Role of vasopressin in stimulation of ACTH secretion by angiotensin II in conscious dogs

1986 ◽  
Vol 251 (1) ◽  
pp. E52-E57
Author(s):  
C. K. Klingbeil ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Conscious Dogs ◽  
Ang Ii ◽  
Acth Secretion ◽  
Series Of Experiments ◽  
Stimulation Of ◽  
Acth Release

Three series of experiments were performed in conscious dogs to test the possibility that the stimulation of adrenocorticotropin (ACTH) release by angiotensin II (ANG II) is mediated by arginine vasopressin (AVP). In the first protocol, the effect of ANG II on ACTH release was studied in dogs in which endogenous AVP levels had been increased by water deprivation. Water deprivation for 24 h increased plasma AVP concentration from 3.0 +/- 0.5 to 7.7 +/- 0.5 pg/ml (P less than 0.01) and increased the AVP response to the highest dose of ANG II (20 ng X kg-1 X min-1). Despite these changes, water deprivation failed to increase the ACTH response to ANG II. Next, the contribution of endogenous AVP to the stimulation of ACTH release by ANG II was examined using the V1-receptor antagonist, d(CH2)5Tyr[Met]-AVP (10 micrograms/kg iv). The ACTH response to ANG II in the presence of the AVP antagonist (66.4 +/- 3.1 to 100.1 +/- 15.9 pg/ml) was not significantly less than that in its absence (53.0 +/- 4.8 to 72.2 +/- 11.1 pg/ml). Finally, ANG II and AVP were infused in combination to determine whether there is a synergism between these two peptides in the release of ACTH. In one protocol, AVP and ANG II were infused separately and in combination. The ACTH response to ANG II and AVP in combination (48.7 +/- 6.5 to 61.5 +/- 8.5 pg/ml) was not enhanced compared with the responses to ANG II (59.8 +/- 7.3 to 71.0 +/- 10.1 pg/ml) or AVP (48.8 +/- 5.7 to 55.6 +/- 6.5 pg/ml) alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of calcium in osmotic and nonosmotic release of vasopressin from rat organ culture

1983 ◽  
Vol 244 (5) ◽  
pp. R703-R708
Author(s):  
S. Ishikawa ◽  
R. W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Organ Culture ◽  
Arginine Vasopressin ◽  
Ionophore A23187 ◽  
Ang Ii ◽  
Ca Uptake ◽  
High Concentrations ◽  
Cellular Ca ◽  
Stimulation Of

In the present study the role of calcium (Ca) in the stimulation of arginine vasopressin (AVP) release from the cultured rat hypothalamoneurohypophyseal complex (HNC) was examined in response to three different stimuli, 56 mM potassium chloride, an increase in medium osmolality from 290 to 310 mosmol/kg H2O, or 1 X 10(-6) M angiotensin II (ANG II). With all three stimuli AVP release from rat HNC explants was enhanced by increasing Ca concentration in the medium from 0 to 1.8 mM Ca. However, high concentrations of Ca (8 mM) inhibited the response of AVP release to either hyperosmolality or angiotensin II. Chemically dissimilar blockers of cellular Ca uptake, verapamil (5.2 X 10(-6) or 5.2 X 10(-5) M) or nifedipine (5.8 X 10(-6) or 5.8 X 10(-5) M), completely abolished AVP release from rat HNC explants in response to the three different stimuli in 1.8 mM Ca. In a normal concentration of medium Ca (1.8 mM) a Ca ionophore, A23187 (3.8 X 10(-5) M), significantly enhanced the osmotic and nonosmotic (ANG II-stimulated) release of AVP from rat HNC explants compared with controls without Ca ionophore. This effect of Ca ionophore to enhance AVP release was more evident in a lower Ca medium (0.9 mM Ca in the hyperosmolality study and 0.3 mM Ca in the ANG II study). These results therefore indicate that cellular Ca uptake is an important modulator of osmotic and nonosmotic AVP release from the intact rat hypothalamoneurohypophyseal system. The influence of extracellular Ca on the osmotic and nonosmotic release of AVP is also demonstrated.

