SEARCH · PubMed Health

Results for “VASOPRESSIN”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources

PubMed1991

Effect of vasopressin on myocardial capillary recruitment and coronary blood flow in the anesthetized rabbit.

The effects of infusion of arginine vasopressin (20 mU.kg-1.min-1) on coronary blood flow and the proportion of the coronary microvasculature perfused was studied in rabbit myocardium. Fluorescein isothiocyanate--dextran was injected into anesthetized open-chest rabbits to identify the perfused vessels and an alkaline phosphatase stain was employed to locate the total microvasculature. Coronary blood flow (radioactive microspheres) was studied in separate groups of rabbits. Vasopressin infusion caused bradycardia (243 +/- 19 to 165 +/- 22 beats/min, mean +/- SD) and an increase in mean blood pressure (92 +/- 18 to 104 +/- 12 mmHg) (1 mmHg = 133.32 Pa). Coronary blood flow decreased significantly with vasopressin from 209 +/- 68 to 97 +/- 36 mL.min-1.100 g-1. The proportion of the arteriolar bed per millimeter squared perfused decreased significantly after vasopressin from 54 +/- 13 to 44 +/- 21%, while the percentage of capillaries per millimeter squared increased significantly from 57 +/- 6 to 67 +/- 11%. There were no subepicardial versus subendocardial differences in any measured parameter. Thus, both coronary blood flow and the proportion of the arteriolar bed perfused decreased with vasopressin. However, compensation occurred in that the proportion of capillaries perfused increased. This indicated an independent level of control of the coronary arteriolar and capillary beds. These microvascular changes may help to maintain oxygen supply-demand balance with vasopressin in the heart.

Alkaline Phosphatase↗

PubMed1998

Posterior lobe of the pituitary gland: correlation between signal intensity on T1-weighted MR images and vasopressin concentration.

PURPOSE: To correlate the signal intensity on magnetic resonance (MR) images in the posterior lobe of the pituitary gland with the vasopressin content. MATERIALS AND METHODS: Fourteen rabbits were studied: 12 water-deprived rabbits (two each at 48, 74, 96, 120, 144, or 168 hours of deprivation) and two control rabbits. Sagittal T1-weighted MR images were obtained before and after water deprivation. The signal intensity ratio of the posterior lobe to the pons was correlated with the vasopressin content in the posterior lobe, which was measured by means of radioimmunoassay. RESULTS: Before water deprivation, high signal intensity in the posterior lobe was demonstrated clearly in all rabbits. The signal intensity ratio and vasopressin content in the posterior lobe gradually decreased with water deprivation. The signal intensity ratio correlated strongly with the vasopressin content in the posterior lobe (Pearson correlation coefficient, .809; P < .001). CONCLUSION: The signal intensity ratio on T1-weighted MR images may be used as an indicator for the quantitative evaluation of the vasopressin content in the posterior lobe. The results strongly suggest that the origin of the high signal intensity in the posterior lobe on T1-weighted MR images is the vasopressin-neurophysin II-copeptin complex.

Animals↗

PubMed1987

Vasopressin-induced changes in the three-dimensional structure of toad bladder apical surface.

The apical plasma membrane of toad bladder granular cells undergoes a rapid and dramatic increase in water permeability in response to vasopressin stimulation. Previous studies have shown that this permeability increase is accompanied by characteristic changes in the morphology of this membrane and that these changes may be involved in the hormonal response. In this report, we have used the technique of rapid freezing and freeze drying to obtain high resolution stereo images of the surface of the granular cell apical plasma membrane before and during vasopressin stimulation. Using this approach, we confirmed that vasopressin induces a ridge-to-villus transformation of the cell surface even in the absence of osmotic water flow, but now show that this transformation occurs at least in part via a retraction of segments of preexisting ridges, rather than by the growth of new microvilli from the apical cell surface. This is also demonstrated by the finding that vasopressin induces the ridge-to-villus transformation of the cell surface even in the presence of cytochalasin D. In addition, the rapid-freeze, freeze-dry technique reveals that the surface glycocalyx of the epithelial cells consists of a complex, three-dimensional network of filaments that is heterogeneous among different cells. Finally, vasopressin-induced tubular invaginations of the apical plasma membrane were visualized in stereomicrographs, and the number and size of such invaginations were altered in the presence of cytochalasin D. These may represent surface images of vasopressin-induced exo- and endocytotic events that are related to membrane permeability changes.

