," its steady-state venous outflow was taken as the collateral blood flow from the nonischemic into the ischemic segment. Without drugs, collateral blood flow was equal to 29 +/- 4 ml/min X 100 gm or, 56% +/- 8% of normal, well above the level needed to sustain oxygen consumption and thereby prevent ischemic injury. Local intra-arterial infusion of the vasodilators isoproterenol and papaverine not only failed to increase collateral flow but actually caused a small but (with isoproterenol) significant reduction, caused by vasodilation in the nonischemic bed, and a resulting drop in arterial pressure distal to the occlusion in the ischemic segment (i.e., a steal phenomenon). The vasoconstrictors levarterenol and vasopressin also reduced collateral flow but by direct and preferential vasoconstriction of the dilated ischemic bed. These findings suggest that collateral blood flow may be optimal without drugs and is decreased only by vasoactive agents, including vasodilators. This contradicts the rationale for vasodilator therapy for the direct augmentation of collateral blood flow in acute occlusive intestinal ischemia.
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PMID:Collateral blood flow in segmental intestinal ischemia: effects of vasoactive agents. 373 47

Experiments were designed to separate effects of myocardial oxygen tension and oxygen consumption on coronary autoregulation. The approach was to measure coronary hemodynamic and metabolic responses to decreases in perfusion pressure during interventions that altered the balance between myocardial oxygen supply and demand. Studies were conducted in anesthetized heart-blocked dogs with the left coronary artery perfused from a pressure-controlled blood reservoir. Decreasing oxygen consumption by lowering heart rate from 120 to 40 bpm increased coronary venous oxygen tension and reduced the degree of flow autoregulation between 120 and 80 mm Hg by threefold. In contrast to effects of bradycardia, coronary constriction with vasopressin or indomethacin (heart rate 120 bpm), which produced comparable increases in baseline vascular resistance, decreased coronary venous oxygen tension, and augmented flow autoregulation by nearly twofold. Initial coronary venous oxygen tension but not oxygen consumption was strongly correlated with a quantitative index of autoregulation (-0.052 PO2 + 2.01, R2 = 0.86) over the pressure range of 120 to 80 mm Hg. When heart rate was lowered to 40 bpm and coronary venous oxygen tension subsequently reduced with vasopressin to control values (120 bpm), autoregulation was completely restored. Parallel studies examined the effects of metabolic and pharmacologic interventions on coronary pressure-flow relations over a wide range of pressures. For each 20 mm Hg decrement in pressure between 160 and 80 mm Hg, lowering heart rate attenuated autoregulation whereas pharmacologic coronary constriction augmented autoregulation. The observed variations in the autoregulation index were largely explained by differences in the prevailing venous oxygen tension. Furthermore, the upper pressure limit for autoregulation was dependent on venous oxygen tension with a threshold oxygen tension for autoregulation of 32 mm Hg. These results indicate that coronary autoregulation is closely coupled to the prevailing venous oxygen tension but not oxygen consumption and is facilitated at low venous oxygen tension.
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PMID:Myocardial oxygen tension determines the degree and pressure range of coronary autoregulation. 374 44

We have synthesized three oxytocin analogs containing an oxygen atom in the amino acid side chain in position 3 to determine the influences of increased side chain length and of hydrophilicity on the potencies and specificities of the resulting analogs. These three analogs: [3-O-methylhomoserine] oxytocin, [3-O-ethylserine] oxytocin, and [3-O-methylthreonine] oxytocin - have the following activities in U/mg: 490, 208, 265, milk ejection; 125, 129, 63, uterus in vivo; 0.2, 16, 0.03, antidiuretic; and 0.1, 0.5, 0.1, pressor. The results show that a longer side chain, [3-O-methylhomoserine] and [3-O-ethylserine] vs. [3-O-methylthreonine], tends to increase all activities. Moving the hydrophilic oxygen farther away from the peptide backbone, on the other hand, decreases vasopressin-like activities but increases or has no effect on oxytocin-like activities.
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PMID:Oxytocin analogs with oxygen-containing side chains in position 3. 375 39

Plasma fluid, electrolyte, protein, renin, and vasoactive hormone (epinephrine, norepinephrine, vasopressin) responses were measured in six women (21-23 yr) and four men (21-38 yr) before and immediately following an orthostatic tolerance test (70 degrees head-up tilt) and a +Gz (head-to-foot) acceleration tolerance test (0.5 G X min-1 linear ramp to grayout). These tests were conducted before and after 12 consecutive days of exercise-heat acclimation when the subjects exercised on a cycle ergometer at a relative oxygen uptake of 44% to 49% peak oxygen uptake in a hot environment (Ta = 40 degrees C, 42% rh). During acclimation plasma volume increased by 10.6% (p less than 0.05) in the women and by 11.9% (p less than 0.05) in the men; in both groups exercise heart rate decreased significantly. After acclimation, acceleration tolerance was unchanged in both groups (range 3.1 to 3.4 G); the women's tilt tolerance was unchanged (range 33.6 to 39.5 min), but the men's tilt tolerance increased from 30.4 min before to 58.3 min (delta = 91%, p less than 0.05) after acclimation. Since the pattern of fluid, electrolyte, and protein shifts and acceleration tolerances in the women and men were virtually the same, the hormone responses were highly variable, and the men's tilt tolerance increased significantly after acclimation, it is clear that responses to tilting cannot be used to predict responses to acceleration. Analysis of data from the present study and the literature suggests that current exercise training regimes should be unrestricted for astronauts who have not previously been highly endurance trained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of exercise-heat acclimation on fluid, electrolyte, and endocrine responses during tilt and +Gz acceleration in women and men. 402 52

