Effects of sodium depletion and angiotensin II on osmotic regulation of vasopressin

1986 ◽  
Vol 250 (2) ◽  
pp. R287-R291
Author(s):  
C. E. Wade ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Angiotensin Ii ◽  
Hypertonic Saline ◽  
Intravenous Infusion ◽  
Plasma Osmolality ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Relationship Of ◽  
The Relationship

After alterations in sodium balance, osmotic reactivity of vasopressin (AVP) release was evaluated in seven conscious dogs during bilateral intracarotid infusions of hypertonic saline. A low-sodium diet reduced plasma sodium concentration by 3%; deoxycorticosterone acetate (30 mg/day for 2 days) elevated the concentration by 1%. Neither treatment altered resting plasma AVP. Hypertonic intracarotid infusions increased jugular plasma osmolality by 20 +/- 2 mosmol/kg independent of manipulations. Plasma AVP values were significantly increased (P less than 0.05) in sodium-depleted dogs compared with values of the control animals. In addition, the osmotic reactivity of AVP release was evaluated during exogenous administration of angiotensin II (ANG II). Intravenous infusion of ANG II (5 ng . kg-1 . min-1) increased plasma concentration of ANG II but did not alter concentration of plasma AVP. The slope for the relationship of jugular plasma osmolality to plasma AVP during hypertonic intracarotid infusions was significantly increased with intravenous infusion of ANG II. Sodium depletion and intravenous ANG II potentiate the relationship of plasma osmolality and plasma AVP when evaluated with intracarotid hypertonic saline infusions in dogs.

Plasma vasopressin response to peripheral administration of angiotensin in conscious rats

1985 ◽  
Vol 248 (2) ◽  
pp. R249-R256 ◽  
Author(s):  
K. Yamaguchi ◽  
M. Koike ◽  
H. Hama
Keyword(s):  
Angiotensin Ii ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Mannitol Solution ◽  
Injection Volume ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Series Of Experiments

To assess a role for peripherally administered angiotensin II (ANG II) in regulating vasopressin (antidiuretic hormone, ADH) release, the effects on plasma ANG II and ADH of intraperitoneal injections of ANG II dissolved in various solutions were examined in conscious rats. Plasma ANG II and ADH were determined by radioimmunoassay using the trunk blood collected after decapitation. Injections of 150 mM NaCl containing ANG II (6, 12, or 24 micrograms X 2 ml-1 X 100 g body wt-1) caused dose-related increases in plasma ANG II 15 and 30 min after, but plasma ADH remained unchanged. The lack of effect on plasma ADH of the ANG II dissolved in isotonic saline was also confirmed in another series of experiments in which the solution with a higher ANG II concentration was loaded by much smaller injection volume (14.3 micrograms X 0.1 ml-1 X 100 g-1). However, when given together with 600 mM NaCl, ANG II (8 micrograms X 2 ml-1 X 100 g-1) significantly potentiated the plasma ADH response to the vehicle at 15, 30, and 60 min, without affecting those of plasma osmolality, sodium, and hematocrit. The elevations of plasma ANG II and osmolality brought about by the treatment were comparable with those previously observed in rats deprived of water for 46 h. ANG II was without effect on the plasma ADH responses to the intraperitoneal injections of hypertonic sucrose or mannitol solution that did not alter plasma sodium, although these solutions were equipotent to 600 mM NaCl in augmenting plasma ADH and osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II-induced Akt activation is mediated by metabolites of arachidonic acid generated by CaMKII-stimulated Ca2+-dependent phospholipase A2

2005 ◽  
Vol 288 (5) ◽  
pp. H2306-H2316 ◽  
Author(s):  
Fang Li ◽  
Kafait U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Ii ◽  
Ang Ii ◽  
Akt Phosphorylation ◽  
Akt Activation ◽  
Interfering Rna ◽  
Relationship Of ◽  
The Relationship ◽  
Cytochrome P 450 ◽  
Hydroxyeicosatetraenoic Acids

