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PubMed2003

Serotonin receptors involved in vasopressin and oxytocin secretion.

Serotonin (5-HT), 5-HT agonists, the 5-HT precursor 5-hydroxytryptophan, 5-HT-releasers and -reuptake inhibitors stimulate the release of vasopressin and oxytocin. We investigated the involvement of 5-HT receptors in the serotonergic regulation of vasopressin and oxytocin secretion. Vasopressin and oxytocin secretion was stimulated by 5-HT, the 5-HT(1A+1B+5A+7) agonist 5-carboxamidotryptamine (5-CT), the 5-HT(2A+2C) agonist DOI, the 5-HT(2C+2A) agonist mCPP, the 5-HT(2C) agonist MK-212, the 5-HT(3) agonist SR 57277 and the 5-HT(4) agonist RS 67506. The 5-HT(1A) agonist 8-OH-DPAT, which had no effect on vasopressin secretion, stimulated oxytocin secretion. The 5-HT-induced release of vasopressin and oxytocin was inhibited by central infusion of the 5-HT antagonists WAY 100635 (5-HT(1A)), LY 53857 (5-HT(2A+2C)), ICS 205-930 (5-HT(3+4)) and RS 23597 (5-HT(4)). The 5-HT2+6+7 antagonist metergoline in combination with the 5-HT1A+2+7 antagonist methysergide inhibited the stimulatory effect of 5-CT on both hormones, whereas the 5-HT1A+1B antagonist cyanopindolol only inhibited the oxytocin response. The 5-HT(2A) antagonist 4-(4-flourobenzoyl)-1-(4-phenylbutyl)-piperidine oxalate had no effect on DOI-induced hormone response. The 5-HT(2C) antagonist Y 25130 partly inhibited the stimulating effect of MK-212. ICS 205-930 and RS 23597 inhibited vasopressin and oxytocin secretion induced by RS 67506. WAY 100635 inhibited 8-OH-DPAT-induced oxytocin secretion. We conclude that 5-HT-induced vasopressin secretion primarily is mediated via 5-HT(2C), 5-HT(4) and 5-HT(7) receptors, whereas 5-HT(2A), 5-HT(3) and 5-HT(5A) receptors seem to be of minor importance. 5-HT-induced oxytocin secretion involves 5-HT(1A), 5-HT(2C) and 5-HT(4) receptors; in addition an involvement of 5-HT(1B), 5-HT(5A) and 5-HT(7) receptors seems likely, whereas 5-HT(2A) and 5-HT(3) receptors seem to be less important.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

A new nausea model in humans produces mild nausea without electrogastrogram and vasopressin changes.

UNLABELLED: The standard human vection model utilized for nausea has been an optokinetic drum. This model may be difficult to extrapolate to the usual clinical setting. Our goals were to develop an experimental model which could induce low grade nausea in humans and to determine the relationship between mild nausea and changes in the electrogastrogram and plasma vasopressin concentrations. METHODS: Twenty-one volunteers (11 males, mean age: 37 years) participated. At baseline and throughout the study the electrogastrogram was monitored, blood was drawn for vasopressin assay and symptoms of nausea, dizziness and headache were rated on a 0-10-point scale. Subjects were semireclined in a darkened room while viewing moving bars of light rotating at a rate of 85 degrees s-1. Subjects were asked to rate their proneness to motion sickness and their current level of anxiety at baseline. RESULTS: Eight subjects developed mild to moderate (mean: 3.6) nausea during vection. Symptoms of nausea were correlated with a reported history of motion sickness (r = 0.49, P < 0.05) but not with anxiety (r = 0.14, P = 0.54). Degrees of nausea correlated with degrees of dizziness (r = 0.47, P < 0.05) but not with headache (r = 0.29, P = 0.14). Subjects who developed mild nausea were not significantly more likely to exhibit altered electrogastrogram or vasopressin than subjects who did not report nausea. Vasopressin levels during baseline and experimental conditions were highly correlated (r = 0.66, P < 0.005 and r = 0.55 P < 0.005, respectively) with reported baseline anxiety. CONCLUSIONS: (1) This new model in humans induced mild nausea that was unrelated to electrogastrogram and vasopressin abnormalities, (2) high correlation between anxiety and vasopressin suggests that vasopressin may not be directly related to nausea, and (3) these data indicate that onset of nausea mediated centrally can occur without associated electrogastrogram changes.

