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PubMed1982

Continuous intravenous vasopressin in active upper gastrointestinal bleeding.

Sixty patients with active upper gastrointestinal bleeding were randomized to received either continuous intravenous infusions of vasopressin (29 patients) or placebo (31 patients) at a rate of 40 U/h. Six hours after beginning the study, 13 patients in the vasopressin group and 11 in the placebo group] had ceased bleeding (p = 0.46). By 24 hours. 17 patients in the vasopressin group and 14 in the placebo group had stopped bleeding (p = 0.30). Restriction of the analysis to patients bleeding from varices showed no advantage with vasopressin treatment after 6 or 24 hours. No consistent trend favoring use of vasopressin to stop hemorrhage was noted during the 30-month study period. There was little difference between the two groups in the number of patients needing surgery (13 on vasopressin, 18 on placebo; p = 0.30) or the number of deaths (eight on vasopressin, 11 on placebo; p = 0.51); the transfusion requirement was the same. In our patients, a continuous intravenous infusion of vasopressin neither controlled bleeding nor altered outcome.

Clinical Trials as Topic↗
PubMed2002

Cardiovascular regulation of supraoptic vasopressin neurons.

A number of laboratories have identified several key areas in the central nervous system that relay information from arterial baroreceptors to the supraoptic nucleus. Two of these regions are the diagonal band of Broca and the perinuclear zone of the supraoptic nucleus. Recent findings suggest that the inhibition of vasopressin neurons in the SON by caval-atrial stretch may also involve the perinuclear zone. Using Fos immunocytochemistry in combination with volume expansion in unanesthetized rats, we observed that volume expansion activates a number of regions in the CNS including the area postrema, the nucleus of the solitary tract, the caudal ventrolateral medulla, the paraventricular nucleus, the perinuclear zone and oxytocin neurons in the supraoptic nucleus. Further experiments using pericardial catheters demonstrate that the activation of the nucleus of the solitary tract, the ventrolateral medulla, the paraventricular nucleus and the perinuclear zone by volume expansion is dependent on cardiac afferents. However, the Fos in the area postrema and oxytocin neurons of the supraoptic nucleus is not affected by removal of cardiac afferents. Similarly, electrophysiological experiments show that stimulation of cardiac receptors in the caval-atrial junction inhibits supraoptic vasopressin neurons but does not significantly affect the activity of supraoptic oxytocin neurons. These experiments suggest that while the inhibition of supraoptic vasopressin neurons during volume expansion is mediated by cardiac afferents, the activation of supraoptic oxytocin is independent of cardiac afferents and may be mediated by other visceral afferents or humoral factors. Additional electrophysiological experiments examined the importance of the perinuclear zone in cardiopulmonary regulation of vasopressin. Excitotoxin lesions of the perinuclear zone region block the inhibitory effects of caval-atrial stretch on supraoptic vasopressin neurons. This lesion has previously been shown to block the inhibitory effects of arterial baroreceptor stimulation on supraoptic vasopressin neurons. Thus, the neural pathways that inhibit vasopressin release in response to an increase in blood pressure and an increase in blood volume may overlap at the perinuclear zone of the supraoptic nucleus. Also while the inhibition of supraoptic vasopressin neurons during volume expansion is mediated by cardiac afferents, the activation of supraoptic oxytocin neurons is independent of cardiac afferents and may be mediated by other visceral afferents or hormonal factors.

Animals↗
PubMed1992

Altered effects of vasopressin on the coronary circulation after ischemia.

