PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “VASOPRESSIN”

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

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

At least 19 recordsLinked to original sources
PubMed1976

Synthesis and some pharmacological properties of deamino(4-threonine,8-D-arginine)vasopressin and deamino(8-D-arginine)vasopressin, highly potent and specific antidiuretic peptides, and (8-D-arginine)vasopressin and deamino-arginine-vasopressin.

Deamino[4-threonine,8-D-arginine]vasopressin (dTDAVP), deamino[8-D-arginine]vasopressin (dDAVP), [8-D-arginine[vasopressin (DAVP), and deamino-arginine-vasopressin (dAVP) were synthesized by the solid-phase method and tested for their biological activities. dTDAVP has an antidiuretic potency of 793+/-95 units/mg and undetectable vasporessor activity, less than 0.02unit/mg. The antidiuretic-pressor (A/P) ratio of dTDAVP is greater than 39 000. dDAVP has an antidiuretic potency of 1200+/-126 units/mg and a vasopressor potency of 0.39+/-0.02; its A/P ratio is thus 3000. DAVP has an antidiuretic potency of 253+/-44 units/mg, a vasopressor potency of 1.1+/-0.04 units/mg, and an A/P ratio of 240. The A/P ratios of dDAVP and DAVP are much higher than those originally reported. dAVP has an antidiuretic potency of 1745+/-385 units/mg, a vasopressor potency of 346+/-13, and an A/P ratio of 5; values are in general agreement with those in the literature. Threonine subsitution has thus brought about a significant enhancement in antidiuretic specificity, a finding entirely consistent with earlier observations that enhancement of lipophilicity at position 4 alone or in combination in arginine-vasopressin can lead to enhanced antidiuretic specificity.

Animals↗
PubMed1986

Interaction of rat adenohypophyseal vasopressin receptors with vasopressin analogues substituted at positions 7 and 1: dissimilarity from the V1 vasopressin receptor.

We readdressed the question of whether or not rat adenohypophyseal vasopressin receptors have a ligand selectivity which is similar to that of the V1 subtype of vasopressin receptors. Vasopressin analogues substituted in positions 7 and 1 were used. By incubating rat anterior pituitary quarters or by perifusing rat isolated anterior pituitary cells, the effect of the vasopressin analogues on the release of beta-endorphin-like or adrenocorticotropin-like immunoreactivity was examined. The replacement of the proline residue in position 7 by sarcosine or N-methyl-alanine did not change the maximum effect reached but increased the EC50 values 20- or 5-fold, respectively, when compared with arginine vasopressin. This decrease in beta-endorphin-releasing activity was no longer observed after additional removal of the alpha-amino group of cysteine in position 1. Since these substitutions are known to drastically reduce vasopressor activity, these data suggest that the beta-endorphin-releasing activity of vasopressin can be dissociated from its V1 receptor activity. Vasopressin analogues substituted in position 7 and with deaminopenicillamine or beta-mercapto-beta,beta-cyclopentamethylenepropionic acid in position 1 were found to be weak antagonists of the beta-endorphin-releasing activity of vasopressin. Since these analogues are potent antagonists at the V1 receptor, these data suggest that the deaminopenicillamine and, more so, the beta-mercapto-beta,beta-cyclopentamethylenepropionic acid residues in position 1 of vasopressin are strong 'binding elements' at the V1 vasopressin receptor but weak 'binding elements' at the adenohypophyseal vasopressin receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

A comparative study of plasma vasopressin levels and V1 and V2 vasopressin receptor properties in congenital hypothyroid rat under thyroxine or vasopressin therapy.

The effects of propylthiouracil (PTU) treatment on the plasma vasopressin level, on the number of hepatic (V1) or renal (V2) vasopressin receptors and on the hormone-sensitive adenylate cyclase activity in the kidney of developing rats were studied in parallel. In addition, we investigated the corrective effects of thyroxine therapy on the plasma vasopressin level and parameters related to the liver, and the effects of vasopressin therapy on the parameters related to the kidney. As already reported in the case of the number of V2 receptors and adenylate cyclase activity in the kidney, the deficient plasma vasopressin level in hypothyroid rats was completely corrected by two daily physiological doses of thyroxine given from birth to the age of sacrifice (1 month). Unlike the V1 receptors, the V2 receptors are known to be highly dependent on their specific circulating ligand. Since, first of all, the deficit was similar in the numbers of V1 and V2 receptors in hypothyroid rats, and, secondly, the treatment of hypothyroid rats by two daily physiological doses of long lasting vasopressin was found ineffective to recover the deficit in the number of V2 receptors, it can be concluded that thyroid deficiency directly alters vasopressin receptor biosynthesis in both liver and kidney, instead of acting via the depressed plasma vasopressin level.

