Arginine Vasopressin Infusion Increases Plasma Levels of Atrial Natriuretic Factor in Humans

Cases, A; Muñoz, Isabel; Jiménez, Wladimiro; Sanz, Ginés; Revert, L; Rivera-Fillat, Francisca

doi:10.1055/s-2007-1003274

Cited by 4 publications

(2 citation statements)

References 9 publications

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“…The possible candidate for the interaction would be norepinephrine (4), as in the case of PGE2. However, whether AVP would release catecholamines from the sympathetic nerve endings has been controversial (17), and therefore the interaction with catecholamines does not definitely seem, at least now, to be a possible explanation for the action of AVP on FBM and LVF activity. Another candidate with which AVP inhibits FBM is ACTH.…”

Section: Discussionmentioning

confidence: 99%

Effect of arginine vasopressin on breathing movements of chronically instrumented fetal lambs

Bessho

Murata

Ninomiya

et al. 1997

Acta Obstet Gynecol Scand

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Section: Discussionmentioning

confidence: 99%

Effect of arginine vasopressin on breathing movements of chronically instrumented fetal lambs

Bessho

Murata

Ninomiya

et al. 1997

Acta Obstet Gynecol Scand

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“…Indeed, ANP reportedly inhibits the secretion (Samson, 1985) and action (Dillingham & Anderson, 1986) of vasopressin, though in an in vitro study synthetic atrial natriuretic peptide induced release of arginine vasopressin from the isolated posterior lobe of the rat hypophysis (Januszewicz, Gutkowska, De Lean, Thibault, Garcia, Genest & Cantin, 1985). It has been shown that AVP Sanz, Revert & Rivera-Fillat, 1992) and in anaesthetized rats stimulates the release of ANP (Manning, Schwartz, Katsube, Holmberg & Needleman, 1985). Morris, Cain & Chalmers (1987) have also reported that reciprocal changes in plasma ANP and AVP concentrations occur in response to volume expansion and haemorrhage in conscious stroke-prone spontaneously hypertensive rats, spontaneously hypertensive rats and normotensive Wistar-Kyoto rats.…”

Section: Introductionmentioning

confidence: 99%

Renal, endocrine and vascular effects of atrial natriuretic peptide in a novel vasopressin‐deficient genetically hypertensive strain of rat

al-Barazanji¹,

Balment²

1995

Experimental Physiology

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SUMMARYIn the absence of the potentially confounding influence of vasopressin in hypertension, the effects of atrial natriuretic peptide (ANP) on arterial blood pressure and renal handling of water and sodium were assessed from comparison of responses to intravenous ANP infusion in anaesthetized vasopressin-deficient New Zealand genetically hypertensive (DI/H) rats and their normotensive substrain (DI/N). After 320 min of hypotonic saline infusion, plasma ANP concentration was significantly higher in DI/H compared with DI/N rats. ANP administration increased circulating ANP concentration in both groups. Plasma angiotensin II concentration was higher in DI/H than in DI/N rats; infusion of ANP raised circulating angiotensin II in both groups though this achieved statistical significance only in DI/N rats. Plasma aldosterone concentrations were initially similar in normotensive and hypertensive animals and, in both, were reduced markedly by i.v. ANP infusion. Administration of ANP produced sustained hypotension in both groups. However, the hypotensive effect of ANP was more pronounced in DI/H compared with DI/N rats. Heart rate was initially similar in the two groups, and infusion of ANP produced no detectable change. By comparison with animals maintained on hormone-free infusate, urine flow increased markedly over the 80 min period of ANP infusion in both groups, by 142 % in DI/H rats and 127 % in DI/N rats. ANP administration produced a natriuresis in both groups but the increase in Na+ excretion was much greater in DI/H (342 %) than in DI/N (139 %) rats. It appears from the current study that vasopressin-deficient hypertensive rats are more sensitive to ANP with regard to effects on blood pressure and renal excretion than their vasopressin-deficient normotensive substrain. These differences may, in part, reflect adjustments to long-term elevation in blood pressure and in plasma ANP concentration in hypertension and, in part, rely on the associated disturbances in related endocrine systems.

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Transient pseudo-hypoaldosteronism following resection of the ileum: Normal level of lymphocytic aldosterone receptors outside the acute phase

Vantyghem

Hober

Evrard

et al. 1999

J Endocrinol Invest

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Pseudo-hypoaldosteronism (PHA) is due to mineralocorticoid resistance and manifests as hyponatremia and hyperkalemia with increased plasma aldosterone levels. It may be familial or secondary to abnormal renal sodium handling. We report the case of a 54-year-old woman with multifocal cancer of the colon, who developed PHA after subtotal colectomy, ileal resection and jejunostomy. She was treated with 6 g of salt daily to prevent dehydration, which she stopped herself because of reduced fecal losses. One month later she was admitted with signs of acute adrenal failure, i.e. fatigue, severe nausea, blood pressure of 80/60 mmHg, extracellular dehydration, hyponatremia (118 mmol/l); hyperkalemia (7.6 mmol/l), increased blood urea nitrogen (BUN) (200 mg/dl) and creatininemia (2.5 mg/dl), and decreased plasma bicarbonates level (HCO3-: 16 mmol/l; N: 27-30). However, the plasma cortisol was high (66 microg/100 ml at 10:00 h; N: 8-15) and the ACTH was normal (13 pg/ml, N: 10-60); there was a marked increase in plasma renin activity (>37 ng/ml/h; N supine <3), active renin (869 pg/ml; N supine: 1.120), aldosterone (>2000 pg/ml; N supine <150) and plasma AVP (20 pmol/l; N: 0.5-2.5). The plasma ANH level was 38 pmol/l (N supine: 5-25). A urinary steroidogram resulted in highly elevated tetrahydrocortisol (THF: 13.3 mg/24h; N: 1.4+/-0.8) with no increase in tetrahydrocortisone (THE: 3.16 mg/24h; N: 2.7+/-2.0) excretion, and with low THE/THF (0.24; N: 1.87+/-0.36) and alpha THF/THF (0.35; N: 0.92+/-0.42) ratios. The number of mineralocorticoid receptors in mononuclear leukocytes was in the lower normal range for age, while the number of glucocorticoid receptors was reduced. Small-bowel resection in ileostomized patients causes excessive fecal sodium losses and results in chronic sodium depletion with contraction of the plasma volume and severe secondary hyperaldosteronism. Nevertheless, this hyperaldosteronism may be associated with hyponatremia and hyperkalemia suggesting PHA related to the major importance of the colon for the absorption of sodium. In conclusion, this case report emphasizes 1) the possibility of a syndrome of acquired PHA with severe hyperkalemia after resection of the ileum and colon responding to oral salt supplementation; 2) the major increase in AVP and the small increase in ANH; 3) the strong increase in urinary THF with low THE/THF and alpha THF/THF ratios; 4) the normal number of lymphocytic mineralocorticoid receptors outside the acute episode.

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Arginine Vasopressin Infusion Increases Plasma Levels of Atrial Natriuretic Factor in Humans

Cited by 4 publications

References 9 publications

Effect of arginine vasopressin on breathing movements of chronically instrumented fetal lambs

Effect of arginine vasopressin on breathing movements of chronically instrumented fetal lambs

Renal, endocrine and vascular effects of atrial natriuretic peptide in a novel vasopressin‐deficient genetically hypertensive strain of rat

Transient pseudo-hypoaldosteronism following resection of the ileum: Normal level of lymphocytic aldosterone receptors outside the acute phase

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