Monophasic and biphasic effects of angiotensin II and III on norepinephrine uptake and release in rat adrenal medulla

1992 ◽  
Vol 70 (6) ◽  
pp. 821-825 ◽  
Author(s):  
M. S. Vatta ◽  
L. G. Bianciotti ◽  
A. S. Locatelli ◽  
M. L. Papouchado ◽  
B. E. Fernández
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Medulla ◽  
Sodium Reabsorption ◽  
Catecholamine Metabolism ◽  
Renal Tubules ◽  
Norepinephrine Release ◽  
Norepinephrine Uptake ◽  
Angiotensin Iii ◽  
Biphasic Effect ◽  
Uptake And Release

Angiotensin II and III have hypertensive effects. They induce vascular smooth muscle constriction, increase sodium reabsorption by renal tubules, stimulate the anteroventral third ventricle area, increase vasopressin and aldosterone secretions, and modify catecholamine metabolism. In this work, angiotensin II and III effects on norepinephrine uptake and release in rat adrenal medulla were investigated. Both angiotensins decreased total and neuronal norepinephrine uptake. Angiotensin II showed a biphasic effect only on evoked neuronal norepinephrine release (an earlier decrease followed by a later increase), while increasing the spontaneous norepinephrine release only after 12 min. On the other hand, angiotensin III showed a biphasic effect on evoked and spontaneous neuronal norepinephrine release. Both angiotensins altered norepinephrine distribution into intracellular stores, concentrating the amine into the granular pool and decreasing the cytosolic store. The results suggest a physiological biphasic effect of angiotensin II as well as angiotensin III that may be involved in the modulation of sympathetic activity in the rat adrenal medulla.Key words: angiotensin II, angiotensin III, norepinephrine uptake, norepinephrine release, adrenal medulla.

B and C Types Natriuretic Peptides Modify Norepinephrine Uptake and Release in the Rat Adrenal Medulla

Peptides ◽  
1997 ◽  
Vol 18 (10) ◽  
pp. 1483-1489 ◽  
Author(s):  
M.S Vatta ◽  
M.F Presas ◽  
L.G Bianciotti ◽  
M Rodriguez-Fermepin ◽  
R Ambros ◽  
...  
Keyword(s):  
Adrenal Medulla ◽  
Natriuretic Peptides ◽  
Norepinephrine Uptake ◽  
Uptake And Release

Modulation of adrenergic transmission by angiotensins in the perfused rat mesentery

1979 ◽  
Vol 236 (2) ◽  
pp. H211-H217 ◽  
Author(s):  
W. B. Campbell ◽  
E. K. Jackson
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Mesenteric Arteries ◽  
Norepinephrine Release ◽  
Sympathetic Nerve Stimulation ◽  
Rat Mesentery ◽  
Angiotensin Iii ◽  
Adrenergic Transmission ◽  
Norepinephrine Reuptake

Isolated rat mesenteric arteries perfused with a modified Krebs solution were utilized to study the effects of angiotensin II (AII), angiotensin III (AIII), and [des-Asp1-Arg2]AII on adrenergic transmission. Angiotensin II potentiated vasoconstrictor responses to both sympathetic nerve stimulation and to exogenous norepinephrine, whereas AIII and [des-Asp1-Arg2]AII potentiated vasoconstrictor responses to exogenous norepinephrine only. When the responses to exogenous norepinephrine were compared, the order of agonist potency was AIII greater than AII greater than [des-Asp1-Arg2]AII. The potentiation of sympathetic nerve stimulation by AII was inhibited by simultaneous administration of AIII (25%), [des-Asp1-Arg2]AII (51%), [Sar1-Ile8]AII (83%), and (Ile7)AIII (80%). The potentiation of exogenous norepinephrine by AII, AIII, and [des-Asp1-Arg2]AII was inhibited by [Sar1-Ile8]AII (110%, 113%, and 108%, respectively) and by [Ile7]AIII (50%, 64%, 91%, respectively). We conclude that AII possesses the capacity both to increase norpinephrine release during sympathetic nerve stimulation and to decrease norepinephrine reuptake, whereas AIII and [des-Asp1-Arg2]AII decrease norepinephrine release and reuptake. Also, under conditions of increased N-terminal degradation of AII, blockade of norepinephrine reuptake would be increased while the release of norepinephrine by nerve stimulation would be reduced.

Stimulation of renal sodium reabsorption by angiotensin II

1977 ◽  
Vol 232 (4) ◽  
pp. F298-F306 ◽  
Author(s):  
M. D. Johnson ◽  
R. L. Malvin
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Filtration Fraction ◽  
Water Diuresis ◽  
Urinary Osmolality ◽  
Anesthetized Dogs ◽  
Renal Sodium Reabsorption

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.

scholarly journals Specific receptors for des-Asp1-angiotensin II (("angiotensin III") in rat adrenals.