Animals↗
PubMed1990

Vasopressin in the brain of the golden hamster: the distribution of vasopressin binding sites and of immunoreactivity to the vasopressin-related glycopeptide.

Using in vitro light microscopic autoradiography and immunocytochemistry, the distribution of vasopressin binding sites and that of the vasopressin-related glycopeptide are described in the brain of golden hamster (Mesocricetus auratus). Vasopressin binding sites and immunoreactive axons were observed in the suprachiasmatic nucleus, in the anterior hypothalamus/median preoptic area, in the medial preoptic nucleus, in the bed nucleus of the stria terminalis, in the habenular complex, in the thalamic paraventricular nucleus, and in the nucleus of the solitary tract. In addition we observed binding sites in regions where no immunoreactivity could be evidenced: the lateral septal nucleus, the central amygdaloid nucleus, the subiculum, the dentate gyrus, the anterodorsal and anteroventral thalamic nuclei, the superior colliculus, the vestibular nuclei, and in the prepositus hypoglossal nucleus. In the golden hamster, exogenous vasopressin excites single neurones located in the suprachiasmatic nucleus and induces flank-marking behavior when microinjected into the preoptic area. Our results provide a morphological basis for similar effects exerted by endogenous vasopressin. A comparison of the present data with those previously described in the rat reveals marked species differences in the brain distribution of vasopressin and of its binding sites.

Animals↗
PubMed1989

N alpha-acetyl-[Arg8]vasopressin antagonizes the behavioral effect of [Cyt6]vasopressin-(5-9), but not of vasopressin.

It has been found recently that N alpha-acetyl-[Arg8]vasopressin (Ac-VP) is present in the brain of rats. The physiological significance of this peptide is as yet unknown. Therefore, the central nervous system effects of this peptide were investigated, namely, its effects on passive avoidance behavior, exploratory behavior and body temperature. The interaction of Ac-VP with the central nervous system effects of vasopressin (VP) was also studied. Ac-VP had a slight agonistic effect on passive avoidance behavior, i.e. it facilitated passive avoidance behavior at a dose 100 times higher than that of VP. Relatively low doses (3-10 ng) of Ac-VP attenuated passive avoidance behavior, which suggests that Ac-VP interfered with an endogenous compound involved in the control of passive avoidance responding. Ac-VP was also able, albeit in higher doses (30 ng), to competitively antagonize the effect of [Cyt6]VP-(5-9), a highly potent, putative endogenous metabolite of vasopressin in the rat brain. This antagonism could be due to an interaction of Ac-VP with sites other than the V1 vasopressin receptor. Ac-VP had no significant influence on other central nervous system effects of the hormonally active nonapeptide VP, such as exploratory behavior and body temperature. These effects were readily antagonized by the V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)VP. Ac-VP may be competitive antagonist of behaviorally active vasopressin metabolite(s) in the brain.

Animals↗
PubMed1977

[1-(L-2-hydroxy-3-mercaptopropanoic acid)] analogues of arginine-vasopressin, [8-D-arginine]vasopressin, and [4-valine,8-D-arginine]vasopressin.

