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PubMed2005

Vasopressin: physiology and clinical use in patients with vasodilatory shock: a review.

Vasopressin is a nonapeptide synthesised in the hypothalamus and released upon stimulations such as hyperosmolality, hypotension and hypovolaemia. In acute shock states serum vasopressin levels increase rapidly and decrease in prolonged septic shock. The administration of vasopressin in healthy subjects has little effect, whereas in vasodilatory shock it increases the mean arterial pressure through V1 receptors and decreases the cardiac output. Vasopressin stimulates the V2 receptors in the kidney leading to reabsorption of water through aquaporin 2. However, in vasodilatory shock the antidiuretic effects are overcome by the effect vasopressin has on the kidneys: improvement of renal blood flow leading to water excretion. Twenty-four studies on the use of vasopressin in patients with vasodilatory shock are reviewed. They show that vasopressin potentiates norepinephrine effects, increases blood pressure significantly in patients with vasodilatory shock and may improve renal function. Side effects ranging from ischaemic skin lesions to possible intestinal ischaemia should not be underestimated. Above a dose of 0.04 U/min it may lead to cardiac arrest. Effects on mortality cannot be interpreted from these studies. Broad clinical use should await controlled trials to clarify its effects on clinical outcomes such as organ failure and mortality.

Animals↗

PubMed2005

Critical care providers' perceptions of the use of vasopressin in cardiac arrest.

BACKGROUND: Although published algorithms and guidelines list epinephrine and vasopressin as either/or choices for treatment of ventricular fibrillation and/or pulseless ventricular tachycardia, little is known about how critical care providers respond to this recommendation. OBJECTIVES: To assess the use of vasopressin as a first-line drug of choice for ventricular fibrillation and/or pulseless ventricular tachycardia and describe factors that may influence decision making for using vasopressin. METHODS: A convenience sample from 4 academic medical centers in the United States was recruited to complete a 20-item survey on demographic factors such as year of last Advanced Cardiac Life Support (ACLS) provider course, specialty certification, predominant practice responsibility, and beliefs related to the use of vasopressin for cardiac arrest. Descriptive statistics, Pearson correlation analysis, and logistic regression were used to analyze the data. RESULTS: A total of 214 critical care providers (80% registered nurses) completed the survey. Year of last ACLS course (r=-0.188, P=.006) was a significant demographic factor, and behavioral beliefs (attitude about using vasopressin) had the strongest relationship (r=0.687, P<.001) and were the best predictor for intentions to use or recommend the use of vasopressin (beta=0.589, P<.001). CONCLUSIONS: Despite the recommendation for vasopressin as an agent equivalent to epinephrine for treatment of ventricular fibrillation and/or pulseless ventricular tachycardia, 63% of respondents used epinephrine as a first-line drug of choice. More research is needed to address the classification system for interpreting the quality of evidence that may influence practice.

Academic Medical Centers↗

PubMedDate not supplied

Role of vasopressin in the blockade of the development of morphine tolerance by footshock and psychological stress.

To elucidate the underlying mechanism for the blockade of the development of morphine analgesic tolerance by footshock and psychological stress, we examined the role of arginine vasopressin in this process. Daily pretreatment with intracerebroventricular anti-arginine vasopressin antiserum suppressed the development of tolerance to morphine. The radioimmunoassayable arginine vasopressin content was decreased in the hypothalamus but not in other regions of mouse brain after exposure to an acute footshock or psychological stress. However, this change disappeared after 5 daily repeated treatments. Neither the development of morphine tolerance nor the brain levels of arginine vasopressin were affected by exposure to forced swimming stress. Neither a single nor 5 daily treatments with morphine induced any appreciable changes in arginine vasopressin content. However, morphine in combination with footshock, lowered this content as did, be it insignificantly, the combination of morphine and psychological stress after chronic treatment. Blockade by footshock and psychological stress of the tolerance development was dose-dependently abolished by daily pretreatment with intracerebroventricular arginine vasopressin. These findings suggest that arginine vasopressin plays a critical role in the blockade, by footshock and psychological stress, of the development of analgesic tolerance to morphine.

