Vascular effects alter early-gestation fetal renal responses to vasopressin

1994 ◽  
Vol 266 (3) ◽  
pp. R722-R729 ◽  
Author(s):  
M. G. Ervin ◽  
K. A. Terry ◽  
G. C. Calvario ◽  
R. Castro ◽  
M. G. Ross ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arginine Vasopressin ◽  
Receptor Agonist ◽  
Free Water ◽  
Vascular Effects ◽  
Receptor System ◽  
Free Water Clearance ◽  
Early Gestation ◽  
V2 Receptor ◽  
Renal Responses

Distinct receptors mediate the vascular (V1) and renal (V2) effects of arginine vasopressin (AVP). Although ovine fetal AVP-induced antidiuresis can be demonstrated in early gestation (< 120 days; term 150 days), the early-gestation fetal renal responses to AVP are variable, including increases in urine flow and glomerular filtration rate (GFR). AVP V1 receptor predominance and/or V2 receptor system immaturity may contribute to variable early-gestation renal responses to AVP. To differentiate these possibilities, we assessed early-gestation fetal V2 receptor function in the presence and absence of V1 receptor-mediated effects by comparing the responses to AVP (a combined V1-V2 receptor agonist; n = 10; 112 +/- 2 days) with the selective V2-receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP) (n = 5; 111 +/- 2 days). AVP infusion increased fetal mean arterial pressure (MAP; 36 +/- 1 to 44 +/- 2 mmHg) and decreased heart rate (197 +/- 2 to 171 +/- 3 beats/min); DDAVP infusion had no effect on MAP or heart rate. Free water clearance decreased in response to AVP (0.13 +/- 0.02 to 0.02 +/- 0.01 ml.min-1.kg-1) and DDAVP (0.21 +/- 0.04 to 0.04 +/- 0.02 ml.min-1.kg-1), and urine osmolality increased in response to both analogues (AVP: 145 +/- 4 to 283 +/- 15 mosmol/kgH2O; DDAVP: 146 +/- 5 to 244 +/- 32 mosmol/kgH2O).(ABSTRACT TRUNCATED AT 250 WORDS)

Antidiuretic effect of subnormal levels of arginine vasopressin in normal humans

1990 ◽  
Vol 259 (1) ◽  
pp. R53-R60 ◽  
Author(s):  
L. J. Andersen ◽  
J. L. Andersen ◽  
H. J. Schutten ◽  
J. Warberg ◽  
P. Bie
Keyword(s):  
Arginine Vasopressin ◽  
Free Water ◽  
Human Kidney ◽  
Urine Osmolality ◽  
Significant Rise ◽  
Constant Infusion ◽  
Free Water Clearance ◽  
Water Load ◽  
Normal Humans ◽  
Renal Responses

The renal responses to 120-min infusions of arginine vasopressin (AVP) were investigated in healthy volunteers undergoing water diuresis induced by an oral water load of 20 ml/kg body wt. AVP at 1 pg.min-1.kg-1 (approximately 10(-15) mol.min-1.kg-1) decreased urine flow (12.2 +/- 1.7 to 7.4 +/- 1.5 ml/min) and free water clearance (9.7 +/- 1.5 to 4.8 +/- 1.4 ml/min) and increased urine osmolality (Uosmol; 71 +/- 6 to 115 +/- 15 mosmol/kgH2O); 5 pg.min-1.kg-1 elicited pronounced antidiuresis (14.4 +/- 0.9 to 0.9 +/- 0.3 ml/min) with maximal Uosmol of 621 +/- 95 mosmol/kg. In response to 25 pg.min-1.kg-1, maximal Uosmol was 869 +/- 38 mosmol/kg. Responses developed gradually and stabilized within the 2nd h of infusion. AVP at 1 and 5 pg.min-1.kg-1 was without effect for at least 20 min. Only 25 pg.min-1.kg-1 caused a significant rise in plasma AVP (1.2 +/- 0.2-2.0 +/- 0.1 pg/ml), and with this dose sodium excretion decreased. The rates of K+ excretion, as well as plasma aldosterone and atrial natriuretic peptide concentrations, were unaffected by AVP. It is concluded that the human kidney is sensitive to changes in the rate of secretion of AVP of less than 1 pg.min-1.kg-1 and that the maximal change occurs after 1-2 h of constant infusion. It is estimated that the rate of infusion of AVP required to produce isosmolar urine during overhydration is approximately 3 pg.min-1.kg-1.

