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PubMedDate not supplied

Lack of vasopressin action on splanchnic hemodynamics during bleeding: a study in conscious, portal hypertensive rats.

Due to the marked effects of hemorrhage on cardiac output and splanchnic hemodynamics, the circulatory actions of vasopressin may differ during bleeding as opposed to stable conditions. We evaluated this hypothesis in conscious rats with portal hypertension due to chronic portal vein stenosis, by comparing the effects of a vasopressin infusion (0.02 IU per kg per min) to those of a control saline infusion, during and after a hypotensive hemorrhage (25 ml per kg). We also studied unbled portal hypertensive rats receiving an identical infusion of vasopressin or saline. During and after hemorrhage, vasopressin induced significant changes in systemic hemodynamics but had no effect on portal pressure, portal tributary blood flow and nonhepatic splanchnic arteriolar resistance. In unbled animals, by contrast, vasopressin decreased portal pressure and portal tributary blood flow and increased nonhepatic splanchnic arteriolar resistance. Our data further indicate that hemorrhage alone caused an early vasoconstriction in the portal tributaries and a delayed vasoconstriction in the nonsplanchnic vascular bed while vasopressin during hemorrhage induced an early and sustained vasoconstriction in the nonsplanchnic vascular bed as well as in the portal tributaries. The results show that, during and after severe bleeding, vasopressin exerts little influence on portal hemodynamics. Although these data do not allow firm conclusions concerning the therapeutic efficacy of vasopressin in bleeding esophageal varices, they demonstrate that the splanchnic actions of vasoactive substances cannot be readily extrapolated from stable conditions to hemorrhage.

Animals↗
PubMed1989

Association of transdermal nitroglycerin to vasopressin infusion in the treatment of variceal hemorrhage: a placebo-controlled clinical trial.

The aim of this study was to evaluate, using a double-blind technique, the efficacy of the association of transdermal nitroglycerin to vasopressin infusion for the treatment of variceal bleeding. Sixty-nine cirrhotic patients with active variceal bleeding were randomly allocated to receive vasopressin (0.4 to 0.8 unit per min until variceal bleeding has been controlled for 12 hr) associated with nitroglycerin administered transdermically in a slow-release preparation (10 mg in 24 hr) or placebo. An initial control of variceal hemorrhage was achieved in 83% of the patients receiving vasopressin-nitroglycerin and in 74% in the vasopressin-placebo group. Owing to a lower frequency of recurrent bleeding during therapy (18 vs. 42%, p = 0.11), vasopressin-nitroglycerin achieved a definitive control of bleeding in a higher proportion of patients than vasopressin-placebo (73 vs. 54%, p = 0.13). The group treated with the drug combination showed favorable results in relation to transfusion requirements (2.9 +/- 0.4 vs. 4.2 +/- 0.5 units, p = 0.05), total dose of vasopressin required (453 +/- 47 vs. 587 +/- 50 units, p less than 0.05), need of balloon tamponade (6 vs. 15, p less than 0.05) and requirement for emergency surgery (0 vs. 4, p = 0.07). There were no significant differences in the undesirable effects associated with treatment, observed in 37 and 49% of cases, respectively. Hospital mortality was similar (33 vs. 25%). This study demonstrates that transdermal nitroglycerin improves the effectiveness of vasopressin for controlling variceal hemorrhage.

Administration, Cutaneous↗
PubMed2001

Regulation of the abundance of renal sodium transporters and channels by vasopressin.

