Effects of angiotensin II and atrial natriuretic peptide alone and in combination on urinary water and electrolyte excretion in man

1988 ◽  
Vol 74 (4) ◽  
pp. 419-425 ◽  
Author(s):  
J. McMurray ◽  
A. D. Struthers
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Normal Male ◽  
Urinary Flow ◽  
Ang Ii ◽  
Electrolyte Excretion ◽  
Water Excretion ◽  
Background Infusion ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide (ANP) has previously been shown to inhibit the renin–angiotensin–aldosterone system (RAAS) at several different levels. We have now investigated a further non-endocrine, renal interaction between ANP and the RAAS. 2. The effects of ANP and angiotensin II (ANG II) alone, and in combination, on urinary electrolyte and water excretion were studied in eight normal male subjects undergoing maximal water diuresis. 3. ANP caused a significant increase in urine flow and sodium excretion. ANG II alone was antidiuretic, antinatriuretic and antikaliuretic. When ANP was given against a background infusion of ANG II, urinary flow rate and electrolyte excretion increased from a new lower level to reach a value intermediate between that found with ANG II alone and ANP alone. 4. It is concluded that the renal effects of ANP are modified in the presence of simultaneously elevated levels of ANG II and that net water and electrolyte excretion reflect the sum of the opposing influences of each peptide. While this interplay may be non-specific, it is possible that ANP may exert some of its actions by specifically inhibiting the intrarenal effects of ANG II.

scholarly journals Extrarenal resistance to atrial natriuretic peptide in rats with experimental nephrotic syndrome

1998 ◽  
Vol 274 (3) ◽  
pp. F556-F563
Author(s):  
Jean-Pierre Valentin ◽  
Wei-Zhong Ying ◽  
William G. Couser ◽  
Michael H. Humphreys
Keyword(s):  
Nephrotic Syndrome ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Fluid Distribution ◽  
Ang Ii ◽  
Hypotensive Action ◽  
Heymann Nephritis ◽  
Atrial Natriuretic

Nephrotic syndrome is associated with resistance to the renal actions of atrial natriuretic peptide (ANP). We performed experiments in anesthetized, acutely nephrectomized rats 21–28 days after injection of adriamycin (7–8 mg/kg iv) or 9–14 days after injection of anti-Fx1A antiserum (5 ml/kg ip) (passive Heymann nephritis; PHN) to test whether extrarenal resistance also occurred. Proteinuria was significantly elevated in both models compared with controls before study. ANP infusion (1 μg ⋅ kg−1 ⋅ min−1) caused arterial pressure to decrease similarly in control rats, adriamycin-treated rats, and rats with PHN (by 8.2 ± 1.0, 9.4 ± 2.3, and 9.0 ± 2.0%, respectively; all P < 0.05 vs. both baseline and vehicle-infused control rats). In control rats, hematocrit increased progressively to a maximal value 9.5 ± 0.9% over baseline as a result of the infusion, an increase corresponding to a reduction in plasma volume of 16.1 ± 0.9%. The ANP-induced increase in hematocrit was preserved in adriamycin-treated rats (9.2 ± 1.3%) but was markedly blunted in rats with PHN (2.4 ± 1.3%; P < 0.0001 vs. ANP infusion in control rats). ANP infusion increased plasma ANP levels to the same extent in the three groups, whereas plasma guanosine 3′,5′-cyclic monophosphate was significantly lower in rats with PHN compared with both control and adriamycin-treated rats. Infusion of a subpressor dose of angiotensin II (ANG II, 2.5 ng ⋅ kg−1 ⋅ min−1) fully restored the ANP-induced increase in hematocrit in rats with PHN. This study demonstrates that 1) the hemoconcentrating and hypotensive actions of ANP are preserved in adriamycin-treated rats, 2) the effect of ANP on hematocrit and fluid distribution is blunted in rats with PHN while its hypotensive action is preserved, and 3) low-level ANG II infusion normalizes the hemoconcentrating effect of exogenously infused ANP in rats with PHN. Thus deficient ANG II generation in rats with PHN, but not adriamycin nephrosis, may contribute to extrarenal ANP resistance.