1. Amiloride reduces short-circuit current and potential difference across the isolated frog skin.2. Isotopically measured sodium influx and efflux are diminished.3. Total electrical conductance and partial sodium conductance are diminished, the reduction in total conductance being entirely accounted for by the reduction in partial sodium conductance.4. The effect of antidiuretic hormone (ADH), cyclic 3'5'-adenosine monophosphate (cyclic AMP) and theophylline can be antagonized by pretreatment with amiloride but the antagonism can be abolished by increasing the concentration of these compounds.5. Amiloride has no effect on oxygen consumption in concentrations which inhibit sodium transport. However, it prevents the stimulatory effect of ADH on oxygen consumption.6. The results are consistent with an action of amiloride at the passive outside membrane of the transporting cells of isolated frog skin.
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PMID:Effects of amiloride on active sodium transport by the isolated frog skin: evidence concerning site of action. 431 93

1. The effect of val(5)-angiotensin II amide, noradrenaline and vasopressin, on kidney volume and intrarenal distribution of carbon particles and thioflavine S was examined in the rat.2. Angiotensin produced a dose-dependent shrinkage of the kidney coinciding with the rise in systemic blood pressure. Noradrenaline and vasopressin, however, produced reduction in kidney volume only in much higher doses than were necessary to produce a pressor effect.3. An intravenous infusion of angiotensin sufficient to produce a diuretic response resulted in a striking increase in glomerular content of injected carbon particles, and a marked reduction in filling of the capillary plexuses of the subcortex and outer medulla. The reduction in outer medullary filling was also observed using the thioflavine S technique.4. Noradrenaline infused in amounts sufficient to produce diuresis, aortic constriction above the kidney and vasopressin injection produced no measurable change in carbon particle distribution.5. The reduction in capillary blood flow produced by angiotensin may result in impaired tubular reabsorptive capacity by reducing peritubular removal of reabsorbate, or by reducing oxygen availability. Thus the vasoconstrictor effects of angiotensin may explain its diuretic action.
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PMID:The effect of angiotensin, noradrenaline and vasopressin on blood flow distribution in the rat kidney. 433 28

1. The sodium-dependent oxygen consumption of pieces of toad bladder (Bufo marinus) has been investigated using an oxygen electrode.2. The effect of polyvalent cations (Ca(2+), Sr(2+), Mg(2+), Eu(3+), La(3+) and Mn(2+)) on sodium-dependent oxygen consumption has been measured. All cations inhibited oxygen consumption, the order of effectiveness being Ca(2+) > Sr(2+) > Mg(2+) > Mn(2+) > Eu(3+) > La(3+).3. Treatment of bladder pieces with antidiuretic hormone (50 m-u./ml.) decreased the effectiveness of Ca(2+) and Sr(2+) as inhibitors of sodium-dependent oxygen consumption. Mn(2+), Eu(2+) and La(2+) were more effective after hormonal treatment, while the effectiveness of Mg(2+) was unaltered.4. The results have been interpreted in terms of a model in which sodium entry to the transporting mechanisms of the epithelium is controlled by Ca(2+), and in which antidiuretic hormone alters Ca(2+) binding and so affects sodium transport.
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PMID:The effect of metal ions and antidiuretic hormone on oxygen consumption in toad bladder. 500 82

Purified staphylococcal alpha toxin was found to inhibit the active transport of sodium across the isolated toad bladder when applied to the serosal but not to mucosal surface. Heating or the addition of specific antitoxin abolished this effect. Low temperatures reduced this activity significantly. Application of vasopressin to the bladder serosa shortly after toxin resulted in only weak and transient stimulation of sodium transport; once maximal toxin activity had been established, exposure to the hormone was without effect. Transport in bladders previously stimulated by vasopressin was rapidly inhibited by alpha toxin. Concentrations that suppressed active sodium transport completely within 30-45 min produced a significant increase in oxygen consumption by minced bladder tissue within the same period; antitoxin neutralized this activity. 2,4-dinitrophenol also inhibited sodium transport and stimulated oxygen consumption by the toad bladder. The addition of 2,4 dinitrophenol to bladder tissue in which respiration was maximally stimulated by alpha toxin resulted in a further increase in respiratory rate. The addition of toxin to bladder tissue after its exposure to a concentration of 2,4 dinitrophenol known to uncouple oxidative phosphorylation produced a significant stabilization but no increment in respiratory rate. The data are consistent with the previously suggested action of staphylococcal alpha toxin on cell membranes and suggest that energy-dependent transport processes are inhibited. The stimulation of oxygen consumption may be due to an additional effect on oxidative phosphorylation.
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PMID:Effect of purified staphylococal alpha toxin on active sodium transport and aerobic respiration in the isolated toad bladder. 565 91

Previous reports have indicated that calcium is necessary to support active sodium transport by the toad bladder, and may be required as well in the action of vasopressin on both toad bladder and frog skin. The structure and function of the toad bladder has been studied in the absence of calcium, and a reinterpretation of the previous findings now appears possible. When calcium is withdrawn from the bathing medium, epithelial cells detach from one another and eventually from their supporting tissue. The short-circuit current (the conventional means of determining active sodium transport) falls to zero, and vasopressin fails to exert its usual effect on short-circuit current and water permeability. However, employing an indirect method for the estimation of sodium transport (oxygen consumption), it is possible to show that vasopressin exerts its usual effect on Q(oo2) when sodium is present in the bathing medium. Hence, it appears that the epithelial cells maintain active sodium transport when calcium is rigorously excluded from the bathing medium, and continue to respond to vasopressin. The failure of conventional techniques to show this can be attributed to the structural alterations in the epithelial layer in the absence of calcium. These findings may provide a model for the physiologic action of calcium in epithelia such as the renal tubule.
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PMID:The effect of calcium withdrawal on the structure and function of the toad bladder. 584 Jul 97


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