Animals↗

PubMed2000

Aquaporin 2 is a vasopressin-independent, constitutive apical membrane protein in rat vas deferens.

Aquaporin 2 (AQP2), the vasopressin-regulated water channel, was originally identified in renal collecting duct principal cells. However, our recent description of AQP2 in the vas deferens indicated that this water channel may have extra-renal functions, possibly related to sperm concentration in the male reproductive tract. In this study, we have examined the regulation and membrane insertion pathway of AQP2 in the vas deferens. The amino acid sequence of vas deferens AQP2 showed 100% identity to the renal protein. AQP2 was highly expressed in the distal portion (ampulla) of the vas deferens, but not in the proximal portion nearest the epididymis. It was concentrated on the apical plasma membrane of vas deferens principal cells, and very little was detected on intracellular vesicles. Protein expression levels and cellular localization patterns were similar in normal rats and vasopressin-deficient Brattleboro homozygous rats, and were not changed after 36 h of dehydration, or after 3 days of vasopressin infusion into Brattleboro rats. AQP2 was not found in apical endosomes (labeled with Texas Red-dextran) in vas deferens principal cells, indicating that it is not rapidly recycling in this tissue. Finally, vasopressin receptors were not detectable on vas deferens epithelial cell membranes using a [(3)H]vasopressin binding assay. These data indicate that AQP2 is a constitutive apical membrane protein in the vas deferens, and that it is not vasopressin-regulated in this tissue. Thus AQP2 contains targeting information that can be interpreted in a cell-type-specific fashion in vivo.

Animals↗

PubMed1983

Osmoregulation of thirst and vasopressin secretion in human subjects: effect of various solutes.

Various hypertonic solutions were infused in healthy human volunteers to determine their effect on thirst and vasopressin secretion. Hypertonic saline and mannitol produced prompt and parallel increases in plasma osmolality and vasopressin concentration. For both of these solutes, there was a high degree of correlation between these measurements. The slope describing this relationship varied considerably between individuals, but the same subjects showed similar slopes with either saline or mannitol. Both solutions stimulated thirst. Hypertonic urea infusions produced a comparable rise in osmolality but produced a smaller increase in plasma vasopressin and stimulated thirst in only one of the subjects. With urea, the correlation between plasma osmolality and vasopressin was significantly lower. Within individuals, the slope describing this relationship was significantly correlated with that seen during hypertonic saline. Hypertonic glucose significantly increased plasma osmolality but decreased plasma vasopressin and had no detectable effect on thirst. We conclude that osmoregulation of vasopressin in humans is mediated by a selective osmoreceptor that is located primarily outside of the blood-brain barrier and that individual differences in osmoregulatory sensitivity are not solute specific.

Adult↗

PubMed2000

Dehydration-induced vasopressin secretion in humans: involvement of the histaminergic system.

In rats, the hypothalamic neurotransmitter histamine participates in regulation of vasopressin secretion and seems to be of physiological importance, because blockade of the histaminergic system reduces dehydration-induced vasopressin secretion. We investigated whether histamine is also involved in regulation of vasopressin secretion during dehydration in humans. We found that 40 h of dehydration gradually increased plasma osmolality by 10 mosmol/kg and induced a fourfold increase in vasopressin levels. Pretreatment with the H(2)-receptor antagonists cimetidine or ranitidine significantly reduced the dehydration-induced increase in vasopressin levels approximately 40% after 34 and 37 h of dehydration, whereas this was not the case with the H(1)-receptor antagonist mepyramine. Dehydration reduced aldosterone secretion by approximately 50%. This effect of dehydration was reduced by both H(1)- and H(2)-receptor blockade after 16 and/or 34 h of dehydration. We conclude that vasopressin secretion in response to dehydration in humans is under the regulatory influence of histamine and that the effect seems to be mediated via H(2)-receptors. In addition, the regulation of aldosterone secretion during dehydration also seems to involve the histaminergic system via H(1) and H(2) receptors.