Ischemia and reperfusion alter the reactivity of large coronary arteries, but the effect of ischemia and reperfusion on the coronary microcirculation has been less well defined. Elevated circulating levels of vasopressin are associated with cardiopulmonary bypass and numerous other clinical states in which vascular ischemia and reperfusion may occur. We examined the effects of ischemia with and without reperfusion on the responses to vasopressin of both large coronary arteries and coronary arterial microvessels. Studies were performed on vessels from control dogs (n = 8), dogs undergoing 1 hour of ischemia only (n = 8), and dogs undergoing 1 hour of ischemia followed with 1 hour of reperfusion (n = 9). Rings of proximal obtuse marginal coronary arteries distal to the site of circumflex coronary artery occlusion were studied in isolated organ chambers. Coronary microvessels (110 to 220 microns in diameter) were studied in a pressurized (20 mm Hg), no-flow state with a microvessel imaging apparatus and electronic dimension analyzer. Microvessels were preconstricted with the thromboxane A2 analog U46619. Responses of large vessel rings were studied in the nonpreconstricted state and after preconstriction with prostaglandin F2 alpha. Large vessel response to vasopressin was minimal and not altered by ischemia with or without reperfusion. In contrast, ischemia markedly affected the coronary microvascular response to vasopressin (10 to 1000 microU/ml). Control coronary microvessels constricted minimally to vasopressin (4% +/- 2% of the baseline diameter), while microvessels after either ischemia alone or ischemia followed by reperfusion constricted 22% +/- 5% and 21% +/- 3%, respectively (p less than 0.05 versus control for both). Hemoglobin, which inactivates the endothelium-derived relaxing factor, augmented microvascular constrictions to vasopressin in all groups to a similar extent. Relaxations to the endothelium-independent agent nitroglycerin were not altered by ischemia. Constrictions of the coronary microcirculation to vasopressin in conditions such as cardiopulmonary bypass or myocardial ischemia, in which circulating levels of vasopressin are increased, may predispose to persistent myocardial ischemia in the perioperative setting.

Animals↗
PubMed1992

Oxytocin and vasopressin release in discrete brain areas after naloxone in morphine-tolerant and -dependent anesthetized rats: push-pull perfusion study.

The effects of naloxone on the release of oxytocin and vasopressin in discrete brain areas were investigated in control and morphine-tolerant/dependent female rats anesthetized with urethane. Two or three consecutive push-pull perfusates were collected for 30-40 min each and the peptide contents measured by radioimmunoassay; naloxone (5 mg/kg, i.v.) was given after the first perfusion. In control rats, naloxone did not increase oxytocin release from any of the regions studied: mediolateral septum, dorsal hippocampus, nucleus of tractus solitarius, or supraoptic nucleus. After naloxone, vasopressin release was approximately doubled in the nucleus of tractus solitarius (p less than 0.05), indicating endogenous opioid inhibition of vasopressin release. Naloxone increased oxytocin concentration in the circulation 3.7-fold (p less than 0.001) but did not affect vasopressin secretion. In rats made morphine tolerant/dependent by intracerebroventricular infusion of morphine for 5 d, oxytocin and vasopressin release in the perfused brain was initially similar to that in control rats, indicating tolerance to any initial morphine effects. In these rats, naloxone increased oxytocin release in the septum threefold relative to control rats (p less than 0.02) but did not alter oxytocin release in hippocampus or nucleus of tractus solitarius. Thus, the oxytocin neurons projecting to septum can develop morphine dependence and may be inhibited acutely by opioids acting via mu-receptors. The results indicate morphine acts selectively on oxytocin neurons projecting to mediolateral septum compared with other central projection areas and compared with centrally projecting vasopressin neurons. In the supraoptic nucleus, naloxone increased oxytocin release 2.3-fold (from 9.2 +/- 3.1 pg/30 min) and increased oxytocin release from axons of these neurons fivefold (from 7.8 +/- 3.2 pg/30 min). Naloxone had no significant effect on vasopressin release from any of the central sites, or on vasopressin secretion into blood, although oxytocin secretion was increased 36-fold (from 17.2 +/- 2.6 pg/ml; p less than 0.001), confirming dependence of magnocellular oxytocin neurons. The central processes of magnocellular supraoptic neurons may be a major source of central oxytocin released during morphine withdrawal.

Anesthesia↗
PubMed1992

Jugular venous vasopressin increases during carotid endarterectomy after cerebral reperfusion.