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

2011 ◽  
Vol 300 (3) ◽  
pp. R624-R629 ◽  
Author(s):  
Toshiyoshi Matsukawa ◽  
Takenori Miyamoto
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Intravenous Infusion ◽  
Ang Ii ◽  
Blood Pressure Elevation ◽  
Arterial Blood ◽  
Atrial Natriuretic

We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg−1·min−1) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg−1·min−1) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure and central venous pressure (CVP). Because the elevation in blood pressure could have potentially inhibited AVP secretion via baroreceptor reflexes, the effect of ANG II on blood pressure was attenuated by the simultaneous infusion of nitroprusside. ANG II alone produced a remarkable increase in plasma AVP levels when infused with nitroprusside, whereas the simultaneous ANP intravenous infusion (10 ng·kg−1·min−1) abolished the increase in plasma AVP levels induced by ANG II when blood pressure elevation was attenuated by nitroprusside. Thus, ANG II increased AVP secretion and ANP inhibited not only basal AVP secretion but also ANG II-stimulated AVP secretion in humans. These findings support the hypothesis that circulating ANP modulates AVP secretion, in part, by antagonizing the action of circulating ANG II.

scholarly journals Angiotensin II-induced proliferation of cultured murine mesangial cells: inhibitory role of atrial natriuretic peptide.

1992 ◽  
Vol 3 (6) ◽  
pp. 1270-1278
Author(s):  
G Wolf ◽  
F Thaiss ◽  
W Schoeppe ◽  
R A Stahl
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mesangial Cell ◽  
Nuclear Antigen ◽  
Ang Ii ◽  
Cyclic Monophosphate ◽  
Intracellular Cgmp ◽  
Atrial Natriuretic

Angiotensin II (ANG II), as a single factor, induces proliferation in a cultured murine mesangial cell line (MMC). This study was undertaken to evaluate a possible influence of atrial natriuretic peptide (ANP) on this ANG II-induced proliferation. ANP (10(-7) M) for 2 min significantly increased intracellular cGMP levels in MMC. This increase in cGMP was totally abolished when cells were preincubated for 5 min with 10(-7) M ANG II. Stimulation of intracellular cGMP formation by sodium nitroprusside was also decreased in the presence of ANG II. The ANG II-mediated inhibition of ANP-stimulated intracellular cGMP levels was blocked by Dupont 753, suggesting signal transduction through ANG II receptors of the AT1 class. ANP (10(-7) M) for 24 h completely abolished the ANG II-induced proliferation in MMC. However, 10(-7) M ANP had no significant effect on mitogenesis induced by platelet-derived growth factor or epidermal growth factor. Furthermore, ANP reduced the ANG II-stimulated expression of the proliferating cell nuclear antigen, a cofactor of polymerase delta that is active in the S-phase of the cell cycle. The addition of 10(-3) M N-monobutyryl-guanosine 3':5'-cyclic monophosphate or 8-bromo-guanosine 3':5'-cyclic monophosphate also blocked the ANG II-induced proliferation. ANP (10(-7)) M for 24 h had no significant influence on the expression (number and dissociation constant) of ANG II receptors as determined by binding assays. These results suggest that, besides the previously shown vasoconstrictive and vasodilating effects, complex interactions between ANG II and ANP exist that can modulate mesangial cell growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic and osmotic responses to atrial natriuretic peptide and angiotensin II in the duck (Anas platyrhynchos)

1987 ◽  
Vol 65 (9) ◽  
pp. 1995-1999 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Anas Platyrhynchos ◽  
Plasma Norepinephrine ◽  
Osmotic Regulation ◽  
Ang Ii ◽  
Salt Glands ◽  
Diuretic Response ◽  
Atrial Natriuretic

There is evidence that analogues of atrial natriuretic peptide (ANP) and angiotensin II (ANG II) occur in birds. The present experiments studied the adrenergic and osmoregulatory responses to synthetic ANP and ANG II in salt-loaded ducks (Anas platyrhynchos). Excretion of water and salt through the nasal salt glands was abolished by ANG II. This extrarenal, salt-retaining effect of ANG II was not altered by ANP. However, ANP did augment the diuretic response to ANG II. ANP also potentiated the stimulatory effect of ANG II on plasma norepinephrine. The data are consistent with physiological roles for native analogues of ANP and ANG II in adrenergic and osmotic regulation in the duck.