Renal responses to the κ-opioid-receptor agonist U-50488H in conscious lambs

2007 ◽  
Vol 293 (1) ◽  
pp. R162-R168 ◽  
Author(s):  
Wei Qi ◽  
K. Kumar Ebenezar ◽  
Mohamed A. Samhan ◽  
Francine G. Smith
Keyword(s):  
Opioid Receptor ◽  
Opioid Receptors ◽  
Receptor Agonist ◽  
Age Groups ◽  
Free Water ◽  
Urinary Flow ◽  
Free Water Clearance ◽  
Postnatal Maturation ◽  
Opioid Receptor Agonist ◽  
Renal Responses

In adult animals and humans, activation of κ-opioid receptors results in a diuresis. The aim of the present study was to investigate whether κ-opioids are also diuretic early in life and whether this is altered during postnatal maturation. Therefore, the renal effects of the κ-opioid-receptor agonist U-50488H were measured in two separate age groups of conscious lambs at two stages of postnatal maturation (∼1 wk and ∼6 wk) under physiological conditions. To evaluate whether the renal responses to U-50488H resulted from receptor-dependent effects, responses to U-50488H were also tested in the presence of the specific κ-opioid-receptor antagonist 5′-guanidinonaltrindole (GNTI). Urinary flow rate, free water clearance, and electrolyte excretions and clearances were measured for 30 min before and for 90 min after intravenous injection of U-50488H or vehicle. An increase in urinary flow rate accompanied by an increase in free water clearance occurred in response to administration of U-50488H but not vehicle. There were no effects of U-50488H on electrolyte excretions or clearances at either 1 or 6 wk of postnatal life. Although there were no effects of GNTI on any of the measured or calculated variables, the aforementioned diuretic response to U-50488H was abolished by pretreatment with GNTI in both age groups. We conclude that κ-opioid receptors are diuretic early in life and that this response does not appear to be altered as postnatal maturation proceeds. Therefore, these data provide evidence that activation of κ-opioid receptors early in life may lead to alterations in fluid balance.

Interaction of somatostatin with PTH and AVP: renal effects.

1979 ◽  
Vol 237 (5) ◽  
pp. E428
Author(s):  
N Brautbar ◽  
B S Levine ◽  
J W Coburn ◽  
C R Kleeman
Keyword(s):  
Antidiuretic Hormone ◽  
Arginine Vasopressin ◽  
Free Water ◽  
Treated Group ◽  
Free Water Clearance ◽  
Parathyroid Extract ◽  
Renal Tubular ◽  
Vehicle Treated Group ◽  
Experimental Group ◽  
Antidiuretic Action

Six conscious intact dogs were studied to evaluate the interactions of somatostatin (SRIF) with exogenous antidiuretic hormone arginine vasopressin (AVP). SRIF administration caused a significant increase in free water clearance compared to a vehicle-treated group: -0.91 (+/- 0.41 SD) ml/min to 0.21 (+/- 0.32 SD) ml/min in the experimental group (P less than 0.01) versus 0.21 (+/- 0.81 SD) ml/min to -0.21 (+/- 0.68 SD) ml/min in the control (P greater than 0.5). Six conscious, thyroparathyroidectomized dogs were studied to test the interaction of SRIF and parathyroid extract (PTE). There were no significant changes in the phosphaturic and hypocalciuric effects of PTE with SRIF administration. We conclude that acute systemic SRIF administration interferes with the antidiuretic action of AVP, probably at the renal-tubular level, but does not antagonize the renal actions of PTE.