Analgesia↗

PubMed1990

Cholestasis, altered junctional permeability, and inverse changes in sinusoidal and biliary glutathione release by vasopressin and epinephrine.

The mechanism for the vasopressin- and epinephrine-induced decrease in bile formation and increase in sinusoidal efflux of glutathione was investigated in rat livers perfused with recirculating fluorocarbon emulsion. Vasopressin and epinephrine transiently decreased bile flow and excretion of endogenous bile acids and glutathione and increased the bile/perfusate ratio of [14C]sucrose, suggesting an increase in junctional permeability, but had no effect on the bile/perfusate ratio of [3H]polyethylene glycol-900. The decreased biliary glutathione was balanced by an increase in sinusoidal efflux, such that total hepatic release remained unchanged. The adrenergic antagonist dihydroergotamine blocked the effects of epinephrine. To examine whether an increase in junctional permeability per se could account for the changes in glutathione efflux, biliary permeability was increased by either bile duct ligation, lowering of perfusate Ca2+ concentration with ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), or addition of taurolithocholate, a cholestatic bile acid. All three maneuvers produced a decrease in biliary glutathione excretion and a concomitant increase in sinusoidal glutathione efflux, whereas total glutathione release was largely unaffected. The effects of EGTA were partially reversed if CaCl2 was reintroduced into the perfusate. Because the GSH/GSSG ratio in perfusate could not be measured in this experimental system due to the spontaneous oxidation of GSH to GSSG, additional experiments in the nonrecirculating mode examined the effects of vasopressin and bile duct ligation on sinusoidal release of GSH and GSSG. In control livers there was no detectable GSSG in perfusate (less than 0.5 nmol.min-1.g-1). After vasopressin administration, the additional sinusoidal glutathione was mainly as GSH, although there was also a significant amount of GSSG (1-2 nmol.min-1.g-1). The additional glutathione released into perfusate after bile duct ligation was 47% as GSSG. When vasopressin was administered to livers whose bile duct had been ligated, its ability to enhance sinusoidal glutathione release was diminished, suggesting that the effects of vasopressin and bile duct ligation are not additive. These observations support previous findings that vasopressin and epinephrine can modulate hepatocyte tight junctional permeability and demonstrate that these hormones produce cholestasis and inverse changes in sinusoidal and biliary glutathione efflux. Other maneuvers that increased biliary permeability to [14C]sucrose also produced cholestasis and a redistribution of glutathione efflux from bile to perfusate, suggesting that an increase in junctional permeability may allow biliary glutathione to reflux from bile to plasma.

Animals↗

PubMed1978

The neurohypophysial vasopressin content as influenced by modified cholinergic or adrenergic transmission during long-term dehydration in the white rat.

In rats dehydrated up to 12 days the neurohypophysial vasopressin content was determined by Dekański's method. Carbamylcholine inhibited somewhat the vasopressin depletion in the neurohypophysis, but not earlier than under severe dehydration (8th and 12th day). A single dose of atropine given 24 h prior to sacrifice to not dehydrated animals resulted in a diminution of the vasopressin content in the neurohypophysis; in animals dehydrated for four days and parallely atropinized the decrease of the neurohypophyseal vasopressin content was, on the contrary, considerably inhibited. Under severe dehydration, the treatment with atropine did not change the vasopressin stores in the neural lobe. Phenoxybenzamine inhibited the vasopressin depletion in the neural lobe following four days of dehydration. Under severe dehydration, amphetamine potentiated the effect of osmoreceptor stimulation. It is supposed that impulses of osmoreceptor origin are of some importance in determining the vasopressin release following changes of cholinergic or adrenergic transmission.

Amphetamine↗

PubMed1986

Vasopressin in hyponatremia: what stimuli?

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.

Creatinine↗

PubMed1977

Role of pituitary vasopressin in the formation and dynamics of aqueous humour.