Several recent reports have suggested that pressor hormones may be released during and after carotid endarterectomy and that release of these factors may be associated with postoperative hypertension and other postoperative morbidity. We measured vasopressin, adrenocorticotropic hormone, and cortisol in jugular venous blood during carotid endarterectomy under general anesthesia in 43 patients with routine carotid shunting. Jugular venous vasopressin increased significantly after the second period of carotid occlusion for shunt removal and remained increased at closure. Vasopressin did not change during the initial carotid occlusion for shunt placement or during the endarterectomy itself, and neither ACTH nor cortisol changed at any sample time. Greater resting vasopressin and cortisol and larger responses of vasopressin were observed in patients receiving phenylephrine to correct intraoperative hypotension. There were no correlations between postoperative hypertension or postoperative complications and intraoperative hormone values. These results suggest (1) basal intraoperative vasopressin values reflect the blood volume of the patient, (2) increased vasopressin was not related to postoperative morbidity, and (3) intraoperative increases in pressor hormones are most likely physiologic responses to specific stimuli such as hypovolemia or hypotension rather than pathologic phenomena. We speculate that the increase of vasopressin after the second carotid occlusion and reperfusion of the brain may be due to the action of humoral factors released into the carotid circulation from the endarterectomy site.

Aged↗
PubMed1991

Chronic ethanol ingestion decreases vasopressin mRNA in hypothalamic and extrahypothalamic nuclei of mouse brain.

Endogenous arginine vasopressin was previously shown to modulate the rate of loss of functional (CNS) tolerance to ethanol, suggesting that chronic ethanol ingestion might alter vasopressin synthesis and/or release. Since extrahypothalamic vasopressin is believed to be involved in the CNS effects of the peptide, we determined the effect of ethanol on vasopressin mRNA in the bed nucleus of the stria terminalis (BST), as well as in several hypothalamic nuclei. Chronic ethanol ingestion, that produced functional tolerance and physical dependence in mice, resulted in decreased vasopressin mRNA levels in all areas examined. In contrast, as expected, dehydration resulted in increases in vasopressin mRNA in the BST and in all hypothalamic nuclei except the suprachiasmatic nucleus. In the BST, both ethanol ingestion and dehydration affected cells in the central region of the nucleus, while cells in the caudal portion were only affected by ethanol treatment. The results indicate that chronic ethanol ingestion generally reduces the synthesis of vasopressin, and that increased vasopressin synthesis is not necessary in order for the peptide to affect ethanol tolerance.

Animals↗
PubMed1991

[Endogenous vasopressin and fibrinolysis in patients with angina pectoris].

A relationship was examined between blood vasopressin levels and the fibrinolytic system in 35 patients with angina pectoris (16 with vasospastic angina (VA) and 19 with exercise-induced angina) who had undergone vein occlusion testing. There was a positive correlation between the post-testing vasopressin levels and the activity of tissue plasminogen activator inhibitor (TPAI) (r = 0.54) which was more high in patients with VA (r = 0.61). Only did the patients with VA show a direct relationship between the vasopressin concentrations and the activity of tissue plasminogen activator (TPA) (r = 0.63), the concentration of fibrinogen-fibrin degradation products (FFDP) (r = 0.88). Thirteen patients having higher vasopressin levels (over 3.4 ng/ml) displayed a greater TPAI activity than did the patients with vasopressin levels of at least 3.4 ng/ml (26.2 +/- 4.9 and 15.0 +/- 1.42 IU/ml, respectively; p less than 0.05). There was a direct relationship between the vasopressin levels and the activity of TPA (r = 0.65), the concentration of FFDP (r = 0.78) in patients having a vasopressin level of above 3.4 ng/ml. The findings are in agreement with the concept that endogenous vasopressin is involved in the regulation of the blood fibrinolytic system.

Adult↗
PubMed1979

The role of calcium ion as a mediator of the effects of angiotensin II, catecholamines, and vasopressin on the phosphorylation and activity of enzymes in isolated hepatocytes.