Enhanced renal vasoconstriction induced by vasopressin in SHR is mediated by V1 receptors

1996 ◽  
Vol 271 (2) ◽  
pp. F304-F313 ◽  
Author(s):  
J. J. Feng ◽  
W. J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Arginine Vasopressin ◽  
Receptor Agonist ◽  
Vascular Reactivity ◽  
Spontaneously Hypertensive Rat ◽  
Rat Kidney ◽  
Strain Difference ◽  
Renal Vasoconstriction ◽  
V2 Receptor

The development of hypertension in the spontaneously hypertensive rat (SHR) is associated with renal dysfunction; the observed renal vasoconstriction may reflect an imbalance of constrictor and dilator systems. The present studies evaluated renal vascular reactivity to arginine vasopressin (AVP) and mediation by V1 and/or V2 receptors. Renal blood flow (electromagnetic flowmetry) was measured in water-loaded, 8-wk-old SHR, Wistar-Kyoto rats (WKY), and Munich-Wistar rats. Injection of AVP (2 and 5 ng) into the renal artery caused dose-dependent renal vasoconstriction. The maximum blood flow response was approximately twofold larger in SHR than both normotensive strains. The strain difference was largely unaffected by indomethacin administration, although the reduction in blood flow produced by 5 ng AVP was 4-6% larger in both SHR and WKY during cyclooxygenase inhibition. The V1 receptor antagonist, [D-(CH2)5,Tyr(Me)2,Tyr(NH2)9]Arg8-vasopressin, blocked up to 90% of the renal vasoconstriction elicited by AVP. Intrarenal injection of the V1-receptor agonist [Phe2,Ile3,Org8]vasopressin produced renal hemodynamic effects similar to AVP; this agonist reduced renal blood flow, with twofold larger responses in SHR (-40 vs. -18% for 10 ng). In contrast, similar doses of the V2-receptor agonist 1-desamino-8-D-arginine vasopressin had no effect. These results indicate that AVP-induced vasoconstriction is mediated predominantly by the V1 receptor in the rat kidney. The enhanced vascular reactivity in 8-wk-old SHR may reflect an increased V1 receptor density and/or affinity or postreceptor signaling pathways, largely independent of buffering by the vascular V2 receptor or vasodilator prostaglandin activity. The strain difference in the vascular response to AVP may contribute to the renal vasoconstriction observed during the development of genetic hypertension.

Baroreflex buffering of pressor response to vasopressin is mediated by V1, not V2, receptors in conscious rats

1993 ◽  
Vol 264 (2) ◽  
pp. R345-R349
Author(s):  
K. Shimizu ◽  
J. Schwartz ◽  
B. P. McGrath
Keyword(s):  
Heart Rate ◽  
Receptor Agonist ◽  
Pressor Response ◽  
Conscious Rat ◽  
Conscious Rats ◽  
Pressor Responses ◽  
Autonomic Blockade ◽  
V2 Receptor ◽  
Intact Rats

Arginine vasopressin (AVP) enhances reflex buffering of its own pressor response, thus attenuating its vasoconstrictor potential in vivo. To investigate the extent to which this effect of AVP is mediated by V1 or V2 receptors, mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of AVP or [Phe2,Orn8]oxytocin, a potent, selective V1-receptor agonist, in the absence and presence of infusion of [Val4,D-Arg8]VP, a selective V2-receptor agonist. Responses were compared in intact and autonomically blocked conscious rats. During autonomic blockade with methscopolamine and hexamethonium, the pressor sensitivities to AVP and [Phe2,Orn8]oxytocin were similarly increased. Infusion of the V2-receptor agonist had no effect by itself on MAP or HR in conscious intact rats. It also did not alter the pressor responses to the V1 agonist, in either intact or autonomically blocked rats. In the presence of the V2 agonist, the decrease in heart rate induced by the V1 agonist was enhanced. These results indicate that reflex buffering of the pressor response to AVP in the conscious rat is mediated by V1 and not V2 receptors. However, V2 receptors may be involved in modulating the heart rate response to AVP.