The role of pituitary vasopressin (antidiuretic hormone--ADH) in the formation and dynamics of aqueous humour was studied in rabbits employing different techniques. Using isolated ciliary body preparations the changes in transepithelial short-circuit current were measured, and natural vasopressin and Lys8-vasopressin were found to increase the transepithelial short-circuit current at concentrations less than 10 muU/ml (i.e. within the physiological range), indicating increased sodium transport across the ciliary epithelium. In another series of experiments with intact rabbits given an ethanol load to suppress endogenous ADH, administration of exogenous vasopressin raised the intraocular pressure, and a similar effect was observed when endogenous ADH production was stimulated with nicotine. Direct measurements of outflow showed that vasopressin was without effect when given intravenously and that the only effect when given intracamerally was to increase the facility which would tend to lower rather than raise the intraocular pressure. Finally, the intra-arterial and intravenous effects of vasopressin on circulation in the iris and on the intraocular and systemic arterial pressures were studied. Local effects on the vascular bed in the eye and changes in systemic blood pressure were observed only at rates of administration well in excess of the physiological range for endogenous vasopressin production. It is concluded that, at physiological levels, antidiuretic hormone can stimulate active sodium transport into the eye thereby tending to raise the intraocular pressure, and it is suggested that this may act as a homeostatic regulating mechanism limiting changes in the rate of formation of aqueous humour and in intraocular pressure which might otherwise result from diurnal variations in the state of body hydration. This also offers some explanation for the ocular hypotensive action of ethanol.

Animals↗

PubMed1987

Desensitization of immature rat testicular ornithine decarboxylase to arginine vasopressin.

Prior exposure of immature rat testis to arginine vasopressin caused the testis refractory at 24 h in terms of ornithine decarboxylase activity. Arginine vasopressin caused desensitization both in Leydig cells and seminiferous tubules. Arginine vasopressin induced desensitization was found to be both time and dose-dependent. Arginine vasopressin desensitized testis was refractory to luteinizing hormone, follicle stimulating hormone, norepinephrine, dibutyryl cAMP, phorbol-myristate acetate and cholera toxin at 24 h. Arginine vasopressin desensitized testis showed recovery of response to norepinephrine at 48 h after the first injection. On the contrary arginine vasopressin could stimulate ornithine decarboxylase in luteinizing hormone desensitized testis. These results indicate that in arginine vasopressin desensitized testis the block is at post cAMP step which is common to both cAMP dependent and protein kinase C-diacylglycerol system in stimulating testicular ornithine decarboxylase.

Animals↗

PubMed1985

Synergistic stimulation of the Ca2+ influx in rat hepatocytes by glucagon and the Ca2+-linked hormones vasopressin and angiotensin II.

Glucagon was added to isolated rat hepatocytes, either alone or together with vasopressin or angiotensin II, and the effects on the initial 45Ca2+ uptake rate were investigated. Addition of glucagon alone which increased cyclic AMP content of the cells slightly increased the initial 45Ca2+ uptake rate. When glucagon was added together with vasopressin or angiotensin II--both of which when added separately increase the initial 45Ca2+ uptake rate but did not affect the cellular content of cyclic AMP--the measured initial 45Ca2+ uptake rate was larger than the sum of that seen with each hormone alone. This indicates that glucagon and Ca2+-linked hormones synergistically enhanced the Ca2+ influx in rat hepatocytes. These effects of glucagon can be mimicked by dibutyryl cyclic AMP or forskolin, suggesting that cyclic AMP augments both the resting Ca2+ and the vasopressin- or angiotensin II-stimulated influx. Measurement of the initial 45Ca2+ uptake rate as a function of the extracellular Ca2+ concentration indicated that the increase in the Ca2+ influx resulting from single or combined glucagon and vasopressin administration occurred through a homogeneous population of Ca2+ gates. These hormones were found to raise both the apparent Km for external Ca2+ and the apparent Vmax of the Ca2+ influx. The maximal increase in these two parameters was observed when the two hormones were added together. This suggests that glucagon and vasopressin synergistically stimulate the same Ca2+ gating mechanism. The dose-response curves for the action of glucagon or vasopressin applied in the presence of increasing concentrations of vasopressin or glucagon, respectively, showed that each hormone increases the maximal response to the other without affecting its ED50. It is proposed that glucagon and the Ca2+-linked hormones control the cellular concentration of two intermediates which are both necessary to allow Ca2+ entry into the cells.

