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

Abstract

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...

Effect of Bilateral Atrial Appendectomy on Postprandial Sodium Excretion in Conscious Monkeys

“…If this is the case, then ATX may have attenuated the release of this factor. This hypothesis is supported by other investigations (10,27,28). Cowley et al (27,28) found that ANF did not increase after acute saline expansion and that bilateral atrial resection attenuated the increase in sodium excretion.…”

“…They concluded that an unidentified factor, with diuretic and natriuretic capabilities, is released after volume expansion, and that the release of this factor is removed by atrial resection. Sakata et al (10) carried out a similar experiment in conscious rats and demonstrated that ATX attenuated volume expansion-induced increases in sodium excretion. Volume expansion also did not increase ANF in these animals.…”

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

“…The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion. serotonin; natriuresis; atrial natriuretic peptide; oxytocin; vasopressin ISOTONIC BLOOD VOLUME expansion, by reflex mechanisms, induces a series of regulatory responses, including the inhibition of the sympathetic outflow to the kidney, heart, and blood vessels, reduction of renin and vasopressin (VP) secretion, and increase in the levels of circulating atrial natriuretic peptide (ANP) and oxytocin (OT) that leads to diuresis and natriuresis (1,2,12,14,20,24,45,53).There are several reports demonstrating the correlation between natriuresis and diuresis and plasma ANP levels in response to systemic volume expansion, e.g., atrial balloon inflation, blood volume expansion, salt load, and water immersion (4,7,17,32,50,59). These responses depend on the activation of sinoaortic baroreceptors and/or cardiopulmonary receptor afferents located in the atria, lungs, great veins, and ventricles that project to the nucleus of the solitary tract (NTS) (1, 12, 22).…”

“…There are several reports demonstrating the correlation between natriuresis and diuresis and plasma ANP levels in response to systemic volume expansion, e.g., atrial balloon inflation, blood volume expansion, salt load, and water immersion (4,7,17,32,50,59). These responses depend on the activation of sinoaortic baroreceptors and/or cardiopulmonary receptor afferents located in the atria, lungs, great veins, and ventricles that project to the nucleus of the solitary tract (NTS) (1, 12, 22).…”

Metoclopramide Does Not Affect Renal Function and Atrial Natriuretic Peptide Release in Response to Acute Saline Loading in Conscious Rats

“…Although the role of ANP in the natriuresis ofisoncotic ECFV expansion in the conscious rat is still controversial [41], most data are in favor of its role in the natriuresis following ECFV expansion [for ref., see 15], Whatever its role in fluid expansion may be, our present data also exclude DA as mediator of ANP secretion or of a renal action of ANP via DA-2 receptors during acute ECFV expansion.…”