Receptors for Arg8-vasopressin, angiotensin II, and atrial natriuretic peptide in the mesenteric vasculature of pregnant rats

1991 ◽  
Vol 69 (2) ◽  
pp. 137-144 ◽  
Author(s):  
Angèle Parent ◽  
Ernesto L. Schiffrin ◽  
Jean St-Louis
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ang Ii ◽  
Receptor Density ◽  
Pregnant Rats ◽  
Receptor Kinetics ◽  
Vasoactive Peptides ◽  
Mesenteric Vascular Bed ◽  
Atrial Natriuretic

Blood pressure and sensitivity of blood vessels to vasoconstrictors are decreased in term-pregnant rats (20–21 days). To determine if changes in receptors for vasoactive peptides could account for these observations, receptor kinetics were measured for Arg8-vasopressin (AVP), angiotensin II (Ang II), and atrial natriuretic peptide (ANP) in the mesenteric vascular bed of the rat throughout pregnancy. Receptors for AVP were statistically similar in the five groups of animals (nonpregnant; pregnant 9, 15, and 21 days; and postpartum). The dissociation constant (KD) for [3H]AVP varied from 0.41 to 0.52 nmol/L (NS), while receptor density (Bmax) varied from 310 ± 110 to 455 ± 135 fmol/mg protein for six experimental measurements. Similar observations were made for Ang II receptors where KD of 125I-labelled Sar1, Ile8-Ang II was between 0.60 and 0.97 nmol/L and Bmax between 215 ± 30 and 250 ± 40 fmol/mg protein in the different groups. 125I-labelled ANP (101–126) receptors were markedly modified in terms of number of sites. Bmax was significantly increased during pregnancy (9 days, 429 ± 86; 15 days, 541 ± 54; 20 days, 438 ± 72) and decreased in the postpartum period (133 ± 21) by comparison with the nonpregnant group (245 ± 35 fmol/mg protein), while KD was similar in the different experimental groups (57 to 82 pmol/L). Despite these increases in receptor density, the vasorelaxant effects of ANP was only increased at 9 days of pregnancy. These results indicate that receptors for vasoconstrictor peptides (AVP and Ang II) are not altered during pregnancy and that receptor homospecific downregulation does not explain the decrease in sensitivity to vasoconstrictors at the end of pregnancy in the rat. Receptors for ANP are, however, markedly increased in number, but this did not result in an increase in the vascular action of the peptide throughout pregnancy.Key words: pregnancy, receptors, angiotensin, vasopressin, atrial natriuretic peptide.

scholarly journals Protein kinase C-dependent prostaglandin production mediates angiotensin II-induced atrial-natriuretic peptide release

1994 ◽  
Vol 298 (2) ◽  
pp. 451-456 ◽  
Author(s):  
D J Church ◽  
S Braconi ◽  
V van der Bent ◽  
M B Vallotton ◽  
U Lang
Keyword(s):  
Protein Kinase C ◽  
Angiotensin Ii ◽  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ang Ii ◽  
Rat Cardiomyocytes ◽  
Kinase C ◽  
Alpha Production ◽  
Atrial Natriuretic

The respective roles of protein kinase C (PKC) and endogenous prostaglandin formation in angiotensin II (Ang II)-induced myocardial secretion of atrial natriuretic peptide (ANP) was studied in cultured, spontaneously beating, neonatal-rat cardiomyocytes. Incubation of cardiomyocytes with 0.1 microM Ang II led to a rapid but transient increase in particulate-bound PKC activity, a response accompanied by marked increases in cellular 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) generation and ANP secretion. A role for PKC in Ang II-induced 6-oxo-PGF1 alpha formation and ANP secretion was apparent, insofar as both responses were suppressed in the presence of the PKC inhibitors staurosporine (1 microM) and CGP 41251 (1 microM), as well as in cells in which PKC had been previously down-regulated by pretreatment with phorbol diester. Furthermore, Ang II-induced 6-oxo-PGF1 alpha production was found to be strongly correlated with Ang II-induced ANP release (r = 0.87, P < 0.001, n = 6), indicating a role for prostacyclin (PGI2) in Ang II-induced ANP secretion in these cells. This hypothesis was confirmed by finding that both Ang II-induced 6-oxo-PGF1 alpha production and ANP release were abolished in the presence of the respective phospholipase A2 and cyclo-oxygenase inhibitors quinacrine (10 microM) and indomethacin (10 microM), whereas exogenously applied PGI2 (1 microM) and prostaglandin E2 (0.1 microM) mimicked Ang II-induced ANP secretion in this system. Taken together, these results suggest that Ang II induces ANP secretion in spontaneously beating rat cardiomyocytes via a PKC-dependent autocrine pathway involving a cyclo-oxygenase product and a yet-to-be-identified myocardial prostanoid receptor.

Effects of homologous atrial natriuretic peptide on drinking and plasma ANG II level in eels

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Drinking Rate ◽  
Plasma Sodium Concentration ◽  
Atrial Natriuretic

The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.

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