Vasopressin plays a role in both salt and water balance in the kidney. Classic studies, utilizing isolated perfused tubules, have revealed that vasopressin increases sodium reabsorption in the kidney thick ascending limb and the collecting duct. Furthermore, the activity of several sodium transport proteins expressed in these segments, such as the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) and the epithelial sodium channel (ENaC), have been shown to be directly increased by vasopressin. Increased protein abundance might be one means through which sodium transporter and channel activity is enhanced. We have used immunoblotting and immunohistochemistry in order to investigate the regulation of abundance of the major sodium transporters and channels expressed along the renal tubule in response to vasopressin. Chronic (7-day) studies were performed in which vasopressin levels were elevated either endogenously by water restriction of Sprague-Dawley rats or exogenously through infusion of the vasopressin V2-receptor-selective agonist, dDAVP (1-deamino-8d-arginine-vasopressin), to Brattleboro rats. We found a significant increase in protein abundance for NKCC2 and the beta- and gamma-subunits of ENaC with either water restriction or dDAVP infusion. The alpha-subunit of Na-K-ATPase was increased by water restriction, but not by dDAVP infusion, and alpha-ENaC and the thiazide-sensitive cotransporter (NCC) were increased by dDAVP infusion but not by water restriction. Acute (60-min) in vivo exposure to dDAVP led to an increase in both beta- and gamma-ENaC abundance in kidney cortex homogenates, displaying the rapid nature of some of these changes. Overall these increases in sodium transporter and channel abundances likely contribute to both the antidiuretic and antinatriuretic actions of vasopressin.

Animals↗
PubMed1998

Studies of renal aquaporin-2 expression during renal escape from vasopressin-induced antidiuresis.

In animal models of the syndrome of inappropriate antidiuresis (SIADH), sustained administration of vasopressin and water results in free-water retention and progressive hyponatremia for several days, which is then followed by escape from the vasopressin-induced antidiuresis. With the onset of vasopressin escape, water excretion increases despite sustained administration of vasopressin, allowing water balance to be re-established and the serum sodium to be stabilized at a steady, albeit decreased, level. Studies from our laboratories have investigated whether this escape phenomenon can be attributed to altered regulation of aquaporin water channels. After four-day pre-treatment with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) by osmotic minipump, rats were divided into control (continued dDAVP) and water-loaded (continued dDAVP plus a daily oral water load) groups. A significant increase in urine volume in the water-loaded rats was observed by the second day of water loading, indicating escape from antidiuresis. The onset of escape coincided temporally with a marked decrease in renal aquaporin-2 protein (measured by semi-quantitative immunoblotting), which began at day 2 and fell to 17% of control levels by day 3. In contrast, there was no decrease in the renal expression of aquaporins 1, 3, or 4. The marked suppression of whole kidney aquaporin-2 protein was accompanied by a concomitant suppression of whole kidney aquaporin-2 mRNA levels. Immunocytochemical localization and differential centrifugation studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact during vasopressin escape. Additional studies have indicated that the observed down-regulation of aquaporin-2 expression also occurs in the renal cortex as well as the inner and outer medullas, and can be reversed simply by water restriction despite maintenance of hyponatremia. Our results therefore suggest that escape from vasopressin-induced antidiuresis is attributable, at least in part, to a vasopressin-independent and osmolality-independent decrease in aquaporin-2 water channel expression in the renal collecting duct. Similar mechanisms likely contribute to the phenomenon of escape from antidiuresis seen clinically in patients with SIADH as well.

Animals↗
PubMed1986

Vasopressin has general rate-decreasing effects on schedules maintaining either high or low response rates.

Male and female Wistar rats were treated with different doses of vasopressin (0.05, 0.25, 1.25, 3.75 and 6.25 micrograms/kg) after responding had stabilized on either a differential reinforcement of low rate 15 s (DRL 15 s) or a differential reinforcement of high rate 0.75 s (DRH 0.75 s) schedule of reinforcement. Low to moderate doses of vasopressin did not affect response rates, response efficiency or the number of reinforcers obtained during vasopressin sessions on both the DRL and DRH schedules. Administration of 6.25 micrograms/kg vasopressin reduced low response rates and the number of reinforcers obtained during vasopressin sessions, but increased response efficiency. High response rates and response efficiency were reduced after administration of 3.75 and 6.25 micrograms/kg vasopressin, while the number of reinforcers obtained during vasopressin sessions was reduced at 6.25 micrograms/kg. Sex differences in the effects of vasopressin were not observed on either schedule.

Animals↗
PubMed1995

ACTH, cortisol and glucose responses after administration of vasopressin in cattle and sheep.

