The Renal Response to Acute Hypervolemia is Caused by Atrial Natriuretic Peptides

Hirth, C.; Jp, Stasch; John, A.; Kazda, S; Morich, F.; Neuser, D; Wohlfeil, Stefan

doi:10.1097/00005344-198603000-00008

Cited by 97 publications

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“…Atrial distension produced by elevation of atrial pressure or head-out water immersion (1), volume expansion (2)(3)(4)(5), and administration of pressor agents (1,6) lead to release of atriopeptin (AP) from the atria. Many investigators have reported that AP immunoreactivity (APir) release appears to be stimulated by atrial distension through acute volume expansion both in animals (2,3,7,8) and in humans (4)(5)(6)(7)(8)(9).…”

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confidence: 99%

“…Many investigators have reported that AP immunoreactivity (APir) release appears to be stimulated by atrial distension through acute volume expansion both in animals (2,3,7,8) and in humans (4)(5)(6)(7)(8)(9). Removal of right atrial appendages in anesthetized rats attenuated the urinary volume (UV) and urinary sodium excretion (UNaV) in response to volume expansion (10).…”

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Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Sakata

Greenwald

Needleman

1988

Proc. Natl. Acad. Sci. U.S.A.

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Surgical removal of one or both atrial appendages was employed in rats to reduce the intrinsic stores of atriopeptin (AP). In conscious rats (with intact baroreceptor reflexes), bilateral or unilateral atrial appendectomy suppressed the diuresis and natriuresis produced by acute volume expansion. Surprisingly, volume expansion (with 4% bovine serum albumin in saline at 1.5 ml/kg per min for 15 min) did not result in an increase in plasma AP immunoreactivity (APir) in control or atrial-appendectomized conscious rats. Previous studies demonstrated that acute volume expansion in anesthetized animals caused increased plasma APir. Indeed, we found that volume expansion causes comparable diuresisnatriuresis in conscious and chloral hydrate-anesthetized rats, but only the latter group exhibits an increase in plasma APir. Brattleboro rats, which are deficient in vasopressin, exhibit the same response as Long-Evans controls in that acute volume expansion in conscious animals produces a pronounced diuresis and natriuresis but no APir release, but when these same animals are anesthetized, there is a simultaneous induction of diuresis-natriuresis and APir release by volume expansion. Plasma AP does not increase in conscious rats despite a large volume load, 3040% of the total blood volume given in 15 min, and the natriuresis-diuresis appears to also be independent of vasopressin. On the other hand, the diuresis induced by acute volume expansion in anesthetized rats seems dependent on the elevated APir, since rats made autoimmune to AP (which are nonresponsive to exogenous AP infusions) exhibit a diuresis in conscious but not anesthetized rats. We therefore conclude that the participation of AP in volume homeostasis is more likely in pathophysiological states and that another mechanism or possibly another atrial factor mediates the diuresis-natriuresis induced by volume expansion in conscious rats.Atrial distension produced by elevation of atrial pressure or head-out water immersion (1), volume expansion (2-5), and administration of pressor agents (1, 6) lead to release of atriopeptin (AP) from the atria. Many investigators have reported that AP immunoreactivity (APir) release appears to be stimulated by atrial distension through acute volume expansion both in animals (2,3,7,8) and in humans (4-9). Removal of right atrial appendages in anesthetized rats attenuated the urinary volume (UV) and urinary sodium excretion (UNaV) in response to volume expansion (10).Similarly, conscious rats 2 weeks after bilateral atrial appendectomy exhibited reduced UV and UNaV during volume expansion (11 In the present study we examined the changes in plasma APir in atrial appendectomized rats. We decided to perform these experiments in conscious precannulated animals because we had observed that basal plasma APir levels were considerably higher in chloral hydrate-anesthetized animals compared to unanesthetized controls. The choice of these conditions led us to an unanticipated finding: the diuresis caused by volume expansion of conscio...

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confidence: 99%

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confidence: 99%

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Sakata

Greenwald

Needleman

1988

Proc. Natl. Acad. Sci. U.S.A.