Adult↗

PubMed1980

Hepatic artery response to vasopressin.

As vasopressin began to be used widely to control gastrointestinal hemorrhage, there was concern over the effect of vasopressin on the hepatic circulation. Although an initial vasoconstrictor effect of the drug has been described on the hepatic artery, a secondary increase in blood flow ensues. This increase has been attributed to the accompanying decrease in portal blood flow produced by vasopressin. The present study was done to investigate the mechanism of the response of hepatic artery to vasopressin in dogs. Anesthetized dogs were studied with flow probes placed on hepatic, superior mesenteric, femoral, and renal arteries, and the animals were prepared so that portal blood was diverted into jugular vein, with portal inflow to liver delivered at varying rates with blood pumped from a femoral artery. Vasopressin (0.5-1.0 U/kg) was administered intravenously. Results in dog indicate the biphasic response of hepatic artery blood flow to vasopressin is not dependent on changes in portal blood flow. Rather, it appears to be a characteristic response of this vessel. The biphasic response was not observed in other vascular beds studied and was not modified by atropine. beta-Adrenergic blockade enhanced the vasoconstrictor portion of the response, but this did not significantly alter the secondary blood flow increase.

Animals↗

PubMed2004

Differing effects of epinephrine, norepinephrine, and vasopressin on survival in a canine model of septic shock.

During sepsis, limited data on the survival effects of vasopressors are available to guide therapy. Therefore, we compared the effects of three vasopressors on survival in a canine septic shock model. Seventy-eight awake dogs infected with differing doses of intraperitoneal Escherichia coli to produce increasing mortality were randomized to receive epinephrine (0.2, 0.8, or 2.0 microg.kg(-1).min(-1)), norepinephrine (0.2, 1.0, or 2.0 microg.kg(-1).min(-1)), vasopressin (0.01 or 0.04 U/min), or placebo in addition to antibiotics and fluids. Serial hemodynamic and biochemical variables were measured. Increasing doses of bacteria caused progressively greater decreases in survival (P <0.06), mean arterial pressure (MAP) (P <0.05), cardiac index (CI) (P <0.02), and ejection fraction (EF) (P=0.02). The effects of epinephrine on survival were significantly different from those of norepinephrine and vasopressin (P=0.03). Epinephrine had a harmful effect on survival that was significantly related to drug dose (P=0.02) but not bacterial dose. Norepinephrine and vasopressin had beneficial effects on survival that were similar at all drug and bacteria doses. Compared with concurrent infected controls, epinephrine caused greater decreases in CI, EF, and pH, and greater increases in systemic vascular resistance and serum creatinine than norepinephrine and vasopressin. These epinephrine-induced changes were significantly related to the dose of epinephrine administered. In this study, the effects of vasopressors were independent of severity of infection but dependent on the type and dose of vasopressor used. Epinephrine adversely affected organ function, systemic perfusion, and survival compared with norepinephrine and vasopressin. In the ranges studied, norepinephrine and vasopressin have more favorable risk-benefit profiles than epinephrine during sepsis.

Animals↗

PubMed1983

Blood pressure maintenance in awake dehydrated rats: renin, vasopressin, and sympathetic activity.