The present study compared the effects of vasopressin on plasma concentrations of corticotropin, cortisol and glucose in cattle and sheep. After intravenous injection of 1, 0.1 and 0.01 microgram vasopressin per kg body weight, the plasma vasopressin concentration increased proportionally to the injected dose, and this increase was similar in cattle and sheep. Doses of 1 and 0.1 microgram per kg body weight of vasopressin triggered significant responses of corticotropin, cortisol and glucose in cattle and sheep. The corticotropin response to both doses was significantly greater in sheep, whereas the glucose response was greater in cattle. The cortisol response did not differ between species. The lowest dose of vasopressin (0.01 microgram per kg body weight) still induced a significant cortisol response without a substantial effect on plasma corticotropin, suggesting that a direct action of vasopressin on the adrenals may contribute to the observed cortisol response. The results demonstrate that vasopressin increases plasma levels of corticotropin, cortisol and glucose in cattle, as it does in sheep, but the intensities of the corticotropin and glucose responses to vasopressin differ between cattle and sheep. The reasons for these differences remain to be clarified.

Adrenocorticotropic Hormone↗
PubMed1988

The physiological effects of vasopressin when used to control intra-abdominal bleeding.

Vasopressin was used in ten critically ill patients with massive intra-abdominal bleeding unresponsive to conventional therapy. Vasopressin controlled bleeding in four patients, three of whom had continued to bleed following laparotomy for haemostasis; in two other patients, bleeding was reduced. All the patients were intensively monitored throughout the period of the vasopressin treatment; this enabled other physiological effects of vasopressin to be documented and reported. Mean arterial pressure and central venous pressure increased following the administration of vasopressin and there was a decrease in heart rate. Core body temperature rose significantly. Although all the patients had impaired renal function before receiving vasopressin, five had a prompt diuresis following its administration. Eight patients died but only three of intra-abdominal bleeding; two patients survived to leave hospital. Four patients had post-mortem evidence of ischaemia in the heart, liver and gastrointestinal tract; vasopressin may have contributed to the development of this. Vasopressin may have a place in the management of patients with life-threatening intra-abdominal haemorrhage but its use should be confined to those patients in whom conventional therapy has failed.

Abdomen↗
PubMed1982

Immunohistochemical identification of the oxytocin and vasopressin neurons in the hypothalamus of the monkey (Macaca fuscata).

The hypothalamic oxytocin and vasopressin neurons of the monkey, Macaca fuscata, were demonstrated in Golgi-like images by a modified immunoperoxidase method. The magnocellular oxytocin and vasopressin neurons were distributed mainly in the supraoptic and paraventricular nuclei. In addition to these main nuclei, both types of magnocellular neurons were found in the accessory supraoptic nucleus, the periventricular and perifornical areas, the nucleus of the stria terminalis, the lateral hypothalamic area, and the pars interna of the globus pallidus. Magnocellular oxytocin neurons were seen immediately ventral to the anterior commissure, and parvocellular vasopressin neurons were localized in the medial portion of the suprachiasmatic nucleus. The preferential distribution of the oxytocin and vasopressin neurons was recognized not only in the supraoptic and paraventricular nuclei, but also in other areas. In all areas observed, the cytological difference between the oxytocin and vasopressin neurons could be identified. The area of the perikarya of the vasopressin neurons was determined to be larger than that of the oxytocin neurons. Most of the axons of the oxytocin neurons issued from the perikarya, while the axons of the vasopressin neurons originated in most cases from the thick proximal dendrites. These results show that the oxytocin and vasopressin neurons are distributed in areas much broader than has hitherto been assumed, and that these two peptidergic neurons can be definitely differentiated morphologically as well as functionally.

Animals↗
PubMed1986

Modulation by fenoldopam (SKF 82526) and bromocriptine of the electrically evoked release of vasopressin from the rat neurohypophysis. Effects of dopamine depletion.