Angiotensin II (ANG II) promotes vascular smooth muscle cell (VSMC) growth, stimulates Ca2+-calmodulin (CaM)-dependent kinase II (CaMKII), and activates cytosolic Ca2+-dependent phospholipase A2 (cPLA2), which releases arachidonic acid (AA). ANG II also generates H2O2 and activates Akt, which have been implicated in ANG II actions in VSMC. This study was conducted to investigate the relationship of these signaling molecules to Akt activation in rat aortic VSMC. ANG II increased Akt activity, as measured by its phosphorylation at serine-473. ANG II (200 nM)-induced Akt phosphorylation was decreased by extracellular Ca2+ depletion and calcium chelator EGTA and inhibitors of CaM [ N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide] and CaMKII {(2-[ N-(2-hydroxyethyl)]- N-(4-me-thoxybenzenesulfonyl)]amino- N-(4-chlorocinnamyl)- N-methylbenzyl-amine)}. cPLA2 inhibitor pyrrolidine-1, antisense oligonucleotide, and retroviral small interfering RNA also attenuated ANG II-induced Akt phosphorylation. AA increased Akt phosphorylation, and AA metabolism inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA) blocked ANG II- and AA-induced Akt phosphorylation (199.03 ± 27.91% with ANG II and 110.18 ± 22.40% with ETYA + ANG II; 405.00 ± 86.22% with AA and 153.97 ± 63.26% with ETYA + AA). Inhibitors of lipoxygenase (cinnamyl-3,4-dihydroxy-α-cyanocinnamate) and cytochrome P-450 (ketoconazole and 17-octadecynoic acid), but not cyclooxygenase (indomethacin), attenuated ANG II- and AA-induced Akt phosphorylation. Furthermore, 5( S)-, 12( S)-, 15( S)-, and 20-hydroxyeicosatetraenoic acids and 5,6-, 11,12-, and 14,15-epoxyeicosatrienoic acids increased Akt phosphorylation. Catalase inhibited ANG II-increased H2O2 production but not Akt phosphorylation. Oleic acid, which also increased H2O2 production, did not cause Akt phosphorylation. These data suggest that ANG II-induced Akt activation in VSMC is mediated by AA metabolites, most likely generated via lipoxygenase and cytochrome P-450 consequent to AA released by CaMKII-activated cPLA2 and independent of H2O2 production.

Sodium-dependent hypertension produced by chronic central angiotensin II infusion

1985 ◽  
Vol 249 (2) ◽  
pp. H321-H327 ◽  
Author(s):  
C. A. Bruner ◽  
J. M. Weaver ◽  
G. D. Fink
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Fluid Intake ◽  
Sodium Intake ◽  
Plasma Osmolality ◽  
Plasma Aldosterone ◽  
Plasma Sodium ◽  
Ang Ii ◽  
High Sodium ◽  
Sodium Dependent

Experiments were performed to characterize the hypertension produced by chronic intracerebroventricular (ICV) infusion of angiotensin II (ANG II) in conscious rats. Infusion of ANG II into a lateral cerebral ventricle for 5 days (1 or 6 micrograms/h) produced dose-dependent increases in mean arterial pressure associated with increased water intake. No consistent changes in heart rate, urinary electrolyte excretion, or water balance were observed. Similarly, no alterations in plasma sodium and potassium concentration, plasma osmolality, or plasma ANG II levels were seen during ICV ANG II infusion. Controlling fluid intake at 40 ml/day did not alter the development of hypertension in this model. Hypertension was found to be sodium dependent, with high sodium intake augmenting the increase in arterial pressure in response to chronic ICV ANG II. Although plasma aldosterone concentrations were increased in some situations during ICV ANG II infusion, adrenalectomy failed to alter the course of hypertension. This study demonstrates that chronic selective stimulation of brain ANG II receptors by means of continuous ICV infusion of ANG II produces sodium-sensitive increases in arterial pressure associated with, but not dependent on, increased fluid intake. This form of hypertension cannot be attributed to sodium and water retention, elevations in plasma aldosterone, or leak of significant amounts of ANG II from cerebrospinal fluid into the peripheral circulation.

scholarly journals Assessing the Relationship of Angiotensin II Type 1 Receptors with Erythropoietin in a Human Model of Endogenous Angiotensin II Type 1 Receptor Antagonism