[1-(L-2-Hdroxy-3-mercaptopropanic acid)]arginine-vasopressin (hydroxy-AVP), [1-(L-2-hydroxy-3-mercaptopropanoic acid),8-D-arginine]vasopressin (hydroxy-DAVP), and [1-(L-2-hydroxy-3-mercaptopropanoic acid),4-valine,8-D-arginine]vasopressin (hydroxy-VDAVP) were synthesized by a combination of the solid-phase and solution methods of peptide synthesis. Protected octapeptides synthesized by the solid-phase method were further acylated by 1 + 8 couplings in solution to furnish the key intermediates. Hydroxy-AVP has antidiuretic potency of 470 units/mg and activity in the rat vasopressor assay of 550 units/mg, representing a small enhancement of activity over that of arginine-vasopressin (AVP) in each case. Hydroxy-DAVP and hydroxy-VDAVP have essentially the same high antidiuretic activity (900 units/mg) and very low vasopressor potencies (0.9 and less than 0.02 units/mg, respectively). Hydroxy-AVP, hydroxy-DAVP, and hydroxy-VDAVP thus have antidiuretic-pressor selectivity (A/P) of 1, 1000, and greater than 45 000, respectively. These data are compared with those of other vasopressin analogues. Hydroxy-VDAVP is a highly specific antidiuretic peptids and may be useful in pharmacological studies of antidiuresis.

Arginine Vasopressin↗
PubMed1991

Characterization of the human liver vasopressin receptor. Profound differences between human and rat vasopressin-receptor-mediated responses suggest only a minor role for vasopressin in regulating human hepatic function.

The [Arg8]vasopressin (AVP) receptor expressed by human hepatocytes was characterized, and compared with the rat hepatic V1a vasopressin receptor subtype. In addition to determining the pharmacological profile of the human receptor, the cellular responses to AVP were measured in human and rat hepatocytes by assaying glycogen phosphorylase alpha activity and DNA synthesis. Marked differences were observed between human and rat hepatocytes regarding vasopressin receptors and the intracellular consequences of stimulation by AVP. Data presented in this paper demonstrate the following, (i) Vasopressin V1a receptors are present in low abundance on human hepatocytes. (ii) Species differences exist between human and rat V1a receptors with respect to the affinity of some selective antagonists. (iii) AVP-stimulated glycogen phosphorylase a activation in human hepatocytes was approx. 5% of that observed in rat cells. (iv) In contrast with rat hepatocytes, DNA synthesis in human cells in culture was not stimulated by AVP. It is concluded that vasopressin plays only a minor role in the regulation of human hepatic function. Furthermore, conclusions drawn from observations made with AVP and its analogues on rat hepatic function cannot be directly extrapolated to the human situation.

Animals↗
PubMed1978

The effects of two analogues of arginine-vasopressin (ornithine-vasopressin and desamino-D-arginine-vasopressin) on kidney function in sheep.

The effects of intravenous infusion of ornithine-vasopressin (OVP) and desamino-D-arginine-vasopressin (dDAVP) were studied in normal and hydrated Merino sheep. In normal sheep, OVP resulted in a diuresis, increased urinary sodium and potassium excretion, and a fall in the plasma potassium concentration. Renal plasma flow remained constant but glomerular filtration rate and filtration fraction rose markedly. dDAVP in normal sheep was antidiuretic, but its only significant effect was a small decrease in plasma osmolality. In the hydrated sheep OVP was antidiuretic and resulted in increased urinary excretion of sodium and potassium, and a fall in the plasma potassium level. Renal plasma flow fell, but glomerular filtration and filtration fraction tended to rise. dDAVP in the hydrated sheep was also antidiuretic but urinary sodium and potassium excretion was reduced. Renal plasma flow and glomerular filtration fell, with a small decrease in filtration fraction. These results suggest that the diuretic effect in normal sheep and the electrolyte-excreting effects in both normal and hydrated sheep of OVP are related to the increase in glomerular filtration, which in turn is dependent on the vasopressor activity of the hormone. The increase in glomerular filtration caused by OVP is due to an increase in the filtration fraction of an unchanged renal plasma flow, which could be brought about by an increase in renal efferent arteriolar tone. The effects of hydration of the sheep were the conventional increased urine flow, decreased urine osmolality and decreased solute-free water reabsorption. Sodium and potassium excretion rose slightly and plasma osmolality fell. Renal plasma flow and glomerular filtration both increased with little change in filtration fraction. These effects could be brought about by suppression of endogenous vasopressin and a decrease in both afferent and efferent renal arteriolar tone.