Adult↗
PubMed1991

Elevation of plasma vasopressin in spontaneous migraine.

Vasopressin is a vasoactive hormone secreted from the posterior pituitary. At low concentration its role is in regulating renal water excretion, but at higher concentrations it has a number of extrarenal actions, including effects on blood flow. To investigate the role of vasopressin in spontaneous migraine, paired samples were collected from 14 subjects (a) during an acute attack of spontaneous migraine, and (b) when symptom-free for at least seven days. During an attack, vasopressin was consistently raised (median (range) 3.5 (1.2-9.6) pg/ml v 0.5 (0.5-1.1) pg/ml, p less than 0.001). The highest vasopressin concentration occurred in the only patient who vomited. The results suggest vasopressin rises during an attack of spontaneous migraine, and this may, in part, be related to emesis. In the majority, vasopressin levels only rose sufficiently to have some renal antidiuretic effect, although in some these levels could have been sufficient to cause alteration in peripheral blood flow. Release of vasopressin may be responsible for the facial pallor and antidiuresis observed in migraine.

Adult↗
PubMedDate not supplied

Vasopressin and oxytocin receptor mRNA expression during rat telencephalon development.

We investigated the developmental expression of vasopressin and oxytocin receptor and peptide mRNA using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Southern blot hybridization. Messenger RNAs for both vasopressin receptor subtypes V(1)a and V(2)were present in the telencephalon from embryonic day 12 to day 20. Both V(1)a and V(2)receptor mRNA increased on day 13 and then remained stable from embryonic day 13 to day 20. Messenger RNA for the vasopressin peptide was also detected in the telencephalon from day 12 to day 20, indicating that vasopressin could be synthesized within the rat cerebral cortex during rat embryonic development. Oxytocin receptor mRNA expression was also present in the telencephalon, but expression levels varied considerably from day 12 to day 20. No oxytocin mRNA expression was detected during rat telencephalon development. Temporal patterns of vasopressin receptor and vasopressin peptide mRNA expression along with oxytocin receptor mRNA suggest a temporal role for vasopressin- and oxytocin-mediated actions during rat telencephalon development.

Animals↗
PubMed1983

Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa.

Previous studies have indicated that many patients with anorexia nervosa have defects in urinary concentration or dilution suggestive of abnormal secretion of the antidiuretic hormone arginine vasopressin. To explore this possibility, we examined the response of plasma vasopressin to intravenous hypertonic saline in anorexic patients before and after correction of their weight loss. We also measured basal levels of the hormone in the cerebrospinal fluid. In all four subjects studied before correction of weight loss, the response to hypertonic saline was abnormal: in one, the plasma level of arginine vasopressin increased subnormally relative to the plasma sodium level; in the other three, it fluctuated erratically, with no relation to plasma sodium. These defects persisted in the three patients studied three to four weeks after recovery of body weight. In two patients who were initially studied when they were underweight, the defects were gone six months after recovery; in five of seven other patients studied at least six months after recovery but not while they were underweight, the response was normal. Abnormalities in the osmoregulation of plasma arginine vasopressin were not accounted for by nonosmotic stimuli and were almost always associated with an absolute increase in the level of arginine vasopressin in the cerebrospinal fluid or a reversal of the normal (less than 1.0) cerebrospinal fluid/plasma ratio of arginine vasopressin. These results indicate that most if not all patients with anorexia nervosa have abnormal levels of arginine vasopressin in their plasma and cerebrospinal fluid that are corrected very slowly with weight gain. The cause and consequences of these abnormalities remain to be determined.