Effects of CRF and ANG II on ACTH and vasopressin release in conscious dogs

1988 ◽  
Vol 255 (1) ◽  
pp. E46-E53 ◽  
Author(s):  
C. K. Klingbeil ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Conscious Dogs ◽  
Ang Ii ◽  
Plasma Acth ◽  
Vasopressin Release ◽  
Intravenous Saline ◽  
Acth Concentration ◽  
Dose Dependent ◽  
Stimulation Of ◽  
Acth Release

The aim of the present study was to examine the effects of corticotropin-releasing factor (CRF) in conscious dogs and to determine whether the stimulation of adrenocorticotropic hormone (ACTH) release by angiotensin II (ANG II) results from potentiation of the action of CRF. In addition, the possible role of CRF in the stimulation of vasopressin released by ANG II was investigated. The following experiments were performed: 1) intravenous saline infusion; 2) ANG II (10 ng.kg-1.min-1) alone; 3) vasopressin (1 ng.kg-1.min-1) alone; 4) CRF (0.001, 0.01, or 0.1 microgram/kg iv) bolus; 5) vasopressin (1 ng.kg-1.min-1) and CRF (0.1 microgram/kg) together; 6) CRF (0.001, 0.01, or 0.1 microgram/kg) and ANG II (10 ng.kg-1.min-1) together; 7) ANG II (10 ng.kg-1.min-1) followed 15 min later with CRF (0.001, 0.01, or 0.1 microgram/kg). Each dose of CRF was tested on a different day. Infusion of ANG II alone stimulated the release of ACTH, cortisol, and vasopressin. Administration of CRF produced dose-dependent increases in plasma ACTH and cortisol concentrations, and the highest dose of CRF increased plasma vasopressin concentration. CRF given together with ANG II did not potentiate the stimulation of ACTH release by CRF. Vasopressin at the dose tested did not stimulate ACTH release but potentiated the ACTH response to CRF. ANG II stimulated vasopressin release but did not potentiate the AVP response to CRF. These results show that, in conscious dogs, ANG II and CRF each increase plasma ACTH concentration and that the ACTH response to CRF is potentiated by vasopressin but not by ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Reactive Oxygen Species-Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor Mrna by Angiotensin II

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 688-688
Author(s):  
Toshihiro Ichiki ◽  
Kotaro Takeda ◽  
Akira Takeshita
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Mrna Expression ◽  
Crucial Role ◽  
Oxygen Species ◽  
Ang Ii ◽  
Stimulation Of

58 Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of Angiotensin II (Ang II) through type 1 Ang II receptor (AT1-R). However, the role of ROS in the regulation of AT1-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT1-R by Ang II. Ang II (10 -6 mol/L) decreased AT1-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells (VSMC). Ang II dose-dependently (10 -8 -10 -6 ) suppressed AT1-R mRNA at 6 hours of stimulation. Preincubation of VSMC with N-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT1-R mRNA. The effect of NAC was due to stabilization of the AT1-R mRNA that was destabilized by Ang II. Ang II did not affect the promoter activity of AT1-R gene. Diphenylene iodonium (DPI), an inhibitor of NADH/NADPH oxidase failed to inhibit the Ang II-induced AT1-R mRNA downregulation. The Ang II-induced AT1-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as PD98059 whereas DPI did not inhibit it. To confirm the role of ROS in the regulation of AT1-R mRNA expression, VSMC were stimulated with H 2 O 2 . H 2 O 2 suppressed the AT1-R mRNA expression and activated ERK. These results suggest that production of ROS and activation of ERK are critical for downregulation of AT1-R mRNA. The differential effect of NAC and DPI on the downregulation of AT1-R mRNA may suggest the presence of other sources than NADH/NADPH oxidase pathway for ROS in Ang II signaling. Generation of ROS through stimulation of AT1-R not only mediates signaling of Ang II but may play a crucial role in the adaptation process of AT1-R to the sustained stimulation of Ang II.

Evidence that centrally released arginine vasopressin is involved in central pressor action of angiotensin II

1996 ◽  
Vol 270 (1) ◽  
pp. H167-H173 ◽  
Author(s):  
S. Lon ◽  
E. Szczepanska-Sadowska ◽  
M. Szczypaczewska
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Ang Ii ◽  
Central Administration ◽  
Hypotensive Action ◽  
Series Of Experiments

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.