Animals↗
PubMed1984

Haemodynamic effects of arginine-vasopressin microinjections into the nucleus tractus solitarius: a comparative study of vasopressin, a selective vasopressin receptor agonist and antagonist, and oxytocin.

Arginine-vasopressin (AVP) and related peptides were administered by microinjection into the nucleus tractus solitarius of the rat. AVP produced a rise both in mean arterial pressure and in heart rate. This effect was abolished by pretreatment with a specific antagonist of V1 receptors and was not seen either after injections of oxytocin or of the V2 agonist deamino-D-arginine-vasopressin. This study provides evidence for a specific action of vasopressin on the cardiovascular system in the nucleus of the tractus solitarius, which is mediated neither by V2 nor oxytocin receptors.

Animals↗
PubMed1988

Characterization of human platelet vasopressin receptor and the relation between vasopressin-induced platelet aggregation and vasopressin binding to platelets.

Immunoreactive AVP was found to be much higher in platelets than in platelet-free plasma (PFP) in normal subjects (12.8 +/- 6.3 versus 1.7 +/- 0.8 fmol/ml). AVP levels in PFP were appreciably elevated in parallel with the elevation of plasma osmolality induced by the acute osmotic stimulation, while the AVP levels in platelets did not change before and after the stimulation. Binding studies on intact platelets demonstrated specific binding sites for [3H]AVP. The specific binding was time, temperature and concentration-dependent, saturable and reversible, with the maximal binding capacity (Bmax) of 169.9 +/- 14.4 sites/platelet and affinity of 4.84 +/- 1.15 x 10(8)M-1. The affinity constants for unlabelled AVP, lysine vasopressin (LVP), oxytocin (OT) and dDAVP were 9.0, 8.5, 7.4 and 6.6, respectively, and the inhibition constant for d(CH2)5Tyr(Me)AVP (V1-antagonist) was 7.7. There was a highly significant correlation between the affinity constants of AVP analogues and their relative vasopressor activities in vivo, whereas no such correlation was found between the affinity constants and antidiuretic activities. AVP caused platelet aggregation with the maximal aggregation of 48.0 +/- 25.1% at 230 nM of AVP. A significant correlation was observed between the maximal percentage aggregation and Bmax of [3H]AVP to intact platelets. These results suggest that the platelet vasopressin receptor belongs to the V1 vascular subtype and mediates platelet aggregation.

Adult↗
PubMed1999

The effect of arginine vasopressin, lysine vasopressin or oxytocin on ADP or arginine vasopressin-induced Ca2+ increase in human platelets.

Oxytocin (OT), lysine vasopressin (L8VP), arginine vasopressin (A8VP) or arginine vasotocin (A8VT) are found in plasma from several species and stimulate various cell types by activation of the polyphosphoinositide metabolism and mobilization of intracellular calcium. We therefore studied the effects of the nonapeptides OT, A8VT, L8VP or A8VP on cytoplasmic calcium (Ca2+) and the effect of the nonapeptides on A8VP-induced Ca2+ mobilization. The preincubation of platelets with 'physiological' concentrations of A8VP (2-4 pmol l-1) did not enhance the intracellular calcium increase caused by the agonists used. However, the ADP-induced calcium increase was enhanced by prior addition of subthreshold concentrations of A8VP (less than 1 nmol l-1) to the platelet suspension (by 10%, P = 0.027, n = 12). Neither OT nor A8VT in concentrations from 10(-5) mumol l-1 to 1 mumol l-1 increased the cytoplasmic calcium concentration. We found that both OT and A8VT blocked the effect of subsequent exposure to A8VP. ADP (0.4 mumol l-1) did not block the effect of A8VP.

Adenosine Diphosphate↗
PubMed1989

Vasopressin, vasopressin fragments and a C-terminal peptide of the vasopressin precursor share cardiovascular effects when microinjected into the nucleus tractus solitarii.