Adult↗
PubMed2001

Vasopressin as an etiologic factor for infection in gynecologic surgery: a randomized double-blind placebo-controlled trial.

OBJECTIVE: The purpose of this study was to evaluate the risk of pelvic infection with the use of vasopressin at time of vaginal hysterectomy with a randomized controlled trial. STUDY DESIGN: Women who underwent vaginal hysterectomy and agreed to participate were randomly assigned to pericervical injections of vasopressin or normal saline solution. Surgeons and patients were blinded to the injected substance. Power analysis revealed that a sample size of 116 patients would be sufficient to detect a 4-fold difference in pelvic infection rates between the 2 groups, with 90% power and a probability value of.05. RESULTS: Analysis with 117 patients found no difference in infection rate between the normal saline solution group and the vasopressin groups (7.3% vs 1.6%; P =.19). Estimated blood loss (312 +/- 222 mL vs 446 +/- 296 mL; P =.006) and change in hemoglobin and hematocrit levels (2.1 +/- 1.4 gm vs 2.9 +/- 1.4 gm; P: =.02; and 6.7% +/- 3.4% vs 8.5% +/- 3.8%; P =.01; vasopressin versus normal saline solution, respectively) were significantly less in the vasopressin group. There were no significant differences in interval blood pressure measurements after vasopressin administration between the 2 groups. CONCLUSION: The use of vasopressin during vaginal hysterectomy does not increase the risk of pelvic infection, does decrease operative blood loss, and does not significantly affect blood pressure.

Adult↗
PubMed2001

Transcriptome of a mouse kidney cortical collecting duct cell line: effects of aldosterone and vasopressin.

Aldosterone and vasopressin are responsible for the final adjustment of sodium and water reabsorption in the kidney. In principal cells of the kidney cortical collecting duct (CCD), the integral response to aldosterone and the long-term functional effects of vasopressin depend on transcription. In this study, we analyzed the transcriptome of a highly differentiated mouse clonal CCD principal cell line (mpkCCD(cl4)) and the changes in the transcriptome induced by aldosterone and vasopressin. Serial analysis of gene expression (SAGE) was performed on untreated cells and on cells treated with either aldosterone or vasopressin for 4 h. The transcriptomes in these three experimental conditions were determined by sequencing 169,721 transcript tags from the corresponding SAGE libraries. Limiting the analysis to tags that occurred twice or more in the data set, 14,654 different transcripts were identified, 3,642 of which do not match known mouse sequences. Statistical comparison (at P < 0.05 level) of the three SAGE libraries revealed 34 AITs (aldosterone-induced transcripts), 29 ARTs (aldosterone-repressed transcripts), 48 VITs (vasopressin-induced transcripts) and 11 VRTs (vasopressin-repressed transcripts). A selection of the differentially-expressed, hormone-specific transcripts (5 VITs, 2 AITs and 1 ART) has been validated in the mpkCCD(cl4) cell line either by Northern blot hybridization or reverse transcription-PCR. The hepatocyte nuclear transcription factor HNF-3-alpha (VIT39), the receptor activity modifying protein RAMP3 (VIT48), and the glucocorticoid-induced leucine zipper protein (GILZ) (AIT28) are candidate proteins playing a role in physiological responses of this cell line to vasopressin and aldosterone.

Aldosterone↗
PubMed1979

Trypsin liberates an arginine vasopressin-like peptide and neurophysin from a Mr 20,000 putative common precursor.