Renal water excretion before and after remission of nephrotic syndrome: Relationship between free water clearance and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading

1986 ◽  
Vol 71 (1) ◽  
pp. 97-104 ◽  
Author(s):  
E. B. Pedersen ◽  
H. Danielsen ◽  
S. S. Sørensen ◽  
B. Jespersen
Keyword(s):  
Nephrotic Syndrome ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Free Water ◽  
Control Group ◽  
Ang Ii ◽  
Free Water Clearance ◽  
Water Load ◽  
Control Subjects ◽  
Before And After

1. An oral water load of 20 ml/kg body wt. was given to eight patients with nephrotic syndrome before and after remission of the syndrome, and to 13 healthy control subjects. Urine volume (D), free water clearance (Cwater), plasma concentrations of arginine vasopressin (AVP), angiotensin II (ANG II) and aldosterone (Aldo), were determined before and three times during the first 4 h after loading. 2. D and Cwater increased to a significantly lower level (P < 0.01) after water loading in patients with nephrotic syndrome than in control subjects, but D and Cwater were normal after remission of the syndrome. The maximum increase in Cwater (ΔCwater max.) was 1.07 ml/min (median) before remission and 7.93 ml/min after, compared with 8.01 ml/min in the control group. 3. Creatinine clearance (Ccr) increased significantly after remission (63 ml/min to 88 ml/min, P < 0.01), and the fractional excretion of sodium was enhanced. AVP was higher in the nephrotic syndrome both before (2.9 pmol/l) and after remission (2.9 pmol/l) compared with the control group (1.8 pmol/l). ANG II and Aldo did not change after remission and remained at the same level as in the control group. 4. The elevation in ΔCwatermax after remission was accompanied by an increase in Ccr in all patients and ΔCwatermax. and Ccr were significantly correlated (ρ = 0.600, n = 16, P < 0.05). No relationship was found between the change in ΔCwater max. and ANG II and Aldo. 5. AVP was significantly suppressed in patients with nephrotic syndrome before remission, but not after remission nor in control subjects, so that although AVP did not differ in nephrotic patients before and after remission, AVP cannot be excluded as a contributory factor to the reduction in Cwater in the nephrotic syndrome. 6. It is concluded that patients with nephrotic syndrome excrete an oral water load slower than control subjects and that the excretion rate is normal after remission of the syndrome. It is suggested that the normalization of Cwater may be attributed to an increase in glomerular filtration rate or a decrease in proximal tubular sodium reabsorption, although a possible role for AVP has not been excluded.

Renal responses to plasma volume expansion and hyperosmolality in fasting seal pups

2002 ◽  
Vol 282 (3) ◽  
pp. R805-R817 ◽  
Author(s):  
Rudy M. Ortiz ◽  
Charles E. Wade ◽  
Daniel P. Costa ◽  
C. Leo Ortiz
Keyword(s):  
Free Water ◽  
Elephant Seal ◽  
Mirounga Angustirostris ◽  
Plasma Volume Expansion ◽  
Northern Elephant Seal ◽  
Indwelling Catheter ◽  
Free Water Clearance ◽  
Plasma Arginine ◽  
Renal Responses ◽  
Extreme Conservation