Angiotensin II, catecholamines, and vasopressin are thought to stimulate hepatic glycogenolysis and gluconeogenesis via a cyclic AMP-independent mechanism that requires calcium ion. The present study explores the possibility that angiotensin II and vasopressin control the activity of regulatory enzymes in carbohydrate metabolism through Ca2+-dependent changes in their state of phosphorylation. Intact hepatocytes labeled with [32P]PO43- were stimulated with angiotensin II, glucagon, or vasopressin and 30 to 33 phosphorylated proteins resolved from the cytoplasmic fraction of the cell by electrophoresis in sodium dodecyl sulfate polyacrylamide slab gels. Treatment of the cells with angiotensin II or vasopressin increased the phosphorylation of 10 to 12 of these cytosolic proteins without causing measurable changes in cyclic AMP-dependent protein kinase activity. Glucagon stimulated the phosphorylation of the same set of 11 to 12 proteins through a marked increase in cyclic AMP-dependent protein kinase activity. The molecular weights of three of the protein bands whose phosphorylation was increased by these hormones correspond to the subunit molecular weights of phosphorylase (Mr = 93,000), glycogen synthase (Mr = 85,000), and pyruvate kinase (Mr = 61,000). Two of these phosphoprotein bands were positively identified as phosphorylase and pyruvate kinase by affinity chromatography and immunoprecipitation, respectively. Incubation of hepatocytes in a Ca2+-free medium completely abolished the effects of angiotensin II and vasopressin on protein phosphorylation but did not alter those of glucagon. Treatment of hepatocytes with angiotensin II, glucagon, or vasopressin stimulated phosphorylase activity by 250 to 260%, inhibited glycogen synthase activity by 50%, and inhibited pyruvate kinase activity by 30 to 35% (peptides) to 70% (glucagon). The effects of angiotensin II and vasopressin on the activity of all three enzymes were completely abolished if the cells were incubated in a Ca2+-free medium while those of glucagon were not altered. The results imply that angiotensin II, catecholamines, and vasopressin control hepatic carbohydrate metabolism through a Ca2+-requiring, cyclic AMP-independent pathway that leads to the phosphorylation of important regulatory enzymes.

Angiotensin II↗
PubMed1985

Modulation of vasopressin-induced water permeability of the cortical collecting tubule by endogenous and exogenous prostaglandins.

These experiments were designed to test the thesis that prostaglandins produced by the cortical collecting tubule cells could modulate the vasopressin-induced osmotic water permeability (Pf). The dose-response curve for vasopressin-sensitive Pf showed the Km to be 1 microU ml-1. Exogenous PGE2 and PGF2 alpha (0.1 microM) inhibited the Pf induced by 1 microU ml-1 vasopressin when they were present in the bath solution. PGE2 (0.1 microM) in the lumen failed to inhibit the normal vasopressin-induced Pf, thus indicating an asymmetrical effect. Exposure of the tubule to 10 microM meclofenamate following stimulation of Pf by 0.2, 1.0, 10, or 100 microU ml-1 vasopressin failed to further increase the Pf. Pretreatment with meclofenamate or arachidonic acid (AA) failed to produce a different Pf response from controls. Neither naproxen (10 microM) nor AA altered significantly the Pf induced by 1 microU ml-1 vasopressin while methylisobutylxanthine, as expected, significantly enhanced Pf. The stable endoperoxide analogs U-44069 and U-46619, which mimic the actions of thromboxane A2 in many systems and which can stimulate osmotic water flow in the toad bladder, had no effect on Pf. Acidifying the lumen to pH 5.2 enhanced the Pf induced by 1 microU ml-1 vasopressin but subsequent exposure to meclofenamate did not cause an additional increment. These experiments demonstrate that exogenous prostaglandins are effective only from the basolateral surface of the cortical collecting tubule; that endogenous prostaglandins, if produced by these epithelial cells, do not produce demonstrable effects on vasopressin-sensitive Pf; and that endogenously produced thromboxane is not the likely reason for these results. Finally, the cortical collecting tubule response to many factors modulating Pf is considerably different from salientian urinary bladders.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Vasopressin secretion in the DIDMOAD (Wolfram) syndrome.

The diabetes insipidus which accompanies the DIDMOAD (Wolfram) syndrome is thought to be hypothalamic in origin, though no formal study of vasopressin secretion in the syndrome has been published, and some data in the literature suggest a renal tubular defect. We have studied vasopressin secretion in seven patients with the Wolfram/DIDMOAD syndrome during three dynamic stimuli: an osmotic stimulus (hypertonic saline infusion), hypoglycaemia (insulin tolerance test) and a baroregulatory stimulus (trimetaphan infusion). Hypertonic saline infusion demonstrated three patients to have complete and four to have partial hypothalamic diabetes insipidus; administration of (per nasal) desmopressin excluded nephrogenic diabetes insipidus in all seven patients. Insulin hypoglycaemia failed to stimulate vasopressin release, but trimetaphan-induced hypotension produced significant though subnormal rises in plasma vasopressin in three patients with partial diabetes insipidus, though it produced a negligible rise and no rise in plasma vasopressin in two patients with complete diabetes insipidus. The data suggest a much greater frequency of hypothalamic diabetes insipidus in the Wolfram/DIDMOAD syndrome than is reported, but did not identify nephrogenic diabetes insipidus. The absence of vasopressin responses to non-osmotic stimuli in patients with complete diabetes insipidus suggests global lack of vasopressin secreting neurones, rather than an isolated osmoreceptor defect or selective vasopressin secreting neuronal loss, as the lesion producing diabetes insipidus in the DIDMOAD syndrome.