Although the hypothesis that vasopressin and its associated neurophysin are synthesized together in one macromolecular common precursor was put forward more than a decade ago, direct conformation of this hypothesis has been lacking. A [35S]cysteine-labeled putative precursor for vasopressin-related neurophysin (Mr 20,000, pI 6.1) has been isolated from the supraoptic nuclei of rats. This precursor was subjected to limited proteolysis with trypsin which produced a Mr 10,000 protein and peptide products. The former was identified as neurophysin on the basis of its pH-dependent affinity for vasopressin and its behavior in isoelectric focusing systems (pI 4.6-4.8). The tryptic peptides proved to be vasopressin-like because they: (i) were rich in cysteine, (ii) comigrated with vasopressin on gel filtration columns in 6 M guanidine HCl, (iii) bound to a neurophysin-Sepharose affinity column at pH 5.7, and (iv) were recognized by antibodies against vasopressin. These data on the Mr 20,000, pI 6.1 protein represent direct experimental evidence for a candidate for the common precursor of vasopressin and neurophysin. We propose that this common precursor be called "propressophysin."

Animals↗
PubMed1979

Vasopressin stimulation of mouse 3T3 cell growth.

Vasopressin is shown to be a potent mitogen for Swiss 3T3 cells. The hormone (1--10 ng/ml) causes a striking shift of the dose--response curve for the effect of serum on thymidine incorporation by cultures of 3T3 cells arrested in the G1/G0 phase of the cell cycle. In the absence of added serum, the effect of vasopressin on DNA synthesis is greatly potentiated by insulin, epidermal growth factor, and a factor isolated from medium conditioned by simian virus 40-infected baby hamster kidney cells. The mitogenic effect of vasopressin is dependent on time and hormone concentration. In the presence of insulin, the half-maximal effect elicited by the peptide is obtained at 0.6 ng/ml. [Arg]Vasopressin and [Lys]vasopressin are equally potent. The vasopressins are 10(3)-fold more potent than oxytocin. In the presence of a low (2.5%) concentration of serum, vasopressins stimulate cell proliferation.

Animals↗
PubMed1986

Sensitivities of rat kidney thick ascending limbs and collecting ducts to vasopressin in vivo.

Clearance experiments were performed to characterize the sensitivity to vasopressin of the thick ascending limbs and collecting duct system of the rat kidney. The response of the thick ascending limbs was evaluated by measuring the Mg2+ excretion rate in the urine, since the [arginine-8] vasopressin-mediated effects on Mg2+ excretion are the direct result of a stimulation of Mg2+ reabsorption in this nephron segment, and the response of the collecting ducts was evaluated by changes in urine flow. To avoid the effects of parathyroid hormone, glucagon, and calcitonin, which stimulate Mg2+ reabsorption in the thick ascending limb and distal tubule, and of calcitonin, which increases the permeability of the cortical collecting ducts to water, experiments were performed on Brattleboro D. I. rats (with hereditary diabetes insipidus, due to a lack of [Arg8]vasopressin) acutely deprived of endogenous parathyroid hormone, calcitonin, and glucagon. Vasopressin infused at rates up to 5 pg/min did not reduce the Mg2+ fractional excretion rate, whereas at 5 pg/min water excretion was decreased by 50%. The half-maximal reduction of Mg2+ excretion occurred at vasopressin infusion rates 4-6 times higher than those necessary to diminish the water excretion rate to the same extent. We conclude that in vivo, two segments involved in the production of concentrated urine have different sensitivities to vasopressin and that this difference in sensitivity is very similar for the biological response in vivo and the adenylate cyclase activation in vitro. We suggest that both the magnitude and the nature of the effects of [Arg8]vasopressin on the kidney may vary according to the required antidiuretic response.

Animals↗
PubMed1988

Vasopressin modulates the spontaneous electrical activity in aortic cells (line A7r5) by acting on three different types of ionic channels.