2015 ◽  
Vol 6 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Lorenzo A. Calò ◽  
Paul A. Davis ◽  
Giuseppe Maiolino ◽  
Elisa Pagnin ◽  
Verdiana Ravarotto ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Healthy Subjects ◽  
Renin Angiotensin System ◽  
Human Model ◽  
Inflammatory Factor ◽  
Ang Ii ◽  
Nadph Oxidase 4 ◽  
Relationship Of ◽  
The Relationship

Hypothesis/Introduction: Angiotensin II (Ang II) has been shown to control erythropoietin (EPO) synthesis as Ang II type 1 receptor (AT1R) blockers block Ang-II-induced EPO oversecretion. To further explore the involvement of AT1R in processes controlling EPO levels, plasma EPO and mononuclear cell NADPH oxidase 4 (NOX4) - a NOX family member involved in oxygen sensing, which is a process central to controlling EPO levels - were assessed in Bartter's/Gitelman's syndrome (BS/GS) patients, a human model of endogenous AT1R antagonism and healthy subjects. Heme oxygenase (HO)-1, antioxidant and anti-inflammatory factor related to NOX4 activation, and the relationship of EPO and NOX4 to HO-1 were also assessed. Materials and Methods: EPO was measured by chemiluminescent immunoassay, HO-1 by sandwich immunoassay and NOX4 protein expression by Western blot. Results: EPO was increased in BS/GS patients compared to healthy subjects (7.64 ± 2.47 vs. 5.23 ± 1.07 U/l; p = 0.025), whereas NOX4 did not differ between BS/GS and healthy subjects (1.76 ± 0.61 vs. 1.65 ± 0.54 densitometric units; p = n.s.), and HO-1 was increased in BS/GS patients compared to healthy subjects (9.58 ± 3.07 vs. 5.49 ± 1.04 ng/ml; p = 0.003). NOX4 positively correlated with HO-1 only in BS/GS patients; no correlation was found between EPO and either NOX4 or HO-1 in those two groups. Conclusions: The effect of the renin-angiotensin system on EPO cannot be solely mediated by Ang II via AT1R signaling, but rather, EPO levels are also determined by a complex interrelated set of signals that involve AT2R, nitric oxide levels, NOX4 and HO-1 activity.

Pulmonary Endothelial Cells / Metabolism of Vasoactive Substances

1975 ◽  
Author(s):  
J. W. Ryan ◽  
Una S. Ryan
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Angiotensin I ◽  
Clotting System ◽  
Arterial Circulation ◽  
Pulmonary Endothelial Cells ◽  
Vasoactive Substances ◽  
Metabolic Products ◽  
Relationship Of ◽  
The Relationship

The lungs metabolize a variety of vasoactive substances, including bradykinin (BK), angiotensin I (AT I), PGE2 and F2α, norepinephrine, 5-HT, 5’-ATP and 5’-AMP. In contrast, the lungs od not metabolize angiotensin II (AT II), PGA2, histamine and epinephrine. Of the substances metabolized, all (with the possible exceptions of the prostaglandins) are processed primarily by the pulmonary endothelial cells. Furthermore, the means by which the substances are processed suggest that endothelial cells determine the vasoactive substances allowed to enter the systemic arterial circulation. BK is inactivated while AT I is converted to its potent homolog, AT II. AT II enters the arterial circulation. The metabolism of BK and AT I may be effected by the same enzyme. Pulmonary endothelial cells are a rich source of thromboplastin, an enzyme capable of degrading BK and AT I. However, the relationship of thromboplastin to the fates of these hormones is not clear : The metabolic products produced are not those produced by intact lungs nor by endothelial cells in culture. In addition, thromboplastin degrades substances (e.g. AT II), which are not degraded by intact lungs. Possibly the extrinsic clotting system plays a role when activated but not under physiologic conditions.