Single neurointermediate lobes were fixed by their stalks to a platinum wire electrode and incubated in Krebs-bicarbonate solution. Vasopressin release into the medium was determined by a radioimmunoassay. Vasopressin secretion was increased by electrical stimulation (15 Hz, 10 s trains with 10 s intervals for 10 min). Fenoldopam (SKF 82526) had a dual effect on vasopressin release, 30 nM decreasing (by 30%) and 3 microM increasing (by 32%) the evoked vasopressin secretion. The facilitatory effect of fenoldopam was antagonized in a concentration-dependent manner by flupenthixol but not by sulpiride. Sulpiride (1 microM) prevented the inhibitory effect of fenoldopam (30 microM). After pretreatment of the rats with the dopamine depleting agent, Ro4-1284 (2 mg/kg i.p. 1 h before the experiments), the evoked vasopressin release was decreased by 21% and the inhibitory effect of fenoldopam disappeared, but the facilitatory effect of fenoldopam was already seen at 30 nM. Similarly, bromocriptine (1-10 microM) decreased the evoked vasopressin release from untreated neurointermediate lobes by 30-40% but increased the vasopressin release by 30% after pretreatment with Ro4-1284. The present findings further support the concept that vasopressin from the neurohypophysis is modulated by dopaminergic mechanisms. Facilitatory effects are mediated via D 1 and inhibition via D 2 receptors. The presence of endogenous dopamine seems to be necessary for the inhibitory effects to occur.

Animals↗
PubMed1995

Enhancement of phospholipid hydrolysis in vasopressin-stimulated BHK-21 and H9c2 cells.

The hydrolysis of phospholipids in vasopressin-stimulated baby hamster kidney (BHK)-21 and H9c2 myoblastic cells was investigated. Phosphatidylcholine and phosphatidylethanolamine in these cells were pulse labelled with [3H]glycerol, [3H]myristate, [3H]choline or [3H]ethanolamine, and chased with the non-labelled precursor until linear turnover rates were obtained. When cells labelled with [3H]glycerol or [3H]myristate were stimulated by vasopressin, no significant decrease in the labelling of phosphatidylcholine was detected, but the labelling of phosphatidic acid was elevated. However, the labellings of phosphatidylethanolamine and its hydrolytic product were not affected by vasopressin stimulation. When the cells were pulse labelled with [3H]-choline, vasopressin stimulation caused a decrease in the labelled phosphatidylcholine with a corresponding increase in the labelled choline. The apparent discrepancy between the two types of labelling might be explained by the recycling of labelled phosphatidic acid back into phosphatidylcholine, thus masking the reduction in the labelled phospholipid during vasopressin stimulation. Alternatively, the labelled choline produced by vasopressin stimulation was released into the medium, thus reducing the recycling of label precursor back into the phospholipid and making the decrease in the labelling of phosphatidylcholine readily detectable. Further studies revealed that vasopressin treatment caused an enhancement of phospholipase D activity in these cells. The presence of substrate-specific phospholipase D isoforms in mammalian tissues led us to postulate that the differential stimulation of phospholipid hydrolysis by vasopressin was caused by the enhancement of a phosphatidylcholine-specific phospholipase D in both BHK-21 and the H9c2 cells.

Animals↗
PubMedDate not supplied

Effect of vasopressin on phasic coronary blood flow.