The role of vasopressin, the renin system, and sympathetic activity in sustaining blood pressure in the dehydrated state was investigated in normotensive nonanesthetized male Wistar rats. After 48-h dehydration, plasma arginine vasopressin was 14.0 +/- 1.7 pg/ml and plasma norepinephrine 0.46 +/- 0.05 ng/ml. In another group of rats in which the angiotensin converting enzyme inhibitor (MK 421, 5 mg po twice daily) was administered throughout the dehydration period, blood pressure was reduced by more than 20% (P less than 0.001), and both plasma arginine vasopressin and norepinephrine were higher at 23.4 +/- 3.9 pg/ml (P less than 0.01) and 0.83 +/- 0.07 ng/ml (P less than 0.01), respectively. Taken together, in rats with or without converting enzyme blockade, there was an inverse correlation between mean blood pressure and plasma arginine vasopressin (r = 0.67, P less than 0.01) as well as plasma norepinephrine (r = 0.82, P less than 0.01) levels. The acute administration of a specific vasopressin pressor inhibitor (dPVDAVP) reduced mean blood pressure in the rats with a blocked renin system by 16.9 mmHg (P less than 0.001). In rats without converting enzyme inhibition, the induced fall was only 6.4 mmHg. These results indicate that following 48-h dehydration the renin angiotensin system interacts with the vasopressin secretory mechanism to sustain blood pressure, with renin playing a predominant role. They further suggest that, following blockade of the renin system, activation of the sympathetic nervous system probably also contributes to blood pressure maintenance.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1989

Absent effect of plasma vasopressin on rat brain blood flow during hemorrhage.

We investigated whether a reflex increase in plasma vasopressin level due to hemorrhagic hypotension affects brain blood flow. In 60 lightly anesthetized, artificially ventilated rats, the flow was determined with radiolabeled microspheres. We found excellent maintenance of blood flow throughout all brain regions during the hypotensive state (71 mmHg on average), and such maintenance of flow was not modulated at all by a supramaximal intravenous dose of the selective vasopressin V1-receptor antagonist [d(CH2)5 Tyr-(Me)]AVP. The latter finding also implies that the V1 antagonist failed to unmask the vasodilator type actions of V2 receptors on the maintenance of flow during hemorrhagic hypotension. These were true also when the cervical sympathetic bundles were severed bilaterally. The plasma level of endogenous vasopressin was increased during hypotension, ranging from 118 to 973 pg/ml. Despite this increase, the brain blood flow was entirely independent of the plasma vasopressin level in all the brain regions studied. We conclude that the brain circulation of rats can maintain its blood flow during hemorrhagic hypotension without any apparent contribution from a concomitant reflex increase in plasma vasopressin. Despite our negative results for the brain blood flow, the possible segmental effects of circulating vasopressin on the brain arterial caliber remain to be clarified under conditions of hemorrhagic hypotension.

Animals↗

PubMed1990

Role of endocardial endothelium in positive inotropic action of vasopressin.

We have studied the effects of vasopressin on isolated cat papillary muscle both before and after damaging the endocardium. The experiments were performed in physiological conditions of temperature (35 degrees C) and calcium concentration (1.25 mM Ca2+). Isometric and isotonic twitches as well as maximal unloaded velocity of shortening (Vmax) were measured. In muscles with an intact endocardium (n = 13), vasopressin (10(-12) to 10(-6) M) induced early twitch relaxation with a significant reduction of time to half isometric tension decline and with concomitant significant decrease in peak twitch performance. In a second group of muscles (n = 13) the endocardial endothelial surface was damaged by briefly (1 s) exposing the muscles to a 0.5% Triton X-100 followed by abundant wash with Krebs-Ringer solution, thereby irreversibly decreasing time to half twitch relaxation and peak twitch tension without significantly affecting Vmax. After this intervention, vasopressin had a positive inotropic effect with a significant increase in peak twitch tension and Vmax with no significant changes in twitch duration. Accordingly, in the presence of a functional endocardium, the direct myocardial positive inotropic effect of vasopressin was reversed, with early twitch relaxation and diminished peak twitch performance. At the highest concentrations of vasopressin, vasopressin-induced functional and morphological damage of the endocardium was observed.

Animals↗

PubMed1992

Baroreflex modulation of sympathetic outflow during physiological increases of vasopressin in humans.