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“…5). Hirth et al (1986) have provided evidence suggesting that ANP is of primary importance in the natriuresis of volume expansion. They have shown, in rats, that the renal response to acute volume expansion, with homologous blood transfusion, can be blocked by the addition of monoclonal antibodies to ANP.…”

Section: Discussionmentioning

confidence: 99%

“…Although increases in central blood volume produce a number of hormonal and neural reactions it has been suggested that ANP is the primary mediator of these responses. Blocking of the natriuretic response to volume expansion by monoclonal antibodies to ANP provides evidence to support this suggestion (Hirth, Stasch, John, Kazda, Morich, Neuser & Wohlfeil, 1986). On the other hand cardiac denervation, both in an animal model (Goetz, Wang, Geer, Leadley & Reinhardt, 1986; Knapp, Hicks, Linden & Mary, 1986) and in human cardiac transplant recipients (Wilkins, Gammage, Lewis, Bun Tan & Weissberg, 1988), has been shown to antagonize the natriuresis associated with atrial stretch but not to affect the ANP release, suggesting a dissociation between these two responses.…”

Section: Introductionmentioning

confidence: 90%

A comparison of head‐down tilt with low‐dose infusion of atrial natriuretic peptide in man.

Allen

Ang

Bennett

1989

The Journal of Physiology

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SUMMARY1. Procedures that increase atrial pressure, such as head-down tilt, result in an increase in plasma atrial natriuretic peptide (ANP) and a natriuresis, but a direct cause-and-effect relationship between these two responses has not been established. This study was undertaken to compare the effects of head-down tilt with exogenous ANP on renal function.2. Eight normal sodium-replete volunteers underwent a 3 h placebo infusion, a 3 h ANP infusion at 1-2 pmol kg-' min-' and a 3 h period of head-down tilt. Each procedure was performed on a separate day, in random order.3. ANP and head-down tilt produced similar increases in sodium excretion (65 + 24 and 68 + 16 %, respectively). ANP did not increase urine flow significantly more than placebo. Head-down tilt increased urine flow significantly more than placebo and ANP.4. Plasma ANP rose from 8-1 +1P0 to 11-4 + 2-5 pg ml-' during head-down tilt and from 6-5 + 1-4 to 32-3 + 107 pg ml-' with ANP infusion.5. ANP infusion had no significant effects on systemic haemodynamics whilst head-down tilt increased cardiac output and reduced heart rate and an index of systemic vascular resistance.6. ANP infusion, whilst achieving a natriuretic response similar to that of tilt, was associated with a 3-fold higher mean plasma ANP level. Although plasma ANP rose during both ANP infusion and tilt, there was a lack of correlation between natriuretic response and plasma ANP.7. The results are not compatible with a direct cause-and-effect relationship between plasma ANP and sodium excretion during head-down tilt.

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“…mediators of this homeostatic mechanism include certain neural and hormonal systems such as atrial natriuretic peptide (ANP) and dopamine (DA) (18). However, the importance of each of these substances in different physiological conditions has not been well defined.…”

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Renal effects of dopamine and ANP in high volume expanded rats

Balaszczuk

Fellet

2001

J Physiol Biochem

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A. M. BALASZCZUK and A. L. FELLET. Renal effects of dopamine and ANP in high volume expanded rats. J. Physiol. Biochem., 57 (2), [81][82][83][84][85][86][87][88] 2001.Both dopamine (DA) and atrial natriuretic peptide (ANP) have been postulated to exert similar effects on the kidney, participating in the regulation of body fluid and sodium homeostasis. In the present study, experiments were performed in anesthetized and isotonic sodium chloride volume expanded rats. After acute volume expansion at 15 % of body weight during 30 min, glomerular filtration rate, urine output, sodium excretion, fractional sodium excretion, proximal and distal sodium excretion and blood pressure were measured. In additional groups we administered ANP or haloperidol or the combination of both to volume expanded animals. Blockade of DA receptors with haloperidol, attenuated diuretic and natriuretic responses to volume load. Proximal sodium excretion was not modified by haloperidol in all experimental groups of rats. Reduction in distal tubular excretion was induced by haloperidol in saline infusion expanded rat but not in ANP treated expanded animals. In conclusion, when exaggerated volume expansion is provoked, both DA and ANP exert renal tubular events, but ANP have a major central role in the regulation of renal sodium handling.An acute increase in sodium intake produced by volume expansion with sodium chloride has shown to evoke a marked diuretic and natriuretic response (29). The mediators of this homeostatic mechanism include certain neural and hormonal systems such as atrial natriuretic peptide (ANP) and dopamine (DA) (18). However, the importance of each of these substances in different physiological conditions has not been well defined. Of particular interest is the observation that DA

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The Renal Response to Acute Hypervolemia is Caused by Atrial Natriuretic Peptides

Cited by 97 publications

References 0 publications

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

A comparison of head‐down tilt with low‐dose infusion of atrial natriuretic peptide in man.

Renal effects of dopamine and ANP in high volume expanded rats

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