Adult↗
PubMed1987

[Vasopressin, the antidiuretic hormone].

Vasopressin is actively involved in the regulation of blood pressure to the same degree as catecholamines and the renin angiotensin aldosterone system are, especially in stressful situations. Vasopressin induces and increase in blood pressure when mechanisms buffering its potent vasoconstrictor effect are altered. Vasopressin binds to specific membrane receptors classified into two main types. The V1 receptors found in blood vessels, platelets and hepatocytes are linked to two intra-cellular messengers, namely 1,2 diacylglycerol and 1,4,5 inositol triphosphate which stimulate protein kinase C and calcium-calmodulin kinase in the presence of calcium. V2-renal receptors stimulate the production of cyclic AMP which activates protein kinase A. Subsequently, the actin network is altered and particles containing pores agregate at the cell surface to produce water molecules reabsorption. Vasopressin modifies human hemostasis via platelet aggregation, stimulation of the three fractions of factor VIII, of factor XII and of fibrinopeptide A. These properties were used to treat hemostasis abnormalities seen in Von Willebrand's disease and hemophilia. There is a feed-back loop between vasopressin and the atrial natriuretic factor: vasopressin stimulates atrial natriuretic factor release via a V1 action whereas the atrial natriuretic factor reduces vasopressin release and inhibits vasopressin antidiuretic action.

Atrial Natriuretic Factor↗
PubMed1987

Fetal vasopressin in late pregnancy. Levels in amniotic fluid and in fetal urine.

The concentrations of vasopressin in the amniotic fluid were measured in 40 patients. The pregnancies were complicated by diabetes, toxemia or imminent premature delivery and in one case by polyhydramnion. The gestation time varied from 33 to 41 weeks. In addition, we measured vasopressin concentrations after transabdominal drainage of fetal bladder in three cases with urethral obstruction. Detectable concentrations of vasopressin in the amniotic fluid were found in all but four of the 40 cases observed. The vasopressin concentrations varied from 0.21 to 1.81 pg/ml. There were no systematic differences in the values in relation to duration of gestation or disease present. The highest vasopressin concentration was observed in the patient with polyhydramnion. No detectable amount of vasopressin was found in the urine of the three fetuses examined. The results suggest that, in contrast to earlier studies, the placenta may be permeable to small amounts of vasopressin or may itself be an origin of this hormone. The maternal complications present seem to have no effect of the vasopressin concentrations in the amniotic fluid.

Amniotic Fluid↗
PubMed1987

Adrenalectomy-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons: anatomic, peptide, and steroid specificity.

Following adrenalectomy (ADX), corticotropin-releasing factor (CRF) and vasopressin immunoreactivity are jointly expressed by a population of parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus (PVH). Because these cells stain positively for CRF, but not for vasopressin, after pretreatment with colchicine, the results suggest the existence of state-dependent alterations in the expression of peptides by neuroendocrine neurons. The present study sought to determine whether other neuropeptides (e.g., neurotensin, met-enkephalin) that have been colocalized with CRF in the parvocellular division of the PVH are influenced similarly by ADX; whether the enhancement of CRF and/or vasopressin immunoreactivity after ADX is limited to neurons of the PVH; and what factors might be involved in the regulation of the expression of these peptides in the PVH. The results confirmed that CRF and vasopressin immunoreactivity are both enhanced, and may be colocalized in a substantial population of parvocellular neurosecretory neurons after ADX; no comparable enhancement of staining for met-enkephalin or neurotensin was observed. The effect of ADX on CRF immunoreactivity was not limited to cells in the PVH, as neurons in the cerebral cortex, amygdala, and the bed nucleus of the stria terminalis also showed heightened CRF immunostaining after ADX; vasopressin immunoreactivity was never colocalized with CRF in these extrahypothalamic sites. Hypophysectomy produced an enhancement of CRF and vasopressin staining in the PVH that was comparable to that seen after ADX, implicating adrenal steroids as primary regulators of peptide expression in this system. Corticosteroid replacement studies in ADX rats indicated that lower doses of dexamethasone attenuated, and higher doses essentially abolished, the expected enhancement of both CRF and vasopressin immunoreactivity after ADX. The relative potency of steroids in mitigating these effects was dexamethasone greater than corticosterone greater than deoxycorticosterone greater than aldosterone. Collectively, these results indicate that the ADX-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons is at least somewhat specific to these peptides and to this cell type. Both peptides would appear to be regulated similarly by adrenal steroids, with glucocorticoids playing a primary role.