A7r5 smooth muscle (aorta) cells have a spontaneous electrical activity. Application of vasopressin produces a hyperpolarization accompanied by an interruption of the spontaneous activity, which is followed by a depolarization associated with a recovery of the spiking activity. Vasopressin action is produced by an action of the peptide on three different types of ionic channels. Vasopressin activates a Ca2+-sensitive K+ conductance, presumably by producing inositol 1,4,5-trisphosphate intracellularly and liberating Ca2+ from internal stores. This activation is transient (0.5-4 min) and is related to the vasopressin-induced hyperpolarization. Intracellular perfusion of inositol trisphosphate triggers by itself a transient K+ current and prevents subsequent activation by vasopressin. Vasopressin inhibits an L-type Ca2+ channel through both protein kinase C activation and a [Ca2+]i-dependent inactivation mechanism triggered by inositol trisphosphate production. The addition of the activation of a Ca2+-sensitive K+ channel and of the inhibition of a voltage-sensitive Ca2+ channel is responsible for the transient blockade of the spontaneous activity. Vasopressin also provokes the activation of an inward current (2-20 min) due to a nonselective channel able to transfer Ca2+, Na+, K+, and Cs+ across the membrane. This effect of the peptide is associated with the depolarization following the hyperpolarization phase.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane.

Water excretion by the kidney is regulated by the peptide hormone vasopressin. Vasopressin increases the water permeability of the renal collecting duct cells, allowing more water to be reabsorbed from collecting duct urine to blood. Despite long-standing interest in this process, the mechanism of the water permeability increase has remained undetermined. Recently, a molecular water channel (AQP-CD) has been cloned whose expression appears to be limited to the collecting duct. Previously, we immunolocalized this water channel to the apical plasma membrane (APM) and to intracellular vesicles (IVs) of collecting duct cells. Here, we test the hypothesis that vasopressin increases cellular water permeability by inducing exocytosis of AQP-CD-laden vesicles, transferring water channels from IVs to APM. Rat collecting ducts were perfused in vitro to determine water permeability and subcellular distribution of AQP-CD in the same tubules. The collecting ducts were fixed for immunoelectron microscopy before, during, and after exposure to vasopressin. Vasopressin exposure induced increases in water permeability and the absolute labeling density of AQP-CD in the APM. In parallel, the APM:IV labeling ratio increased. Furthermore, in response to vasopressin withdrawal, AQP-CD labeling density in the APM and the APM:IV labeling ratio decreased in parallel to a measured decrease in osmotic water permeability. We conclude that vasopressin increases the water permeability of collecting duct cells by inducing a reversible translocation of AQP-CD water channels from IVs to the APM.

Animals↗
PubMed1999

Mutations in the vasopressin prohormone involved in diabetes insipidus impair endoplasmic reticulum export but not sorting.

Familial neurohypophysial diabetes insipidus is characterized by vasopressin deficiency caused by heterozygous expression of a mutated vasopressin prohormone gene. To elucidate the mechanism of this disease, we stably expressed five vasopressin prohormones with a mutation in the neurophysin moiety (NP14G-->R, NP47E-->G, NP47DeltaE, NP57G-->S, and NP65G-->V) in the neuroendocrine cell lines Neuro-2A and PC12/PC2. Metabolic labeling demonstrated that processing and secretion of all five mutants was impaired, albeit to different extents (NP65G-->V >/= NP14G-->R > NP47DeltaE >/= NP47E-->G > NP57G-->S). Persisting endoglycosidase H sensitivity revealed these defects to be due to retention of mutant prohormone in the endoplasmic reticulum. Mutant prohormones that partially passed the endoplasmic reticulum were normally targeted to the regulated secretory pathway. Surprisingly, this also included mutants with mutations in residues involved in binding of vasopressin to neurophysin, a process implicated in targeting of the prohormone. To mimick the high expression in vasopressin-producing neurons, mutant vasopressin prohormones were transiently expressed in Neuro-2A cells. Immunofluorescence displayed formation of large accumulations of mutant prohormone in the endoplasmic reticulum, accompanied by redistribution of an endoplasmic reticulum marker. Our data suggest that prolonged perturbation of the endoplasmic reticulum eventually leads to degeneration of neurons expressing mutant vasopressin prohormones, explaining the dominant nature of the disease.

Biological Transport↗
PubMed2005

Calmodulin is required for vasopressin-stimulated increase in cyclic AMP production in inner medullary collecting duct.