Central angiotensin II stimulation of ovine fetal swallowing

1994 ◽  
Vol 76 (3) ◽  
pp. 1340-1345 ◽  
Author(s):  
M. G. Ross ◽  
L. K. Kullama ◽  
A. Ogundipe ◽  
K. Chan ◽  
M. G. Ervin
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Low Voltage ◽  
Control Period ◽  
Late Gestation ◽  
Ang Ii ◽  
Fetal Plasma ◽  
Plasma Arginine ◽  
Ovine Fetal ◽  
Stimulation Of

In the late-gestation ovine fetus, spontaneous swallowing occurs primarily during fetal low-voltage electrocortical (ECoG) activity in association with fetal breathing movements. Fetal swallowing activity may be stimulated in response to systemic or carotid plasma hyperosmolality, although not to increased plasma angiotensin II (ANG II) levels. In view of the potent dipsogenic effects of central, but not peripheral, ANG II in adult sheep, the present study investigated the effect of intracerebroventricular (ICV) ANG II on fetal swallowing activity. Six ovine fetuses (127 +/- 1 days) were chronically prepared with electromyogram and cortical electrodes and with vascular and lateral ventricle catheters. After a 2-h control period, fetuses received ICV injections of artificial cerebrospinal fluid and increasing concentrations of ANG II (0.1, 1.0, 10, 100, and 500 ng/kg). Fetal ECoG activity did not change, although fetal swallowing activity significantly increased in response to the 100- and 500- ng/kg ANG II doses (1.20 +/- 0.14 to 3.34 +/- 0.59 and 3.46 +/- 0.81 swallows/min of low-voltage ECoG, respectively). In response to the highest ANG II dose, fetal plasma arginine vasopressin levels significantly increased (5.7 +/- 1.2 to 17.2 +/- 4.6 pg/ml). ICV ANG II stimulation of fetal swallowing and arginine vasopressin secretion demonstrates that central ANG II dipsogenic mechanisms are intact by 0.9 of ovine gestation.

Role of periaqueductal gray in the pressor response produced by central injections of angiotensin II

1993 ◽  
Vol 265 (5) ◽  
pp. R1052-R1059
Author(s):  
L. R. Portis ◽  
S. J. Lewis ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Angiotensin Ii ◽  
Fluorescent Dyes ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Ang Ii ◽  
Hemodynamic Responses ◽  
Anesthetized Rats ◽  
Stimulation Of

The present studies were undertaken to determine the role of rostral periaqueductal gray (PAG) in mediating the pressor effect produced by intracerebroventricular (icv) injection of angiotensin II (ANG II, 200 ng). Two functionally and anatomically distinct sites were identified in rostral PAG: a dorsomedial site involved in the hemodynamic responses produced by electrical stimulation of the anteroventral third ventricle (AV3V) region and a ventromedial site required for the pressor response elicited by icv administration of ANG II. In Saffan-anesthetized rats, injection of lidocaine (LIDO, 4%) in dorsomedial PAG, but not in ventromedial PAG, significantly attenuated the decrease in hindquarter resistance (HQR) produced by electrical stimulation of the AV3V region, and the poststimulatory increase in mean arterial pressure (MAP) and HQR. The injection of LIDO in ventromedial PAG had no effect on the hemodynamic responses produced by electrical stimulation of the AV3V region in anesthetized rats but significantly attenuated the pressor response produced by icv administration of ANG II in conscious rats. The hypothesis that these two sites receive separate projections was addressed by microinjecting two retrogradely transported fluorescent dyes, Fluoro-Gold and Fast Blue. The anatomic findings suggest that separation of the pathways activated by electrical and chemical stimulation of the AV3V region occurs at the level of rostral PAG.

scholarly journals Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells

2015 ◽  
Vol 308 (7) ◽  
pp. F720-F727 ◽  
Author(s):  
Benjamin Ko ◽  
Abinash Mistry ◽  
Lauren Hanson ◽  
Rickta Mallick ◽  
Robert S. Hoover
Keyword(s):  
Angiotensin Ii ◽  
Cell Model ◽  
Surface Protein ◽  
Early Time ◽  
Dependent Manner ◽  
Ang Ii ◽  
Biphasic Effect ◽  
Surface Protein Expression ◽  
Stimulation Of