The effects of vasopressin on the coronary circulation have been studied with regard to its general hemodynamic effects. Aortic blood pressure (BP), left ventricular pressure (LVP), aortic blood flow (AoBF), and circumflex blood flow (CBF), were measured in 12 open-chest dogs, under control conditions and during vasopressin infusion (25 mU/kg/min). During vasopressin infusion, the mean aortic blood pressure (MBP) was increased from 104 +/- 23 mm Hg to 161 +/- 23 mm diastolic blood pressure (DBP) was more increased (+55%) than the systolic blood pressure (SBP) (+40%). AoBF was decreased from 2.169 +/- 0.408 l/min to 1.118 +/- 0.303 l/min; and the heart rate was decreased by 18%. The total combined left ventricular power did not change significantly. The increase in total peripheral resistance (TPR) (+200%) was the main change in impedance spectrum. The mean circumflex coronary blood flow (MCBF) was decreased from 48 +/- 8.6 ml/min to 33.4 +/- 9.7 ml/min. This decrease was more important in the diastolic circumflex blood flow (DCBF) (-33%) than in the systolic one (-0.8%). The diastolic pressure time index (DPTI) was more increased than the systolic pressure time index (SPTI). The DPTI/SPTI ratio was increased from 0.91 to 1.3. Long diastoles, induced by vagus nerve stimulation, have permitted to characterise the relationship between pressure and coronary blood flow during diastole. This relationship was linear under basal condition, and during vasopressin perfusion. This made it possible to determine the critical closing pressure (Pf0), and the coronary conductance (the slope of the regression curve). Vasopressin induced an increase in Pf0, from 33.7 +/- 95 to 77.4 +/- 16.07 mm Hg (p less than 0.001), and a decrease in coronary conductance, from 0.8 +/- 0.32 to 0.5 +/- 0.1 ml/min/mm Hg. The effect of an acute change in perfusion pressure on the coronary flow, under control conditions and during vasopressin infusion was studied by opening a large arteriovenous fistula. Unclamping of the fistula, under control conditions, allowed to realize an acute fall in DBP from 82.5 +/- 6.36 to 35.5 +/- 9.19 mm Hg, and in DCBF, from 58.5 +/- 9.2 to 20 +/- 9.8 ml/min. During vasopressin infusion, a similar fall in perfusion pressure lead to a zero diastolic circumflex blood flow, for a diastolic aortic blood pressure of 56 +/- 12 mm Hg. However, vasopressin did not affect the delayed active coronary vasodilatation.

Animals↗
PubMed1997

Possible roles of prostaglandins in the anteroventral third ventricular region in the hyperosmolality-evoked vasopressin secretion of conscious rats.

This study explored the roles of prostaglandins in the anteroventral third ventricular region, a cerebral osmoreceptor site, in the osmoregulation mechanism of vasopressin release. We injected (1 microliter) prostaglandin E2 (12.8 nmol) or meclofenamate (78.3 nmol), an inhibitor of prostaglandin biosynthesis, into the brain region or the lateral cerebral ventricle of conscious rats, examining their effects on plasma vasopressin and its controlling factors in the presence or absence of an osmotic stimulus. The injection of prostaglandin E2 into the anteroventral third ventricular region augmented plasma vasopressin and arterial pressure after 5 min and 15 min, without influencing plasma osmolality, sodium, potassium, or chloride. In contrast, intraventricular injection of prostaglandin E2 did not cause any significant effect on those variables. The i.v. infusion (0.1 ml.kg-1.min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin after 15 min and 30 min; this was accompanied by increased plasma osmolality, sodium, and chloride, and by unaltered or elevated arterial pressure. Meclofenamate given into the anteroventral third ventricular region 30 min before starting the hypertonic saline infusion abolished the osmotic vasopressin response without significantly changing the responses of the other variables. Histological analysis showed that the injection sites of meclofenamate in these rats were close to those of prostaglandin E2 in the anteroventral third ventricular region and included the organum vasculosum of the lamina terminalis and the surrounding area, the medial preoptic area, and periventricular and median preoptic nuclei. When injection cannulae for meclofenamate deviated from those areas incidentally or when the drug was expressly administered into the cerebral ventricle, the osmotic vasopressin response was not inhibited. Plasma vasopressin and the other variables observed during the i.v. infusion of isotonic saline (0.15 mol/l) were not affected significantly by meclofenamate administration into the anteroventral third ventricular region or the cerebral ventricle. On the basis of these results, we concluded that prostaglandins synthesized in and/or near the anteroventral third ventricular region might contribute to the facilitation of vasopressin release in the hyperosmotic state.

Animals↗
PubMed1994

Biphasic modulation of choline uptake and phosphatidylcholine biosynthesis by vasopressin in rat cardiac myocytes.