Angiotensin II↗

PubMed1986

Comparison of the effects of muscarine and vasopressin on inositol phospholipid metabolism in the superior cervical ganglion of the rat.

Both muscarine and vasopressin have been shown previously to increase the accumulation [3H]inositol phosphates in superior cervical ganglia in which the phospholipids were labeled with [3H] inositol. In this study, we have compared the effects of muscarine and of vasopressin on phospholipid metabolism in the ganglion. The effects of these agents on [3H]inositol phosphate accumulation are additive. The response to muscarine levels off after approximately 10 min, whereas the response to vasopressin increases for at least 30 min. The incorporation of [3H]inositol into phospholipids is enhanced in decentralized ganglia and in ganglia maintained in organ culture compared to freshly isolated ganglia. These treatments appear to potentiate the effect of muscarine on [3H]inositol phosphate accumulation, but do not affect the response of the ganglia to vasopressin. Muscarine and vasopressin also increase the incorporation of [3H]inositol into phospholipids in the ganglion. Autoradiographic techniques were used to localize the inositol-containing phospholipids in the ganglion. Muscarine increases phospholipid labeling primarily in the cell bodies of the principal ganglionic neurons, whereas vasopressin increases phospholipid labeling primarily in the neuropil. These data are consistent with the hypothesis that muscarine and vasopressin stimulate the hydrolysis of different pools of ganglionic phospholipids.

Animals↗

PubMedDate not supplied

The hypothalamic and neurohypophysial vasopressin and oxytocin content under various states of adrenergic transmission in dehydrated and subsequently rehydrated rats.

Rats dehydrated for 8 days and subsequently rehydrated were given intracerebroventricularly (i.c.v.) methoxamine hydrochloride (MX) or dihydroergotamine methanosulphonate (DHE), each in a daily dose of 10 micrograms dissolved in 10 microliter of 0.9% sodium chloride. A single dose of MX injected to normally hydrated animals increased the release of hypothalamic and neurohypophysial vasopressin but did not affect significantly the oxytocic activity in the hypothalamus as well as in the neurohypophysis. Under conditions of dehydration MX did not influence the hypothalamic vasopressin content but it stimulated the neurohypophysial vasopressin depletion. On the contrary, MX distinctly inhibited the decrease of hypothalamic and neurohypophysial oxytocin content in dehydrated animals. In rehydrated animals MX restrained some what the renewal of hypothalamic vasopressin and oxytocin storage but intensified this process in the neurohypophysis. A single dose of DHE decreased the vasopressin content in the hypothalamus as well as the oxytocin content both in the hypothalamus and neurohypophysis. Under conditions of dehydration DHE stimulated the depletion of hypothalamic vasopressin and oxytocin. On the contrary, DHE strongly inhibited the depletion of oxytocin in the neurohypophysis of dehydrated rats. DHE restrained the renewal of hypothalamic vasopressin and oxytocin stores as well as intensified this process in the neurohypophysis of subsequently rehydrated rats.

Adrenergic Fibers↗

PubMed1977

Influence of vasopressin on colon blood flow in monkeys.

Inferior mesenteric arterial blood flow was measured with an electromagnetic blood flowmeter in five anesthetized rhesus monkeys. The effects of vasopressin on this vasculature were determined to evaluate the optimal, safe concentration of this agent during its clinical application in the management of hemorrhagic lesions of the colon. Control flow was 29 +/- 3 (SE) ml min-1; aortic pressure was 124 +/- 4 mm Hg. Intraarterial injections of vasopressin, in doses ranging logarithmically from 5 X 10(-5) to 5 X 10(-2) U kg-1, caused dose-dependent decreases in flow. At the highest dose, vasopressin reduced flow by 50% and increased arterial pressure by 9 mm Hg. When infused, at a rate of 5 X 10(-3) U kg-1 min-1, vasopressin produced a significant and sustained reduction in inferior mesenteric arterial blood flow. Autoregulatory escape was not observed. At this rate, vasopressin increased arterial pressure 10 mm Hg, by the 6th minute of infusion. This hypertension was unaccompanied by significant bradycardia. After cessation of the infusion, flow gradually returned to control values over a period of minutes. These observations indicate that vasopressin is a potent constrictor in the inferior mesenteric arterial circulation of the monkey, and support the use of this agent to control lower intestinal bleeding in man. At a dose of 5 X 10(-3) U kg-1 min-1, vasopressin causes a significant reduction in flow without adverse systemic side effects.