Calmodulin plays a critical role in regulation of renal collecting duct water permeability by vasopressin. However, specific targets for calmodulin action have not been thoroughly addressed. In the present study, we investigated whether Ca2+/calmodulin regulates adenylyl cyclase activity in the renal inner medullary collecting duct. Rat inner medullary collecting duct suspensions were incubated in the presence or absence of 0.1 nM vasopressin and the calmodulin inhibitors, monodansylcadaverine, W-7, and trifluoperazine, followed by measurement of cAMP. Vasopressin-stimulated cAMP elevation was significantly attenuated in the presence of calmodulin inhibitors. Analysis of transglutaminase 2 knock-out mice confirmed that these compounds were not acting through inhibition of transglutaminase 2 activity. Calmodulin inhibitors also blocked both cholera toxin- and forskolin-stimulated cAMP accumulation. In isolated perfused tubules, W-7 reversibly blocked vasopressin-stimulated urea permeability, a process that requires a rise in intracellular cAMP but does not appear to involve protein trafficking to the apical plasma membrane. These results suggest that calmodulin is required for vasopressin-stimulated adenylyl cyclase activity in the intact inner medullary collecting duct. Reverse transcription-PCR, immunoblotting, and immunohistochemistry revealed the presence of the calmodulin-sensitive adenylyl cyclase type 3 in the rat collecting duct, an isoform previously not known to be expressed in the collecting duct. Long-term treatment of Brattleboro rats with a vasopressin analog markedly decreased adenylyl cyclase type 3 protein abundance, providing an explanation for long-term down-regulation of vasopressin response in the collecting duct. These studies demonstrate the importance of calmodulin in the regulation of collecting duct adenylyl cyclase activity and transport function.

Adenylyl Cyclases↗
PubMed1998

Deleterious action of vasopressin in gastroduodenal ulceration: experimental and clinical observations.

Vasopressin, released from the posterior pituitary and from the vascular endothelium, can cause vasoconstriction and provoke platelet aggregation, leading to an impaired tissue blood supply. In humans with pituitary diabetes insipidus the central release of vasopressin is diminished, and in the Brattleboro homozygous rat there is congenitally no synthesis of this hormone. The gastroduodenal intramucosal vasopressin level is elevated in normal rats following various acute ulcerogenic challenges (after ethanol, reserpine, indomethacin, cold-restraint stress, endotoxin shock and hemorrhagic shock), and vasopressin-deficient rats are less sensitive to these stimuli. In a hospital- and population-based case-control, age-matched retrospective study, the incidence of human gastroduodenal ulceration is significantly higher in the normal population (in whom the release of vasopressin is presumed to be intact) than in the vasopressin-deficient one (central diabetes insipidus patients). In conclusion, endogenous vasopressin plays an aggressive role in development of gastroduodenal ulceration, especially that related to stress.

Adult↗
PubMed2006

A comparison of vasopressin and glucagon in beta-blocker induced toxicity.

OBJECTIVE: We compared the efficacy of vasopressin and glucagon in a porcine model of beta-blocker toxicity. Our primary outcome was survival over 4 hours. METHODS: Sixteen pigs received a 1-mg/ kg bolus of propranolol IV followed by continuous infusion at 0.25 mg/kg/minute. Toxicity was defined as a 25% decrease in the product of heart rate (HR) and mean arterial pressure (MAP), at which point 20 mL/kg normal saline was rapidly infused. Each pig was randomly assigned to receive either vasopressin or glucagon after the saline bolus. The vasopressin group received a continuous infusion at 0.0028 U/kg/minute, titrated up to a maximum of 0.014 U/ kg/minute. The glucagon group received a 0.05-mg/kg bolus followed by continuous infusion at 0.15 mg/kg/hour. The HR, MAP, systolic BP (SBP), cardiac output (CO), glucose, and pH were monitored for 4 hours from toxicity or until death. RESULTS: One pig survived at 4 hours (vasopressin group). Analysis of the 4-hour Kaplan-Meier survival curves found no differences between the groups (log-rank test 0.059, p = 0.81). No overall differences were identified in MAP, systolic BP, cardiac output, glucose, pH, or HR. However, over the first hour MAP and SBP were significantly higher in the vasopressin group (p = 0.004, p = 0.006, respectively). CONCLUSION: In this beta-blocker toxicity model, there were no differences in the survival curves between vasopressin- and glucagon-treated pigs during a 4-hour analysis period. No overall differences were noted in MAP, systolic BP, CO, HR, pH, or glucose levels, although vasopressin treatment yielded higher MAP and systolic BP early in resuscitation.