Effect of Changes in Sodium Balance on Potassium/Aldosterone Dose-Response Curves in the Dog

1982 ◽  
Vol 62 (4) ◽  
pp. 373-380 ◽  
Author(s):  
M. G. Nicholls ◽  
M. Tree ◽  
J. H. Livesey ◽  
R. Fraser ◽  
J. J. Morton ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Depletion ◽  
Beagle Dogs ◽  
Response Curves ◽  
Dose Response Curves

1. Potassium was infused intravenously in an incremental fashion and the plasma aldosterone responses were measured in conscious beagle dogs at five different intakes of dietary sodium. 2. Potassium/aldosterone dose—response curves were constructed for each dietary sodium regimen. 3. The rate of increase of plasma potassium during graded potassium infusion became progressively greater with increasing sodium depletion. 4. Regression lines of plasma aldosterone on plasma potassium were progressively elevated and steepened with increasing sodium depletion. 5. The alteration of these dose-response curves could in part have been the result of chronic elevation of plasma potassium and angiotensin II, and depression of plasma sodium, with sodium deprivation. 6. By contrast, acute changes in plasma angiotensin II or sodium concentrations across incremental infusions of potassium did not explain the progressive changes in the potassium/aldosterone dose—response curves. 7. The steepest part of the plasma aldosterone response curve was in the plasma potassium range 4–6 mmol/l. 8. Maximum achieved aldosterone levels were similar to or greater than those attained during angiotensin II infusion in previous studies in beagle dogs. 9. Potassium, like angiotensin II and adrenocorticotropic hormone, becomes a more effective stimulus to aldosterone with sodium depletion, thereby facilitating the preservation of sodium homoeostasis.

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

Central oxytocin and ANP receptors mediate osmotic inhibition of salt appetite in rats

1995 ◽  
Vol 269 (2) ◽  
pp. R245-R251 ◽  
Author(s):  
R. E. Blackburn ◽  
W. K. Samson ◽  
R. J. Fulton ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Salt Appetite ◽  
Saline Ingestion ◽  
A Chain ◽  
Anp Receptors ◽  
Atrial Natriuretic

These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.

Ablation of subfornical organ does not prevent angiotensin-induced water drinking in sheep

1986 ◽  
Vol 250 (6) ◽  
pp. R1052-R1059 ◽  
Author(s):  
M. J. McKinley ◽  
D. A. Denton ◽  
R. G. Park ◽  
R. S. Weisinger
Keyword(s):  
Angiotensin Ii ◽  
Hypertonic Saline ◽  
Water Deprivation ◽  
Subfornical Organ ◽  
Ang Ii ◽  
Water Drinking

The subfornical organ (SFO) and surrounding periventricular tissue were ablated in sheep. Such a lesion did not significantly reduce water drinking in response to intracarotid, intravenous, or intracerebroventricular infusions of [Val5]angiotensin II amide (ANG II) but caused reduced intake of water in response to intracarotid infusion of hypertonic saline. The dipsogenic response of these sheep to water deprivation for 3 days was similar to that of normal sheep subjected to water deprivation. Although the results are not conclusive in excluding the SFO from having a role in ANG II-induced drinking, they show that there are receptors outside the SFO sensitive to blood-borne ANG II that are involved in water drinking in sheep. The results also show that tissue in the SFO or its surroundings may be involved in drinking caused by acute hypertonicity.

Effect of intravenous angiotensin II on Fos distribution and drinking behavior in rabbits

1997 ◽  
Vol 272 (5) ◽  
pp. R1515-R1524 ◽  
Author(s):  
E. Badoer ◽  
D. McKinlay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Drinking Behavior ◽  
Ventrolateral Medulla ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Solitary Tract ◽  
Cell Nuclei ◽  
Drinking Response

We investigated the effect of intravenous infusion of angiotensin II (ANG II, 40 ng.kg-1.min-1) on the distribution of Fos in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), and the medulla of the conscious rabbit. ANG II elicited significant increases in the number of Fos-positive cell nuclei in the SFO and OVLT (15- and 10-fold, respectively). Raising blood pressure with phenylephrine did not elicit Fos in these nuclei. These nuclei are believed to be responsible for the dipsogenic actions of ANG II; however, ANG II was not dipsogenic. When blood pressure was held at preinfusion levels by the coadministration of sodium nitroprus-side and ANG II, the rabbits did not drink but Fos production in the lamina terminalis was elevated. In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla (VLM). However, with the coadministration of sodium nitroprusside, there were marked increases in the NTS and VLM. The results suggest that neurons in the SFO and OVLT are either not involved in the dipsogenic pathways or there is disruption further downstream in the central pathways that would normally mediate a drinking response to ANG II.

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