Animals↗

PubMed1979

Plasma vasopressin levels and urinary flow during cardiopulmonary bypass in patients with valvular heart disease: effect of pulsatile flow.

The effect of pulsatile flow on plasma vasopressin levels during cardiopulmonary bypass (CPB) was studied in 20 patients undergoing open valve replacement. Routine bypass was used in 10 patients and the AVCO pulsatile bypass pump was utilized in the other 10. In Group I (nonpulsatile) during CPB, the vasopressin level was markedly elevated (3.1 +/- 2 to 80 +/- 22 pg/ml) as was urine flow (0.6 +/- 0.2 to 5.9 +/- 2 ml/min) and urine Na+ concentration (69 +/- 19 to 116 +/- 7 mEq/L). In Group II (pulsatile) during CPB, the vasopressin level (3.8 +/- 3 to 54 +/- 14 pg/ml), urine flow (0.6 +/- 0.1 to 16.2 +/- 4.8 ml/min), and urine Na+ concentrations (61 +/- 13 to 97 +/- 10 mEq/L) were also elevated. The rise in vasopressin and urine Na+ was less in the pulsatile group (p less than 0.05) whereas the urine flow was higher (p less than 0.05). To maintain comparable blood pressure, the pulsatile flow group required significantly higher flows (4.5 +/- 0.2 compared to 3.8 +/- 0.2; p less than 0.05). These data suggest that CPB produces a marked vasopressin stress response which is beyond the physiological range for an antidiuretic effect on the kidney. At these levels vasopressin can exert a vasopressor effect to maintain resistance and affect renal blood flow, as well as producing an Na+ diuresis. The addition of pulsatile flow creates a more physiological situation attenuating the vasopressin response and producing a decrease in systemic resistance and a less pronounced Na+ diuresis.

Arginine Vasopressin↗

PubMed1980

[Contribution to the study of labeled neurohypophysial hormones. Preliminary data on the properties of the macromolecular compound: vasopressin-dextran (author's transl)].

The neuropeptide binding sites at the level of their target cells can be localized by several morphological methods. For one of the neurohypophysial hormones, vasopressin, not all labelling techniques can be applied: radioiodinated vasopressin has no biological activity; only 3Hvasopressin can be used. Immunocytochemical evidence for vasopressin receptors must be supported by complementary data in order to demonstrate the specificity of the binding. A new labelled ligand is prepared: vasopressin-dextran. In vivo, this macromolecular compound has antidiuretic properties equivalent to those of free vasopressin. In vitro, it gives a cross reaction with specific anti-vasopressin antibodies. For the same macromolecular compound, the ratio between the conjugated vasopressin estimated through R.I.A. and that assayed by biological method was 30.

Animals↗

PubMed1983

Proteolytic conversion of arginine-vasopressin and oxytocin by brain synaptic membranes. Characterization of formed peptides and mechanisms of proteolysis.

This study concerned the fragmentation of the nonapeptides arginine-vasopressin (AVP-(1-9)) and oxytocin (OXT-(1-9)) by proteolytic enzymes present in a brain synaptic membrane preparation. The peptides formed during digestion of arginine-vasopressin and oxytocin were isolated by high pressure liquid chromatography and chemically characterized by amino acid composition, NH2-terminal amino acid residues, and the presence of 14C radioactivity in tyrosine-2 and glycinamide-9. The major peptide fragments of arginine-vasopressin were [Cyt6]-AVP-(2-9), [Cyt6]-AVP-(3-9), [less than Glu4, Cyt6]-AVP-(4-9), and a peptide having the AVP-(4-8) sequence. The characterized fragments of oxytocin were [Cyt6]-OXT-(2-9), [Cyt6]-OXT-(3-9), [Cyt6]-OXT-(4-9), [less than Glu4, Cyt6]-OXT-(4-9), and [Cyt6] OXT-(5-9). Employing differentially 14C-labeled arginine-vasopressin and oxytocin, the proteolysis of the two peptides into fragments was followed with time. The results showed the sequential formation of peptide fragments by proteolytic cleavage from the NH2 terminus onward, demonstrating the action of an aminopeptidase-like enzyme. Arginine-vasopressin was converted significantly more rapidly by the amino-peptidase activity than oxytocin. In contrast to known brain aminopeptidases, the synaptic membrane-associated activity cleaved the nonapeptides without prior reduction of the disulfide bridge. From the present data it is concluded that aminopeptidases predominate in the proteolytic mechanism by which brain synaptic membranes convert arginine-vasopressin and oxytocin. The role of the proteolytic events and the significance of formed peptide fragments is discussed in view of the concept that arginine-vasopressin and oxytocin are precursors for neuropeptides in brain.