Adrenergic beta-Antagonists↗
PubMed2004

Comparison of the role of endothelin, vasopressin and angiotensin in arterial pressure regulation during sevoflurane anaesthesia in dogs.

BACKGROUND: In this study we aimed to clarify the role of endothelin in arterial pressure regulation during anaesthesia with increasing concentrations of sevoflurane (1-3 MAC) and compare it with those of vasopressin and angiotensin. METHODS: After an awake control period, on different days, six dogs underwent each of the following four interventions: sevoflurane anaesthesia alone (1-3 MAC), sevoflurane after block of either endothelin receptors using tezosentan (3 mg kg(-1) followed by 3 mg kg(-1) h(-1)), vasopressin V(1a) receptors using [d(CH(2))(5)Tyr(Me(2))]AVP (40 micro g kg(--1)) or angiotensin receptors using losartan (6 mg kg(-1) h(-1)). Plasma concentrations of endothelin, big endothelin, vasopressin and renin were measured. Effects of sevoflurane in the presence and absence of the respective receptor block were analysed and compared using analysis of variance for repeated measures (ANOVA followed by Fisher's PLSD (protected least significant difference) (P<0.05)). RESULTS: Mean arterial pressure decreased in a dose-dependent manner with sevoflurane during all interventions. At 1 MAC, this decrease was greatest during angiotensin receptor block (mean (SEM), -41 (3) mm Hg), intermediate during vasopressin and endothelin receptor block (-31 (4) and -30 (2) mm Hg respectively), and least during sevoflurane alone (-24 (3) mm Hg). The course of systemic vascular resistance mirrored the course of arterial pressure, while cardiac output did not differ between groups. Plasma concentrations of endothelin, big endothelin and renin did not change during any intervention, whereas vasopressin concentration increased from approximately 0.5 to 40 ng litre(-1) at 3 MAC as arterial pressure decreased in all groups. CONCLUSIONS: At 1 MAC, angiotensin attenuated the decrease in arterial pressure during sevoflurane anaesthesia more than endothelin and vasopressin. However, at higher MAC only vasopressin was specifically activated to partly compensate for the arterial pressure decrease.

Analysis of Variance↗
PubMed1985

Vasopressin-induced coronary constriction at low perfusion pressures.

We studied the effects of intracoronary vasopressin on the relationship between pressure and flow in the coronary circulation of anaesthetised swine. In addition to measurements at control levels, diastolic pressure-flow relationships were constructed from steady-state points below a coronary pressure of 50 mmHg, where endogenous vasodilatation is strongly stimulated. At baseline pressures, flow fell 28% with maximal vasopressin effect. At all levels of diastolic pressure below 50 mmHg vasopressin also decreased flow, eg, at 30 mmHg flow was depressed by 40%. The slope of the steady-state pressure-flow relationship fell from 1.21 to 0.75 ml.min-1.mmHg-1. The diastolic pressure at which coronary flow ceased rose slightly from 13 to 15 mmHg. Intracoronary adenosine completely prevented vasopressin's effect, and the vasodilator response to adenosine was not attenuated by simultaneous administration of vasopressin. The porcine coronary circulation will constrict in response to vasopressin, not only at normal perfusion pressure, but also at low levels when metabolic vasodilatation is intense. Our study has implications about the therapeutic use of vasopressin, and demonstrates interaction of vasoactive stimuli in the coronary circulation.

Adenosine↗