Effect of Atrial Natriuretic Peptide on the Vasopressin Response to Osmotic and Hemorrhagic Stimuli in Dogs

Inoue, Minoru; Kimura, Tokihisa; Ota, Kozo; Miyake, Shoji; Sato, Kazutoshi; Ohta, Makoto; Yamamoto, Takeki; Yoshinaga, Kaoru

doi:10.1111/j.1365-2826.1990.tb00658.x

Cited by 6 publications

(2 citation statements)

References 32 publications

(26 reference statements)

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“…Moreover, there are interactions between AVP and ANH release: AVP enhances ANH release, while ANH attenuates AVP release (10,11). However, the release of AVP and ANH and their interaction in renal water and electrolyte metabolism during the condition of chronic mineralocorticoid excess remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism

Kimura

Yamamoto²,

Ohta³

et al. 1997

European Journal of Endocrinology

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The release of arginine vasopressin (AVP) and atrial natriuretic hormone (ANH) and their involvement in renal water and electrolyte metabolism in primary aldosteronism in humans were studied. An oral acute water load (20 ml/kg body weight) was given to each of 12 patients before and after surgical removal of their aldosterone-producing adenoma(s). Plasma AVP and ANH were measured simultaneously, and renal water and electrolyte metabolism and tubular functions were determined. The same water load was given to seven normal subjects and the same parameters were determined. In the presence of mineralocorticoid excess before the operation, plasma AVP was relatively low compared with plasma osmolality (Posm), but was not suppressed in response to decreases in Posm after the water load. Baseline plasma ANH was high and increased further after the water load; urinary dilution and diuresis both remained normal. After the operation, baseline plasma AVP was normal and decreased in response to the decrease in Posm after the water load, with normal urinary dilution and diuresis. Baseline plasma ANH was normal, and did not increase after the water load. The ratio of urinary K and Na clearances and distal tubular reabsorption of Na increased before the operation. These results suggest that there are perturbations of AVP and ANH release in primary aldosteronism, despite the normal urinary dilution after a water load. European Journal of Endocrinology 137 154-161

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Section: Introductionmentioning

confidence: 99%

Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism

Kimura

Yamamoto²,

Ohta³

et al. 1997

European Journal of Endocrinology

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“…Therefore, it is possible that increased plasma ANH may take part in the suppression of AVP release in response to changes in plasma osmolality within the physiological range because increased blood pressure, which activates the baroreceptor reflex leading to the attenuation of AVP release, was not observed in dextran hypertonic saline administration. Moreover, Inoue et al (20) from our laboratory reported that increases in plasma ANH, produced by exogenous administration of ANH, of more than 233 pmol/1 attenuated the AVP response to hypertonic saline in dogs. In fact, in the present study, real increases in plasma ANH in the 9% dextranhypertonic saline group are in almost the same range as previously reported values (233 pmol/1).…”

Section: Discussionmentioning

confidence: 77%

Role of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion

Sato

Kimura²,

Ota³

et al. 1993

Acta Endocrinologica

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of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion. Acta Endocrinol 1993:129:65-74. ISSN 0001-5598To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume receptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volume expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran (9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/l NaCI alone was administered. Plasma AVP and ANH and cardiovascular and renal functions were determined.Hypertonic saline and 9D-HS also were administered into the vagotomized and sham operated dogs, and the same parameters were determined. Mean blood pressure and heart rate never changed in all the groups, but central venous pressure and plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increased slightly but plasma volume never changed. Plasma AVP increased in the order of hypertonic saline, 6D-HS and 9D\ x=req-\ HS, but plasma ANH increased in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma ANH. Urine sodium and potassium excretion and urine flow increased in hypertonic saline, 6D-HS and 9D-HS groups, but these increases were comparable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an effect on the suppression of the AVP response to osmotic stimuli, and increased plasma ANH release never potentiated the natriuresis under the hypertonic plasma volume expansion.It is well known that arginine vasopressin (AVP) plays an essential role in the regulation of body fluid metab¬ olism. The release of AVP is mainly regulated by the osmoreceptor, atrial volume receptor and aortic and carotid baroreceptors. Namely, a rise in plasma osmolality stimulates AVP release, but increased blood volume suppresses AVP release via the volume receptor and/or baroreceptor reflexes, which act via the afferent vagal and glossopharyngeal nerves (1-5). On the other hand, atrial natriuretic hormone (ANH), known to increase in response to the atrial stretch by the blood volume expansion (6), has been documented to interfere with AVP release (7-12) and AVP to stimulate ANH release (13-15).Thus, it is likely that the blood volume expansion may attenuate the AVP response to osmotic stimuli via both the volume receptor reflex and the increased plasma ANH. However, little is known about the mutual relationship between endogenous ANH release and the volume receptor reflex on AVP release under the hypertonic blood v...

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Natriuretic Peptide Receptors (NPRs) as a Potential Target for the Treatment of Heart Failure

Bekele

2023

Curr Heart Fail Rep

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Effect of Atrial Natriuretic Peptide on the Vasopressin Response to Osmotic and Hemorrhagic Stimuli in Dogs

Cited by 6 publications

References 32 publications

Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism

Impaired vasopressin suppression and enhanced atrial natriuretic hormone release following an acute water load in primary aldosteronism

Role of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion

Natriuretic Peptide Receptors (NPRs) as a Potential Target for the Treatment of Heart Failure

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