Adrenal Cortex Hormones↗
PubMed1985

Oxytocin and vasopressin in the rat do not readily pass from the mother to the amniotic fluid in late pregnancy.

In order to see whether the mother contributes to the vasopressin or oxytocin levels of amniotic fluid, these peptides were measured under conditions (1) in which the fetus lacks vasopressin (Brattleboro strain) and (2) where high maternal oxytocin and vasopressin plasma levels were induced by means of a controlled-delivery Accurel-collodion device. No vasopressin could be demonstrated in amniotic fluid of vasopressin-deficient fetuses present in a heterozygous (i.e., vasopressin-synthetizing mother). High peptide levels on the maternal side of Wistar rats generally failed to affect the amniotic fluid levels. The increase that was occasionally seen in amniotic vasopressin was probably due to fetal release concomitant with growth retardation. Amniotic vasopressin is derived from the fetus. Since amniotic fluid oxytocin is neither derived from the mother nor from the fetal brain, other fetal sources should be considered.

Amniotic Fluid↗
PubMed1982

Effect of somatostatin on vasopressin-induced antidiuresis and renal cyclic AMP of rats.

Effects of somatostatin (SRIF) on vasopressin-stimulated antidiuresis and on cyclic AMP in renal medulla in vivo and in microdissected tubule segments were examined in rats. An intravenous infusion of SRIF abolished vasopressin-induced antidiuresis without significant changes in urinary solutes and creatinine excretion in water diuresing rats: urinary osmolality rose from 131 +/- 12 to 587 +/- 20 mOsm/kg H2O in rats receiving vasopressin while urinary osmolality rose from 103 +/- 7 to only 258 +/- 25 mOsm/kg H2O in response to vasopressin with SRIF. This effect of SRIF was reversible. SRIF diminished only slightly the vasopressin-stimulated increases in cyclic AMP in renal medulla in vivo. In both cortical and medullary collecting tubules as well as in the medullary thick ascending limb of Henle's loop microdissected from rat kidney, SRIF partially inhibited vasopressin-dependent increases in cell cyclic AMP concentrations. These data demonstrate an inhibition by SRIF of vasopressin-stimulated anti-diuresis in rats and suggest that the mechanisms involved may be, at least partly, an inhibition of cyclic AMP formation in response to vasopressin in the collecting tubules.

Animals↗
PubMed1983

Effect of intracarotid administration of morphine and naloxone on plasma vasopressin levels and blood pressure in the dog.

The effects of intracarotid injection of morphine and naloxone on plasma vasopressin levels and arterial blood pressure were examined in pentobarbital-anesthetized dogs. Morphine administration decreased blood pressure in a dose-dependent fashion with a threshold between 10 and 50 micrograms/kg. Plasma levels of vasopressin rose in parallel with the decrease in blood pressure and were significantly elevated after doses of 50 and 100 micrograms/kg of morphine. Intracarotid injection of the opioid antagonist naloxone (1 mg/kg) increased blood pressure slightly, but significantly, and increased plasma concentrations of vasopressin approximately 60%. Pretreatment with naloxone did not blunt the hypotensive effect of morphine at a dose of 50 micrograms/kg, but enhanced the secretion of vasopressin in response to the morphine stimulus; plasma vasopressin levels were 5-fold greater than those found in animals given morphine but not pretreated with naloxone. Pretreatment with the histamine receptor blockers chlorpheniramine and cimetidine blunted morphine-induced (50 micrograms/kg) hypotension by about 50% and prevented a significant increase in the plasma vasopressin concentration. The data are consistent with the hypothesis that stimulation of vasopressin secretion by systemically administered morphine is secondary to the blood pressure fall. However, it also appears that, in the pentobarbital-anesthetized dog, naloxone-sensitive systems exert a tonic inhibitory influence over both vasopressin secretion and blood pressure.