Arginine-vasopressin (VP), the VP fragments VP-(1-8), [pGlu4,Cyt6]VP-(4-9) and -(4-8), and a fragment of the C-terminal glycopeptide of the VP precursor [CPP-(22-39)] decreased blood pressure and heart rate in anesthetized rats when microinjected bilaterally into the nucleus tractus solitarii (NTS). The magnitude of the effect was similar at doses of 20 pg, except for VP-(1-8) which required about 500 pg. The strongest decrease in blood pressure and heart rate was observed with 100 pg VP. Higher doses of other peptides either were ineffective [CPP-(22-39)] or increased blood pressure [( pGlu4,Cyt6]VP-(4-9) and -(4-8)). VP metabolites thus may participate in the control of cardiovascular functions exerted by VP. The effect of CPP-(22-39) indicates that the C-terminal glycopeptide of the VP precursor contains biological activity, which may support the cardiovascular action of VP in the NTS.

Animals↗
PubMed1986

Arginine vasopressin as an intragonadal hormone in Brattleboro rats: presence of a testicular vasopressin-like peptide and functional vasopressin receptors.

We have previously demonstrated the presence of an arginine vasopressin (AVP)-like peptide and AVP receptors in rat testis. We have also shown a direct inhibitory effect of AVP on androgen biosynthesis by cultured testicular cells. This study examined the presence of testicular AVP-like peptides and AVP receptors in homozygous (di/di) Brattleboro rats, a genetic mutant known to be deficient in hypothalamic, pituitary, and circulating AVP. The supernatant of homogenized 0.1 N acetic acid-extracted testis from adult homozygous Brattleboro rats was chromatographed on a Sephadex G-25 column. The elution profile of AVP immunoreactivity, as measured by a specific RIA, showed three distinct peaks. The first peak eluted close to the column void volume, a second peak eluted at the column total volume, while a third peak coeluted with synthetic AVP. The third peak of immunoreactive material (375 pg/g tissue) behaved similarly to authentic AVP on octadecylsilica adsorption chromatography, showed a competition curve parallel to that of AVP in the RIA, and comigrated with AVP on Sephadex G-25 and reverse phase TLC. The first, but not the second, immunoreactive peak contained enzyme activity that degraded labeled AVP in a time-dependent manner. Additional studies investigated the presence of AVP receptors in testes from Brattleboro rats. Saturable and specific [3H]AVP-binding sites were present in an enriched testicular interstitial cell preparation from these animals. Scatchard analysis indicated a Kd of 5.6 X 10(-10) M and a binding capacity of 9.7 fmol AVP bound/10(6) cells. These receptors were of the vasopressor (V1) subtype, as indicated by the potencies of selective AVP analogs for competition of [3H]AVP binding. The functionality of these receptors was shown by AVP inhibition of gonadotropin-induced androgen biosynthesis in cultured testicular cells derived from Brattleboro rats. Thus, testes from Brattleboro rats contain a high amount of an AVP-like peptide even though these animals lack hypothalamic, pituitary, and circulating AVP. Also, an AVP-degrading enzyme and AVP receptors with a Kd and binding capacity similar to those of Sprague-Dawley rats are present in the testes of Brattleboro rats. These findings add further support to the hypothesis that locally produced AVP acts as an intratesticular modulator of androgen biosynthesis.

Animals↗
PubMed1988

The role of vasopressin in acute cerebral vasospasm. Effect on spasm of a vasopressin antagonist or vasopressin antiserum.

An experimental model of subarachnoid hemorrhage (SAH) in the Sprague-Dawley rat induces angiographically demonstrable, reproducible biphasic vasospasm of the vertebrobasilar system. The acute vasospasm is maximum at 10 minutes and the maximum late vasospasm occurs 2 days after the SAH. Brattleboro rats, which are deficient in arginine vasopressin (AVP), do not have acute vasospasm after SAH but exhibit a degree of late vasospasm that is not significantly different from that seen in Sprague-Dawley rats. Cisternal injection of AVP induced acute vasospasm in Sprague-Dawley rats with a duration similar to that seen after cisternal blood injection; however, at 2 days, the vessel diameter was normal. Intravenous AVP antagonist or intracisternal AVP antiserum administered prior to the SAH prevented the development of acute vasospasm without affecting the late phase. The data suggest that an increased release of AVP in the cerebrospinal fluid is involved in the development of acute cerebral vasospasm.

Acute Disease↗
PubMed1998

Coronary vasoconstriction produced by vasopressin in anesthetized goats. Role of vasopressin V1 and V2 receptors and nitric oxide.