The effect of vasopressin on choline uptake and phosphatidylcholine biosynthesis in isolated rat heart myocytes was investigated. Myocytes were incubated with labelled choline in the presence of 0.05-1.0 microM vasopressin. Uptake of choline was enhanced (25%) by a low concentration (0.2 microM) of vasopressin, but was attenuated (19%) by a higher vasopressin concentration (1.0 microM). The biosynthesis of phosphatidylcholine was also affected by vasopressin in a biphasic manner. At low concentrations of vasopressin, a general increase in cytosine triphosphate:phosphocholine cytidylyltransferase activity was observed that caused an enhanced conversion of phosphocholine to phosphatidylcholine via the cytidine diphosphocholine pathway. At high vasopressin concentrations, a decrease in the activity of cytidylyltransferase was detected, which was caused by the translocation of the enzyme from the microsomal fraction to the cytosolic fraction. The decrease in enzyme activity coincides with a reduction in the conversion of labelled phosphocholine to phosphatidylcholine. In view of the fact that phospholipid biosynthesis in rat hepatocytes is inhibited by vasopressin at all concentrations, the biphasic modulation of phosphatidylcholine biosynthesis in rat heart myocytes illustrates the diverse effects of this hormone in different mammalian tissues.

Animals↗
PubMed2004

Effect of carcinomatosis and intraperitoneal 5-fluorouracil on peritoneal blood flow modulated by vasopressin in the rat as measured with the 133Xe-clearance technique.

PURPOSE: Intraperitoneal administration of 5-fluorouracil for the treatment of gastrointestinal malignancies results in a greater total drug exposure in the peritoneal fluid than in plasma. Drugs are eliminated from the peritoneal cavity mainly by capillaries leading to the portal venous system and to a lesser extent by lymphatics. The drug itself and the presence of peritoneal carcinomatosis may affect elimination of the drug. The 133Xe-clearance technique allows the influence of a vasoactive agent on the peritoneal blood flow to be estimated with minimal invasiveness. The aim of the present study was to explore whether intraperitoneal 5-FU or peritoneal carcinomatosis affects the peritoneal blood flow and its reactivity to intravenous vasopressin, as measured indirectly with the 133Xe-clearance technique. METHODS: The animals used in this study were 63 Wistar-Fu (W-Fu) rats and 67 Lister-Hooded (LH) rats. On day 0, either 5-FU at 25 mg/kg body weight in 25 ml/kg isotonic saline was instilled intraperitoneally, or 1 x 10(5) syngeneic tumour cells were inoculated intraperitoneally. On days 1, 2 and 3 in the 5-FU-treated rats, and on days 12-16 in rats inoculated with tumour cells, peritoneal blood flow was analysed with the 133Xe-clearance technique, before and during intravenous infusion of vasopressin at 0.07 IU/min/kg body weight. RESULTS: The basal 133Xe-clearance before administration of vasopressin was similar in all groups except in the LH rats treated with 5-FU in which it was significantly lower. Infusion of vasopressin induced a significant decrease in 133Xe-clearance of the same magnitude in controls and in tumour-bearing rats. In the rats given intraperitoneal 5-FU, vasopressin did not reduce the 133Xe-clearance the first day after administration of 5-FU. CONCLUSIONS: Intravenous vasopressin at 0.07 IU/min/kg decreased peritoneal blood flow as measured indirectly with the 133Xe-clearance method. Intraperitoneal 5-FU abrogated the reduction in peritoneal blood flow with intravenous vasopressin the first day after treatment. In contrast, the presence of peritoneal carcinomatosis did not influence peritoneal blood flow, nor the effect of vasopressin

Animals↗
PubMed2005

Two-channel gastric electrical stimulation accelerates delayed gastric emptying induced by vasopressin.

The aim of this study was to investigate the effects of two-channel gastric electrical stimulation (GES) on delayed gastric emptying, gastric dysrhythmias, and motion sickness-like symptoms induced by vasopressin. Seven dogs implanted with four pairs of gastric electrodes and a duodenal cannula were studied in four randomized sessions (saline, vasopressin, single-channel GES, and two-channel GES). The experiment in each session was conducted sequentially as follows: 30-min baseline, ingestion of a liquid meal, 30-min iv infusion of vasopressin or saline, and two 30-min postprandial recordings. In the GES sessions, GES was applied via the first pair of electrodes for single-channel GES or the first and third pairs of electrodes for two-channel GES. Gastric emptying was collected every 15 min via the cannula for a period of 90 min. Results were as follows. (1) Vasopressin induced gastric dysrhythmias, motion sickness-like symptoms, and delayed gastric emptying (P < 0.01, ANOVA). (2) GES normalized gastric dysrhythmias (P < 0.01) but showed no effects on vasopressin-induced emetic response. (3) Two-channel GES improved delayed gastric emptying induced by vasopressin. In comparison with the vasopressin session, two-channel GES, but not single-channel GES, significantly increased gastric emptying at 30 min (43.9+/-12.6 vs. 27.5+/-7.7%; P < 0.03), 60 min (75.3+/-15.1 vs. 54.0+/-17.8%; P < 0.05), and 90 min (91.6+/-9.8 vs. 80.3+/-9.0%; P < 0.05). GES with long pulses is able to normalize gastric dysrhythmias. Two-channel GES improves delayed gastric emptying induced by vasopressin.