Two studies were carried out to determine whether vasopressin influences the baroreceptor reflex of humans. In protocol 1, eight healthy subjects received sequential infusions of nitroprusside and phenylephrine to alter baroreceptor input. Muscle sympathetic nerve activity (SNA) was recorded to assess baroreceptor reflex modulation of efferent vasoconstrictor drive. Baroreceptor sensitivity (slopes) of the relationship between systolic pressure and R-R interval (cardiac baroslopes) and slopes relating muscle SNA to diastolic pressure were not altered during subpressor infusions of vasopressin, which raised basal plasma levels to 19 +/- 6 and 26 +/- 6 (mean +/- SE) pg/ml. A second protocol (n = 10 subjects) compared the reflex inhibition of SNA and heart rate produced by incremental pressor doses of phenylephrine and vasopressin. The calculated cardiac and sympathetic baroreflex gains did not differ between pressor agents. However, immediately following the peak dose of vasopressin (which elevated plasma levels to 35 +/- 3.6 pg/ml), reflex sympathoexcitation produced by unloading baroreceptors (with a bolus of nitroprusside) was significantly enhanced compared with an identical stress initiated at peak phenylephrine infusion. Thus increased levels of vasopressin ranging from 19 to 26 pg/ml did not alter cardiac or sympathetic baroreflex responses in humans. Higher levels of vasopressin may enhance the sympathetic response to unloading of baroreceptors.

Adult↗

PubMed1992

Effect of protein kinase C inhibitors on endothelin- and vasopressin-induced constriction of the rat basilar artery.

The goal of this study was to determine whether inhibitors of protein kinase C (PKC) attenuate constrictor responses of the basilar artery in vivo to endothelin and arginine vasopressin. In anesthetized rats, the diameter of basilar arteries was measured through a cranial window [control diameter 218 +/- 3 (SE) microns]. Vessel diameter was measured during topical application of agonists and antagonists. Sphingosine (10(-6) M), a PKC inhibitor that binds to the regulatory site of PKC, attenuated vasoconstriction in response to endothelin (10(-9), 10(-8), and 10(-7) M) and vasopressin (10(-9) and 10(-8) M). H-7 (10(-9) M), a PKC inhibitor that binds to the catalytic site of PKC, also inhibited vasoconstriction in response to endothelin and vasopressin. Sphingosine and H-7 did not affect baseline diameter and did not attenuate vasoconstriction in response to prostaglandin (PG) F2 alpha. The V1 antagonist [d(CH2)5Tyr(Me)]arginine vasopressin (10(-8) M) significantly inhibited constriction in response to vasopressin (10(-9) and 10(-8) M) but not PGF2 alpha (10(-6) M). These observations suggest that activation of PKC may contribute to endothelin-induced constriction of the basilar artery in vivo and that PKC may also be a mediator of V1-receptor-mediated constriction of the basilar artery in response to vasopressin.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1993

Endothelium, vasopressin receptors, and resistance to DOCA-salt hypertension.

Mesenteric artery rings from Wistar and Wistar-Furth rats subcutaneously treated with deoxycorticosterone acetate (DOCA) and 1% NaCl drinking water were used to measure endothelial modulation of contractile sensitivity and vasopressin receptor function and affinity. DOCA-salt hypertension reduced contractile sensitivity to arginine vasopressin (AVP) and did not affect contractile sensitivity to norepinephrine in arteries from Wistar rats. Endothelial removal caused a threefold increase in contractile sensitivity to AVP and norepinephrine in DOCA-salt hypertensive Wistar rats. In Wistar-Furth rats, DOCA-salt treatment did not affect contractile sensitivity to AVP, lysine vasopressin, oxytocin, and norepinephrine or the affinity of the vasopressin receptor for agonists or antagonists. Removal of endothelium did not affect vasopressin contractile sensitivity but caused a 15-fold increase in contractile sensitivity to norepinephrine in untreated or DOCA-salt-treated Wistar-Furth rats. These data show that reduced vasopressin receptor function and increased endothelial function that compensate for increased contractile sensitivity in arteries from DOCA-salt hypertensive Wistar rats are not the cause of resistance of DOCA-salt-treated Wistar-Furth rats to the development of enhanced contractile sensitivity and hypertension.