To examine the role of vasopressin V1 and V2 receptors, nitric oxide and prostanoids in the coronary vascular effects of [Arg8]vasopressin, coronary blood flow was measured with an electromagnetic flow transducer placed around the left circumflex (23 goats) or anterior descending (11 goats) coronary artery and vasopressin (0.03-1 microg) was intracoronarily injected in 34 anesthetized, open-chest goats. Basal mean values for coronary blood flow, mean systemic arterial pressure and heart rate, were 34 +/- 2.38 ml/min, 89 +/- 3.34 mmHg and 80 +/- 3.06 beats/min, respectively. Vasopressin produced dose-dependent decreases in coronary blood flow and the maximal reduction of this flow, attained with 1 microg of vasopressin, was 14 +/- 1.49 ml/min (42 +/- 2.64% of basal flow) (P < 0.01). Desmopressin (0.03-1 microg; 8 goats) did not affect significantly coronary blood flow. The intracoronary infusion of the antagonist for vasopressin V1 receptors d(CH2)5Tyr (Me) arginine vasopressin (2 microg/min per kg, 6 animals) significantly diminished the effects of vasopressin on coronary blood flow (the effects of 1 microg of vasopressin were reduced by 28%, P < 0.05). The mixed antagonist for vasopressin V1 and V2 receptors desGly-d(CH2)5-D-Tyr(Et)Val arginine vasopressin (0.2, 0.7 and 2 microg/min per kg, 9 animals) decreased in a dose-dependent manner the effects of vasopressin on coronary blood flow (the effects of 1 microg of vasopressin were decreased by 61% with 2 microg/min per kg, P < 0.01). Intracoronary infusion of saline (vehicle, 3 goats) did not change the effects of vasopressin on coronary blood flow. Intravenous administration of the inhibitor of nitric oxide synthesis N-omega-nitro-L-arginine methyl ester (L-NAME, 47 mg/kg, 9 animals) decreased resting coronary blood flow by 10% (P < 0.01) and augmented mean systemic arterial pressure by 20% (P < 0.01), without changing heart rate. During this treatment the reduction in coronary blood flow produced by vasopressin was higher than under control (the effects of 1 microg of vasopressin were increased by 28%, P < 0.01). Intravenous administration of the inhibitor of cyclooxygenase, meclofenamate (5 mg/kg, 7 animals), neither modified resting coronary blood flow, arterial pressure and heart rate nor the effects of vasopressin on this flow. These data indicate that vasopressin produces marked coronary vasoconstriction and suggest that: (a) it may be mediated by vasopressin V1 receptors, without involvement of vasopressin V2 receptors, (b) it is probably inhibited by nitric oxide under normal conditions and (c) it may be not modulated by prostanoids.

Anesthesia, General↗
PubMed1998

Regulation of hypothalamic arginine vasopressin messenger ribonucleic acid and pituitary arginine vasopressin content in fetal sheep: effects of acute tonicity alterations and fetal maturation.