Renal responses were quantified in northern elephant seal ( Mirounga angustirostris) pups during their postweaning fast to examine their excretory capabilities. Pups were infused with either isotonic (0.9%; n = 8; Iso) or hypertonic (16.7%; n = 7; Hyper) saline via an indwelling catheter such that each pup received 3 mmol NaCl/kg. Diuresis after the infusions was similar in magnitude between the two treatments. Osmotic clearance increased by 37% in Iso and 252% in Hyper. Free water clearance was reduced 3.4-fold in Hyper but was not significantly altered in Iso. Glomerular filtration rate increased 71% in the 24-h period after Hyper, but no net change occurred during the same time after Iso. Natriuresis increased 3.6-fold in Iso and 5.3-fold in Hyper. Iso decreased plasma arginine vasopressin (AVP) and cortisol acutely, whereas Hyper increased plasma and excreted AVP and cortisol. Iso was accompanied by the retention of water and electrolytes, whereas the Hyper load was excreted within 24 h. Natriuresis is attributed to increased filtration and is independent of an increase in atrial natriuretic peptide and decreases in ANG II and aldosterone. Fasting pups appear to have well-developed kidneys capable of both extreme conservation and excretion of Na+.

Vasopressin and oxytocin receptors coupled to Ca2+ mobilization in rat inner medullary collecting duct

1993 ◽  
Vol 265 (1) ◽  
pp. F15-F25 ◽  
Author(s):  
Y. Maeda ◽  
J. S. Han ◽  
C. C. Gibson ◽  
M. A. Knepper
Keyword(s):  
Arginine Vasopressin ◽  
Receptor Agonist ◽  
Collecting Duct ◽  
Oxytocin Receptor ◽  
Receptor Subtype ◽  
Vasopressin Receptor ◽  
Inner Medullary Collecting Duct ◽  
V1b Receptor ◽  
V2 Receptor ◽  
Medullary Collecting Duct

In renal collecting duct epithelial cells, arginine vasopressin (AVP) at greater than nanomolar concentrations has been reported to transiently increase intracellular free calcium ([Ca2+]i) in a manner consistent with activation of the phosphoinositide pathway. To investigate whether any of the known neurohypophysial hormone subtypes are involved, we measured [Ca2+]i in microdissected rat terminal inner medullary collecting duct (IMCD) using fura-2. To allow quantitative comparisons of the response under different conditions, we determined the areas under the response curves (in nM.min) over 1.5 min using numerical integration. AVP, the V1b-receptor agonist [deamino1,D-3-(pyridyl)Ala2,Arg8]vasopressin, the V2-receptor agonist 1-desamino-8-D-arginine vasopressin, oxytocin, and the selective oxytocin-receptor agonist [Thr4,Gly7]oxytocin (TG-OXT), each at 10 nM, significantly increased [Ca2+]i (69.52 +/- 10.25, 27.0 +/- 11.7, 24.33 +/- 5.83, 14.75 +/- 2.81, and 14.57 +/- 3.50 nM.min, respectively). In contrast, a V1a-selective agonist ([Phe2,Ile3,Orn8]vasopressin) did not increase [Ca2+]i (0.43 +/- 2.36 nM.min). In desensitization studies, challenge with 10 nM AVP or TG-OXT completely prevented a rise in [Ca2+]i in response to immediate rechallenge with the same agent, but not the other, demonstrating homologous desensitization. The lack of cross-desensitization implies that at least two receptors are present that can trigger a rise in [Ca2+]i in response to neurohypophysial hormones. Antagonists for oxytocin ([des-glycinamide9,d(CH2)5(1),O-Me-Tyr2,Thr4,Orn8]vaso tocin), V2 ([d(CH2)5(1),D-Ile2,Ile4,Arg8]vasopressin), and V1a ([d(CH2)5(1),O-Me-Tyr2,Arg8]vasopressin) receptors partially inhibited the [Ca2+]i response induced by 10 nM AVP (89.5, 81.6, and 51.4% inhibition, respectively). These data are consistent with the view that both an oxytocin receptor and a vasopressin receptor are coupled to a [Ca2+]i mobilization response in rat terminal IMCD. This vasopressin receptor is distinct from both the V1a receptor and the V2 receptor and may be either the V1b receptor or a novel vasopressin receptor subtype.