1977 ◽  
Vol 74 (9) ◽  
pp. 4029-4032 ◽  
Author(s):  
M. A. Devynck ◽  
M. G. Pernollet ◽  
P. G. Matthews ◽  
M. C. Khosla ◽  
F. M. Bumpus ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Iii ◽  
Rat Adrenals ◽  
Specific Receptors

scholarly journals Signaling pathways in the biphasic effect of angiotensin II on apical Na/H antiport activity in proximal tubule

1996 ◽  
Vol 50 (5) ◽  
pp. 1496-1505 ◽  
Author(s):  
Pascal Houillier ◽  
Régine Chambrey ◽  
Jean Michel Achard ◽  
Marc Froissart ◽  
Josiane Poggioli ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Signaling Pathways ◽  
Biphasic Effect

Local and Downstream Actions of Proximal Tubule Angiotensin II Signaling on Sodium Transporters in the Mouse Nephron

2021 ◽  
Author(s):  
Jonathan William Nelson ◽  
Alicia A. McDonough ◽  
Zhidan Xiang ◽  
Donna L. Ralph ◽  
Joshua A Robertson ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Renin Angiotensin System ◽  
Cell Types ◽  
Sodium Reabsorption ◽  
Electrolyte Balance ◽  
Sodium Transporters ◽  
Lower Abundance ◽  
Angiotensin Ii Signaling ◽  
Distinct Cell

The renal nephron consists of a series of distinct cell types which function in concert to maintain fluid and electrolyte balance and blood pressure. The renin angiotensin system (RAS) is central to sodium and volume balance. We aimed to determine how loss of angiotensin II signaling in the proximal tubule (PT), which reabsorbs the bulk of filtered sodium and volume, impacts solute transport throughout the nephron. We hypothesized that proximal tubule (PT) RAS disruption would not only depress PT sodium transporters, but also impact downstream Na+ transporters. Utilizing a mouse model in which the type 1a angiotensin receptor (AT1aR) is deleted specifically within the PT (AT1aR PTKO), we profiled the abundance of sodium transporters, channels, and claudins along the nephron. Absence of PT AT1aR signaling was associated with lower abundance of PT transporters (NHE3, NBCe2 and claudin 2) as well as lower abundance of downstream transporters (total and phosphorylated NKCC2, medullary Na,K-ATPase, phosphorylated NCC and claudin 7) versus controls. However, transport activities of NKCC2 and NCC (assessed with diuretics) were similar between groups in order to maintain electrolyte balance. Together, these results demonstrate the primary impact of angiotensin II regulation on sodium reabsorption in PT at baseline and the associated influence on downstream Na+ transporters, highlighting the ability of the nephron to integrate sodium transport along the nephron to maintain homeostasis.

Abstract 196: Involvement of Peroxynitrite Formation in Angiotensin II Induced Changes in Na+K+ATPase Activity in HK2 Cells

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Arpan K Maiti ◽  
Mohammed T Islam ◽  
Ryosuke Satou ◽  
Dewan S Majid
Keyword(s):  
Angiotensin Ii ◽  
Colorimetric Assay ◽  
Renin Angiotensin System ◽  
Human Kidney ◽  
Protective Role ◽  
Renal Tubules ◽  
Proximal Tubule Cell ◽  
Wide Range ◽  
Induced Changes ◽  
Hk2 Cells

Angiotensin II (AngII) induces both superoxide (O 2 - ) and nitric oxide (NO) generation forming peroxynitrite (ONOO - ) in biological systems. To determine the role of ONOO - in AngII induced sodium excretory responses, we examined Na + K + ATPase (NKA) activity in cultured HK2 cells (human kidney proximal tubule cell line) incubated for 30 min with a wide range (10 pM to 200 μM) of AngII concentrations (conc) in the presence or absence of a ONOO - scavenger, mercapto-ethyl-guanadine (MEG; 200μM). Post incubation HK2 cellular membrane fractions were used for measurement of NKA activity via colorimetric assay capable of detecting inorganic phosphate (Pi). Baseline value of NKA activity in these HK2 cells was measured as 10.3 ±0.7 μmoles of Pi liberated/mg protein/hr (n=12). AngII exerts dose-dependent differential effects on NKA activity. Compared to the baseline value, NKA activity was increased at lower conc (13.7±1.3% at 10 pM to 19.6±1.5% at 100nM) and decreased at higher conc (-6.0±0.8% at 1 μM to -38±2.1% at 200 μM ) without any significant effect at 500 nM conc (-1.2±0.6%) of AngII. Interestingly, MEG treatment markedly attenuated these AngII induced changes in NKA activity, both at lower conc (activity increased only to 7.8±0.67% at 10 pM and to 8.9±0.57% at 100nM; an average reduction of 33.2±2.4% in stimulatory effects) and at higher conc (activity decreased to -3.0±0.7% at 1 μM and to -20±0.57% at 200 μM; an average reduction of 54.4±4.1% in inhibitory effects). Co-incubation with O 2 - scavenger, tempol (1 mM) or NO synthase inhibitor, nitro-L-arginine methyl ester (100 μM) did not alter these AngII induced responses in HK2 cells indicating that neither O 2 - , nor NO, was directly involved in mediating these responses. AT 1 receptor (AT 1 R) blocker, losartan (10μM) treatment prevented these AngII induced changes on NKA activity confirming the involvement of AT 1 R signaling in these responses. These findings demonstrate a direct contributory role for concomitant ONOO - generation in mediating AngII induced changes in NKA activity in the proximal tubular cells. These data also suggest a reno-protective role for ONOO - in minimizing sodium retaining action of AngII by the renal tubules, particularly in the conditions associated with enhanced renin-angiotensin system.

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