Animals↗

PubMed1994

Renal function contributes to antihypertensive effect of vasopressin in DOCA-salt but not spontaneous hypertension.

The contribution of sodium losses to the dramatic fall in blood pressure that follows cessation of a 3-h intravenous infusion of vasopressin (20 ng.kg-1.min-1) in hypertensive rats was investigated. Cessation of the vasopressin infusion was associated with a large fall in pressure below preinfusion basal levels (30-50 mmHg) in both spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt-hypertensive rats. In contrast, pressure returned to control levels in normotensive rats. Sodium excretion rates increased markedly during the infusions of vasopressin in both SHR and DOCA-salt-hypertensive rats but also in their appropriate normotensive controls. An equinatriuretic dose of furosemide failed to induce any change in pressure in SHR or normotensive controls. In contrast, furosemide decreased pressure in the DOCA-salt-hypertensive group, although the decrease was not as large as with vasopressin. Replacement of the sodium losses that occurred during the vasopressin infusion failed to return pressure toward control levels in SHR but did increase pressure in the DOCA-salt-hypertensive group. The results indicate a major difference between the SHR and DOCA-salt-hypertensive models. In SHR, sodium losses do not contribute to the antihypertensive effect of vasopressin, but in contrast these losses do contribute significantly to this antihypertensive effect in the DOCA-salt-hypertensive model.

Animals↗

PubMed2001

Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension.

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

Angiotensin II↗

PubMed1975

Effect of infusion of pharmacologic amounts of vasopressin on renal electrolyte excretion.

Aqueous vasopressin was infused to bicarbonate- and glucose-loaded dogs and to nonloaded antidiuretic dogs in doses of 50 mU/kg per min or 50 mU/kg per h. Both doses caused a marked increase in sodium, chloride, and water excretion. The larger dose raised the fractional excretion (sodium clearance (C-Na)/glomerular filtration rate (GFR) times 100) of these ions from 2% or less to in excess of 20%. Blocking the pressor effects of these doses of vasopressin with sodium nitroprusside did not alter the marked natriuretic and chloriuretic effect. The maximal rate of bicarbonate and glucose reabsorption was not depressed by vasopressin infusion; fractional phosphate excretion, however, was markedly increased. Inhibiting distal hydrogen ion secretion by inducing selective aldosterone deficiency failed to uncover a vasopressin-induced inhibition of proximal bicarbonate reabsorption that might have been masked by increased distal bicarbonate reabsorption. There was no significant change in GFR, renal plasma flow, or filtration fraction. The distribution of cortical renal blood flow (measured by the radioactive microsphere technique) shifted toward the inner cortex after vasopressin administration. Vasopressin, in pharmacologic doses, is a potent diuretic that most likely exerts this effect by directly inhibiting sodium reabsorption at a point in the nephron distal to the proximal tubule.

Adrenalectomy↗

PubMed1976

Influence of vasopressin and amiloride on shunt pathways of frog skin.

Studies were done to determine the influence of vasopressin and amiloride on the sodium backflux of nonedge-damaged frog skin. As before, the bidirectional fluxes of sodium appeared to be limited primarily to the active transport pathways of control skins. When the skins were treated with vasopressin, the sodium backflux was increased selectively (over that of sucrose) and more so than was expected for the active transportpathway alone. In control skins, amiloride had no effect on the flux of the shunt pathway. However, with vasopressin-treated skins, amiloride at 10(-6) M decreased the sodium backflux of the shunt pathway to levels observed previously for the control skins. These observations are compatible with the idea that the shunt pathway may in part be cellular and in part extracellular. When the changes in open-circuit voltage and shunt resistance caused by vasopressin and amiloride (as determined from the I-V relationships) were examined, the data were also found to be compatible with the idea that vasopressin exerted an influence on the shunt pathway of the frog skin, and this effect of vasopressin could be reversed by amiloride.

Amiloride↗