Amino Acid Sequence↗

PubMed1984

[Is there a relation between the renin-angiotensin-aldosterone system and vasopressin secretion in essential hypertension?].

103 patients with mild or moderately severe essential hypertension and 35 healthy normotensive subjects were examined. In all patients examined plasma osmolality, plasma renin activity and plasma level of vasopressin and aldosterone were estimated twice: first after administration of a diet with a sodium chloride content of 100 to 120 mmol/a day and 8 hours recumbency and a second time after 3 days of dietary sodium chloride restriction (20 mmol/a day) and 3-4 hours upright position. In hypertensives independent of the behaviour of the plasma renin activity similar values of the plasma osmolality, the plasma level of vasopressin and the aldosterone level could be established as in healthy persons. In contrast to normals in hypertensive subjects no significant correlation between plasma osmolality or plasma renin activity and plasma level of vasopressin and aldosterone was stated. In spite of normal levels of vasopressin and aldosterone a significant correlation between the plasma level of vasopressin and aldosterone and the systolic blood pressure was found in hypertensive patients. From the results obtained in this study follows that in hypertensive patients the plasma osmolality is only of secondary importance for the secretion of vasopressin and aldosterone and for the plasma renin activity. The importance of plasma vasopressin and aldosterone in the pathogenesis of hypertension seems to be probable but not yet unanimously proved.

Adult↗

PubMed1983

Verapamil inhibition of vasopressin-stimulated water flow: possible role of intracellular calcium.

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.

Animals↗

PubMed1984

Actions of vasopressin, oxytocin, and synthetic analogs on vascular smooth muscle.

A variety of physiological, pharmacological, and experimental factors are needed to explain why different authors have recorded often confusing and contradictory results of studying blood pressure and blood flow with vasopressin, oxytocin, and their analogs. Vasopressin and a number of synthetic analogs can produce potent constriction of numerous regional arteries and arterioles (e.g., splanchnic, renal, skeletal muscle, carotid, hepatic) in near physiological (i.e., 10(-12) - 10(-10)M) concentrations. Oxytocin appears to be able to elicit much weaker constriction (threshold = 10(-7) - 10(-5)M) and can produce relaxation (i.e., vasodilatation) in the presence of high degrees of tone in skeletal muscle, hepatic, renal, and splanchnic vasculatures; this may account for its blood pressure-lowering actions. With respect to the cerebral, coronary, and pulmonary vasculatures, there appears to be no good direct evidence indicating that either vasopressin or oxytocin can elicit much in the way of constrictor actions. Oxytocin, in contrast to vasopressin, is a potent constrictor of the umbilical-placental vasculature in concentrations found at term pregnancy and during parturition. Blood vessels from animals genetically lacking vasopressin appear to be supersensitive to the contractile actions of neurohypophyseal hormones. The contractile potencies and structure-activity relationships of neurohypophyseal peptides appears to vary with the type of blood vessel; i.v. rat pressor assays do not reflect the latter and cannot be utilized to determine structure-activity relationships of these peptides on vascular smooth muscle. Either a heterogeneity of the vasopressin receptor exists in peripheral blood vessels or there are vasopressin receptor subtypes on vascular muscles. Oxytocin analogs can be designed that are extremely potent splanchnic vasoconstrictors. Further insight into these areas should provide basic information on the role of these peptides in circulatory homeostasis.

Animals↗