Angiotensin II (ANG II) increases thiazide-sensitive sodium-chloride cotransporter (NCC) activity both acutely and chronically. ANG II has been implicated as a switch that turns WNK4 from an inhibitor of NCC into an activator of NCC, and ANG II's effect on NCC appears to require WNK4. Chronically, ANG II stimulation of NCC results in an increase in total and phosphorylated NCC, but the role of NCC phosphorylation in acute ANG II actions is unclear. Here, using a mammalian cell model with robust native NCC activity, we corroborate the role that ANG II plays in WNK4 regulation and clarify the role of Ste20-related proline alanine-rich kinase (SPAK)-induced NCC phosphorylation in ANG II action. ANG II was noted to have a biphasic effect on NCC, with a peak increase in NCC activity in the physiologic range of 10−11 M ANG II. This effect was apparent as early as 15 min and remained sustained through 120 min. These changes correlated with significant increases in NCC surface protein expression. Knockdown of WNK4 expression sharply attenuated the effect of ANG II. SPAK knockdown did not affect ANG II action at early time points (15 and 30 min), but it did attenuate the response at 60 min. Correspondingly, NCC phosphorylation did not increase at 15 or 30 min, but increased significantly at 60 min. We therefore conclude that within minutes of an increase in ANG II, NCC is rapidly trafficked to the cell surface in a phosphorylation-independent but WNK4-dependent manner. Then, after 60 min, ANG II induces SPAK-dependent phosphorylation of NCC.

Analysis of the actions of angiotensin on the central nervous system of conscious dogs

1982 ◽  
Vol 243 (1) ◽  
pp. R82-R91 ◽  
Author(s):  
I. A. Reid ◽  
V. L. Brooks ◽  
C. D. Rudolph ◽  
L. C. Keil
Keyword(s):  
Heart Rate ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Ang Ii ◽  
Acth Secretion ◽  
Vertebral Arteries ◽  
The Central Nervous System ◽  
Series Of Experiments ◽  
The Brain ◽  
Corticosteroid Secretion

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.

Role of angiotensin II, alpha-adrenergic system, and arginine vasopressin on arterial pressure in rat

1984 ◽  
Vol 246 (1) ◽  
pp. H25-H30 ◽  
Author(s):  
M. S. Paller ◽  
S. L. Linas
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Adrenergic Receptor ◽  
Enzyme Inhibitor ◽  
Adrenergic System ◽  
Ang Ii ◽  
Conscious Rat ◽  
Profound Hypotension

Three pressor systems regulate arterial pressure (MAP): angiotensin II (ANG II), the alpha-adrenergic system, and arginine vasopressin (AVP). In this study we determined the ability of each system to support MAP in the conscious rat when the other two systems were inactivated. After administration of the converting-enzyme inhibitor teprotide (CEI) and the alpha-adrenergic receptor antagonist phenoxybenzamine (POB), MAP decreased 40% as a result of a 45% decrease in peripheral vascular resistance (PVR). Despite hypotension, plasma AVP levels were not increased, and an AVP pressor antagonist (AVP-A) did not result in a further decrease in MAP. Thus the profound hypotension after POB plus CEI was the result of inhibition of all three systems. POB, rather than CEI, prevented AVP release since following hypotensive hemorrhage, plasma levels reached 51 +/- 13 pg/ml with CEI but only 4.7 +/- 0.8 pg/ml with POB. To study the pressor effect of AVP alone, AVP was infused in POB plus CEI-treated rats. AVP increased MAP (from 68 +/- 4 to 92 +/- 5 mmHg; P less than 0.005) and plasma AVP (to 13.8 +/- 1.9 pg/ml). Since POB inhibited both the AVP and the alpha-adrenergic system, the role of ANG II alone was determined in POB-treated rats. In the presence of ANG II MAP was 97 +/- 1 mmHg. To study the alpha-adrenergic system, MAP was determined in CEI plus AVP-A-treated rats. In the presence of an intact alpha-adrenergic system MAP was 101 +/- 1 mmHg. We conclude that PVR and MAP are profoundly decreased in the absence of all three pressor systems.(ABSTRACT TRUNCATED AT 250 WORDS)

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