OBJECTIVE: Fetal arginine vasopressin contributes to fetal and amniotic fluid homeostasis by increasing water resorption in the kidney and, at higher plasma levels, circulatory homeostasis by vasopressor effects. In utero and neonatal exposure of rat pups to prolonged alterations in plasma osmolality may permanently alter (imprint) pituitary arginine vasopressin content and adult responses to osmotic challenges. Our objective was to investigate fetal developmental changes and the impact of maternal dehydration and maternal hyponatremia on fetal pituitary arginine vasopressin content and hypothalamic arginine vasopressin messenger ribonucleic acid expression. STUDY DESIGN: Ten pregnant ewes with singleton fetuses (135 +/- 1 day) were chronically prepared with maternal vascular catheters. Ewes were assigned to receive water deprivation (n = 4) [desamino, D-Arg8]-arginine vasopressin-induced plasma hyponatremia (n = 3), or 4 days of observation (n = 3). Three additional pregnant ewes with preterm (110 +/- 1 day) singleton fetuses were also included for a study of maturational effects. Daily maternal blood samples were analyzed for determination of plasma arginine vasopressin, electrolytes, and osmolality. After the study protocol, fetuses were operatively delivered, umbilical blood samples obtained, and fetuses put to death for pituitary and hypothalamic tissues. Pituitary arginine vasopressin content was determined by radioimmunoassay, and hypothalamus arginine vasopressin messenger ribonucleic acid expression was detected by Northern blotting. RESULTS: Dehydration significantly (P < .05) increased, and hyponatremia significantly decreased maternal plasma sodium concentration compared with controls. Fetal plasma sodium concentration significantly changed in parallel with maternal values (dehydration: 139 +/- 1 to 150 +/- 1 mEq/L; hyponatremia: 138 +/- 1 to 128 +/- 5 mEq/L). Fetal hypothalamic arginine vasopressin messenger ribonucleic acid expression and pituitary content did not change in relation to these relatively acute alterations in plasma tonicity. However, among all animals, arginine vasopressin messenger ribonucleic acid expression was significantly negatively correlated with pituitary arginine vasopressin content (r2 = 0.563; P = .02). Arginine vasopressin messenger ribonucleic acid expression was significantly lower in both preterm and near-term fetuses (P < .05) than that in the maternal ewe, although pituitary arginine vasopressin content (in micrograms per milligram of protein) was significantly greater in preterm fetuses (P < .01, vs maternal; P < .05, vs near term). CONCLUSIONS: The significant inverse relation between arginine vasopressin content and arginine vasopressin messenger ribonucleic acid suggests a dynamic arginine vasopressin synthesis-content feedback relationship is functional in the near-term fetus. Although relatively acute periods of maternal hypertonicity or hypotonicity do not alter fetal pituitary arginine vasopressin content or hypothalamic arginine vasopressin messenger ribonucleic acid expression, longer-term plasma tonicity alterations may potentially have an impact on the fetal arginine vasopressin hypothalamic-pituitary axis.

Animals↗
PubMed1995

Effects of arginine vasopressin and 1-desamino-8-D arginine vasopressin on forearm vasculature of healthy subjects and patients with a V2 receptor defect.

OBJECTIVES: To assess which vasopressin receptor subtype mediates the vasodilation occurring in response to arginine vasopressin and 1-desamino-8-D (DD)-arginine vasopressin and whether nitric oxide is involved in these effects. MATERIALS AND METHODS: Vasoactive effects of arginine vasopressin and DD-arginine vasopressin on forearm vasculature were studied in healthy subjects and in patients with congenital nephrogenic diabetes insipidus with a vasopressin type 2 (V2) receptor gene defect. Venous occlusion plethysmography was used to assess the forearm blood flow responses to the infusion of arginine vasopressin and its analogue into the brachial artery, in the presence and the absence of the nitric oxide synthase inhibitor L-NG-monomethyl-arginine (L-NMMA). RESULTS: In healthy subjects (n =10), DD-arginine vasopressin (0.1, 1 and 10 or 5, 10 and 20 ng/min per dl) induced a dose-related increase in forearm blood flow, but did not affect forearm blood flow in the patients with nephrogenic diabetes insipidus (n = 3). In two healthy subjects, seven increasing doses of arginine vasopressin (0.25-12 ng/min per dl) induced an initial decrease in forearm blood flow and then a gradual increase. In one of the patients, the same arginine vasopressin doses produced a persistent decrease in forearm blood flow. In the healthy subjects, infusion of L-NMMA reduced forearm blood flow significantly (n = 10). Subsequent administration of DD-arginine vasopressin during L-NMMA infusion produced a slight reduction in the forearm blood flow increase compared with DD-arginine vasopressin alone, but this was significant only for the absolute forearm blood flow increase induced by 10 ng/min per dl in all subjects. Infusion of arginine vasopressin in the presence of L-NMMA did not increase forearm blood flow significantly. CONCLUSIONS: In human forearm vasculature, extrarenal V2 receptors mediate the vasodilation induced by DD-arginine vasopressin or high doses of arginine vasopressin, whereas these receptors are not necessary for arginine vasopressin-induced vasoconstriction. The DD-arginine vasopressin-induced vasodilation seems to be mediated predominantly by a mechanism other than endothelial nitric oxide release, whereas arginine vasopressin-induced vasodilation seems to involve nitric oxide release only.

Adult↗