Animals↗
PubMed1977

Effect of pharmacologic doses of vasopressin on sodium reabsorption in the rat kidney.

Administration of pharmacologic doses of vasopressin (50 mU./min./kg.) to the rat resulted in significant increases in both the urinary excretion of sodium (0.02 +/- 0.02 to 6.24 +/- 0.76 micronEq/min.) and the urine flow rate (4.5 +/- 0.5 to 30.5 +/- 6.0 micronl/min). Simultaneous free-flow micropuncture studies demonstrated a decrease in end-proximal TF/Pinulin ratios from 2.82 +/- 0.15 to 1.90 +/- 0.90 (p less than 0.01), indicating decreased water reabsorption in this portion of the nephron. To reduce the influence of the pressor effect of these doses of vasopressin on the kidney, the aorta was constricted proximal to the renal arteries and this resulted in a decrease in urinary sodium excretion to 2.87 +/- 0.57 micronEq/min. and in urine flow rates to 16.6 +/- 3.6 micronl/min. compared with animals given vasopressin alone. End-proximal TF/Pinulin ratio was 2.01 +/- 0.15, a value not significantly different than that in animals given vasopressin alone, suggesting a continued proximal inhibitory effect of vasopressin. It is concluded that pharmacologic doses of vasopressin inhibit sodium reabsorption in the proximal convoluted tubule as well as in distal portions of the nephron. The magnitude of sodium excretion observed is a function both of vasopressin inhibition of sodium reabsorption and the pressor effect of vasopressin.

Animals↗
PubMed1996

Differential effects of vasopressin and endothelin-1 on vascular contractile and calcium responses in pressurized small arteries from spontaneously hypertensive rats.

OBJECTIVE: To investigate the effects of vasopressin and endothelin-1 on the intracellular free calcium concentration ([Ca2+]i) and on contractile responses in endothelium-denuded resistance vessels of prehypertensive (5-week-old) and adult hypertensive (17-week-old) spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats. METHODS: Segments (2 mm long) of third-order branches of small mesenteric arteries were mounted in a perfusion myograph and maintained at 60 mmHg pressure. Endothelium was removed by intraluminal passage of air. The vessel [Ca2+]i was measured by fura-2 fluorescence and contraction was determined using a video imaging system to record lumen diameter. RESULTS: Lumen diameter was significantly smaller in 5-and 17-week-old SHR than it was in age-matched WKY rats (5 week-old SHR versus WKY rats: 178 +/- 4.0 versus 195 +/- 4.3 microns; 17-week-old SHR versus WKY rats: 168 +/- 7.0 versus 230 +/- 3.1 microns). The basal [Ca2+]i was significantly higher in 5- and 17-week-old SHR than it was in age-matched WKY rats. Infusions of vasopressin and endothelin-1 increased [Ca2+]i and contractile responses in a dose-dependent manner in all groups. The vasopressin-induced change in [Ca2+]i was significantly greater in 5- and 17-week-old SHR than in age-matched controls. The sensitivity of [Ca2+]i to vasopressin was increased in adult SHR compared with WKY rats (pD2 9.0 +/- 0.1 in SHR, 8.2 +/- 0.3 in WKY rats). Vasopressin-stimulated contractile responses were increased in adult SHR. The endothelin-1-induced change in [Ca2+]i did not differ between WKY rats and SHR. The contractility of vessels in response to endothelin-1 infusion was similar in age-matched groups. CONCLUSIONS: Endothelin-1-induced changes in [Ca2+]i and contractile responses in small arteries are similar in age-matched WKY rats and SHR, whereas responses to vasopressin are significantly enhanced in SHR compared with WKY rats. Thus [Ca2+]i signalling for vasopressin is more active than is that for endothelin-1. Vasopressin but not endothelin-1 might play a role in the development of hypertension in SHR.

Animals↗