RADIOIMMUNOASSAY OF [8-ARGININE]-VASOPRESSIN

1975 ◽  
Vol 80 (3) ◽  
pp. 453-464 ◽  
Author(s):  
U. Merkelbach ◽  
P. Czernichow ◽  
R. C. Gaillard ◽  
M. B. Vallotton
Keyword(s):  
Arginine Vasopressin ◽  
Excretion Rate ◽  
Regression Line ◽  
Plasma Osmolality ◽  
Free Water ◽  
Bartter Syndrome ◽  
Total Output ◽  
Urinary Concentration ◽  
Free Water Clearance ◽  
Significant Difference

ABSTRACT A radioimmunoassay for [8-arginine]-vasopressin (AVP), previously described (Czernichow et al. 1975) has been used for the determination of antidiuretic hormone in a 4 ml urine sample. AVP is extracted from acidified urine with a cation exchanger (Amberlite CG 50) with an overall recovery of 72 %. The blank value measured in extracted samples of urine was 0.29 pg/ml ± 0.21 (sem) and calculated by extrapolation of the regression line of the recovery experiment was 0.49 pg/ml. The coefficient of variation within-assay was 13 % and between-assay 18%. Addition of the amounts of AVP found in each specimen of urine voided gave results nearly identical to those of the amounts found in 24 h pool of urine, indicating that the assay was not affected by changes in concentration of the other urinary components during the day. The daily urinary excretion of AVP measured in 34 subjects was found to be 34 ng in 17 women and 70 ng in 17 men, a significant difference. Urinary concentration and excretion rate of AVP rose during thirst test and during Carter-Robbins test performed in 13 healthy subjects. In the latter test it was observed that the women displayed a strikingly more pronounced AVP elevation after the osmolar stimulus than the men. In both sexes a significant correlation was found between AVP excretion rate and plasma osmolality as well as free water clearance. Three cases of complete or incomplete diabetes insipidus and potomania could be clearly differentiated according to the total output of AVP during the thirst test. Extremely high values of AVP were found in the urine of 5 subjects with Schwartz-Bartter syndrome associated with bronchogenic tumours.

Vasopressin regulation of inner medullary collecting ducts and compensatory changes in mice lacking adenosine A1 receptors

2008 ◽  
Vol 294 (3) ◽  
pp. F638-F644 ◽  
Author(s):  
Timo Rieg ◽  
Kanishka Pothula ◽  
Jana Schroth ◽  
Joseph Satriano ◽  
Hartmut Osswald ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Free Water ◽  
Urinary Flow ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Loading ◽  
Collecting Ducts ◽  
Camp Formation

Activation of adenosine A1 receptors (A1R) can inhibit arginine vasopressin (AVP)-induced cAMP formation in isolated cortical and medullary collecting ducts. To assess the in vivo consequences of the absence of A1R, we performed experiments in mice lacking A1R (A1R−/−). We assessed the effects of the vasopressin V2 receptor (V2R) agonist 1-desamino-8-d-arginine vasopressin (dDAVP) on cAMP formation in isolated inner medullary collecting ducts (IMCD) and on water excretion in conscious water-loaded mice. dDAVP-induced cAMP formation in isolated IMCD was significantly greater (∼2-fold) in A1R−/− compared with wild-type mice (WT) and, in contrast to WT, was not inhibited by the A1R agonist N6-cyclohexyladenosine. A1R−/− and WT had similar basal urinary excretion of vasopressin, expression of aquaporin-2 protein in renal cortex and medulla, and acute increases in urinary flow rate and electrolyte-free water clearance in response to the V2R antagonist SR121463 or acute water loading; the latter increased inner medullary A1R expression in WT. Dose dependence of dDAVP-induced antidiuresis after acute water loading was not different between the genotypes. However, A1R−/− had greater inner medullary expression of cyclooxygenase-1 under basal conditions and of the P2Y2 and EP3 receptor in response to water loading compared with WT mice. Thus vasopressin-induced cAMP formation is enhanced in isolated IMCD of mice lacking A1R, but the adenosine-A1R/V2R interaction demonstrated in vitro is likely compensated in vivo by multiple mechanisms, a number of which can be “uncovered” by water loading.

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