Animals↗
PubMed1983

Vasopressin response to orthostatic hypotension. Etiologic and clinical implications.

Plasma vasopressin was measured before and after tilt testing in 18 patients with orthostatic hypotension of various causes. In six patients, all of whom had normal osmotic regulation of vasopressin, normal stimulation of vasopressin did not occur on tilt testing; all six had clinical evidence of defects in the afferent or central connections of the baroregulatory reflex arc. In the remaining 12 patients, plasma vasopressin increased to levels appropriate for the degree of hypotension; none of these patients had clinical evidence of defects in afferent or central portions of the baroregulatory arc. Those with subnormal vasopressin response had significantly more severe orthostatic hypotension than the patients with normal vasopressin response, but none had plasma hypotonicity, an abnormality present in one-quarter of those with normal response. It is concluded that the vasopressin response to orthostatic hypotension may serve as a test of the integrity of the afferent and central components of the baroregulatory reflex arc. Furthermore, this study suggests that the normal vasopressin response to orthostatic hypotension may moderate the fall in blood pressure but may adversely affect water balance.

Adult↗
PubMed1990

Fetal hemodynamic and fetoplacental vascular response to exogenous arginine vasopressin.

Fetal hemodynamics and fetoplacental blood flow were measured in chronically instrumented ovine fetuses during intravenous infusion of arginine vasopressin. Vasopressin was infused at rates ranging from 1 to 300 ng/min/kg estimated fetal mass. This range of infusion rates produces plasma arginine vasopressin levels observed throughout a wide range of fetal stress. No maternal effects were observed at any infusion rates used in this investigation. Fetal heart rate declined linearly with the log of the infusion rate. Mean fetal arterial pressure showed a sigmoidal response to log arginine vasopressin infusion rate, reaching a plateau at 30 ng/min/kg. Umbilical vascular resistance increased throughout the entire range of infusion rates. Fetoplacental blood flow decreased with increasing infusion rate but decreased only 4% to 13% throughout the range of infusion rates that produce plasma arginine vasopressin levels commonly observed during fetal stress. Because umbilical vascular resistance continued to rise after arterial pressure reached a plateau, fetoplacental blood flow decreased 31% at the highest infusion rate. However, the plasma vasopressin level associated with this infusion rate is probably in excess of that associated with severe fetal distress. The fetoplacental vascular bed is, therefore, either relatively insensitive to arginine vasopressin, or is capable of autoregulation in the face of high circulating levels of arginine vasopressin.

Animals↗
PubMed1975

Isoproterenol in offsetting adverse effects of vasopressin in cirrhotic patients.

Vasopressin administered as a peripheral infusion (40 U/hr) significantly reduced portal vein pressure in ten awake patients with cirrhosis and portal hypertension. A vasopressin-induced reduction in cardiac output occurred in five of the ten patients (50 per cent). Vasopressin-induced changes in systemic arterial pressure, heart rate, and portal venous pressure were independent of alterations in cardiac output. When the five patients with vasopressin-induced reductions in cardiac output were given a combination of vasopressin and isoproterenol, cardiac output was maintained and the reduction in portal vein pressure was equal to that observed with unopposed vasopressin therapy. Thus, the addition of isoproterenol prevented a vasopressin-induced reduction in cardiac output while permitting vasopressin to reduce portal vein pressure.

Blood Pressure↗