Stimulation of ADH release by the renin-angiotensin system

Bonjour, J. P.; Malvin, RL

doi:10.1152/ajplegacy.1970.218.6.1555

Cited by 274 publications

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“…A direct action of angiotensin I1 on free water reabsorption in the tubule has been recently demonstrated in dogs (15). However, it is known that angiotensin I1 enhances vasopressin release (6).…”

Section: Discussionmentioning

confidence: 99%

Plasma Renin Activity Related to Sodium Balance, Renal Function and Urinary Vasopressin in the Newborn Infant

Godard

Geering

et al. 1979

Pediatr Res

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Summary MATERIALS AND METHODSPlasma renin activity was determined in 25 healthy, full-term, newborn infants aged 1 day to 9 weeks. High values were found, the mean level at 1-2 days of life (24.8 +. 8.4 ng/ml/hr, SE) being significantly higher than the mean levels at 7-9 days (5.8 + 1.5) and at 4-9 weeks (8.1 f 13) (P < 0.05). No correlation was found between plasma renin activity and systolic blood pressure, hematocrit, creatinine clearance, serum sodium, or serum potassium. Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium ( r = -OM), and positively with urinary osmolality (r = 0.67). The correlations reached higher coefFicients if only infants aged 5 9 days were considered.In addition, vasopressin was measured by radioimmunoassay in the urine. The daily excretion was lower in newborn infants (9.4 f 1.6 ng/m2/day, SE, at 1-2 days of postnatal life) than in healthy children (37.1 + 5.6), and was significantly correlated with creatinine clearance ( r = 0.69), but not with urinary osmolality. SpeculationThe postnatal changes of plasma renin activity were significantly correlated only with parameters of sodium balance and with urinary osmolality, so that one can speculate that early after birth, the renin-angiotensin system plays a preponderant role not only in sodium homeostasis, but also in water balance.Plasma renin activity (PRA) (8,16,23,27) and angiotensin I1 concentration (7) are relatively high in human newborn infants. PRA decreases progressively over weeks and months (8,16,22); a similar trend is followed by aldosterone secretion rates (4), plasma aldosterone (4), and exchangeable sodium (19).The cause of increased activity of the renin-angiotensin system during the neonatal period is not clear. The low sodium intake, the low blood pressure, the hypovolemia, and the increased sympathetic activity ,have been invoked as possible factors. On the other 'hand, no correlation was found between PRA and plasma aldosterone. either in cord blood (10, 26) or in newborn infants . . , aged 2-3 days (26), suggesting that angiotensin I1 is not a predominant regulatory factor controlling aldosterone secretion at this age.In an effort to gain insight into the interplay between renin, sodium, and renal function during the neonatal period, we have studied the relationship between PRA, sodium intake and output, urine osmolality, and glomerular filtration rate (GFR) in hea6hy, full-term newborns of different ~ostnatal aees. In addition. vaso-" pressin was determined in the urine, because limited data are available concerning this hormone in human newborns. 7

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Section: Discussionmentioning

confidence: 99%

Plasma Renin Activity Related to Sodium Balance, Renal Function and Urinary Vasopressin in the Newborn Infant

Godard

Geering

et al. 1979

Pediatr Res

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“…Bonjour and Malvin (22) demonstrated that systemic administration of angiotensin II caused an increase in the level of plasma ADH, and Gagnon et al (9) provided evidence that ADH liberation from isolated neurohypophysis was increased by angiotensin II. Additional ly, although bradykinin given through the intracarotid artery route rather than intravenously was more effective in an increment of blood ADH concentrations, direct stimulation by the kinin of the pituitary was not observed (10).…”

Section: Discussionmentioning

confidence: 99%

Antidiuresis of Centrally Administered Amines and Peptides and Release of Antidiuretic Hormone from Isolated Rat Neurohypophysis

Hisada

Fujimoto

Kamiya

et al. 1977

Japanese Journal of Pharmacology

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Abstract-Effectsof biogenic amines and peptides on urine outflow and ADH release were studied using intracerebroventricular (i.c.v.) perfusion experiments and isolated neurohypophysis incubation studies. Decrease in the urine outflow was observed after norepinephrine, histamine and angiotensin II had been administered i.c.v.. The effect of norepinephrine was prevented by phentolamine.Phentolamine alone also acted as an antidiuretic.a-Adrenergic and histaminergic mechanisms may thus involved in ADH releasing system and this system might be also responsive to angioten sin II. When the isolated neurohypophysis was incubated in the presence of nore pinephrine, histamine, angiotensin II amide 5-valine or bradykinin, release of ADH was increased, and the effects of norepinephrine and histamine were prevented by phentolamine and promethazine, respectively.Phentolamine but not promethazine alone increased ADH release. On the other hand, serotonin, dopamine and angio tensin II 5-isoleucine did not result in an ADH release from the isolated neural lobes. Our findings suggest that when the local concentration of norepinephrine, histamine or peptides is increased to the extent where the posterior lobe of the pituitary is stimu lated directly, the ADH release is enhanced.Norepinephrine (also probably dopamine)-containing nerve terminals have been found in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus (1). Antidiuretic hormone (ADH) produced in the nerve cells in the SON and PVN is transported to the posterior lobe of the pituitary. It seems likely, therefore, that an adre nergic mechanism is implicated in the production and secretion of ADH. In fact, centrally administered norepinephrine stimulated the release of ADH (2-4). Although relatively high concentrations of histamine (5-7) and angiotensin (8) are found in the brain, particularly in the hypothalamus, little is known about their role in the mechanisms of ADH release.The present experiments dealt with possible roles of these biogenic amines and the peptides on the central antidiuresis using an intracerebroventricular (i.c.v.) perfusion technique in rats.Whether or not biogenic amines and peptides stimulate directly the release of ADH from the isolated neurohypophysis was also studied. It has earlier been shown that angio tensin II increases the ADH release from the isolated neurohypophysis (9), and it was sug gested that the antidiuretic effect of bradykinin was due to its action on the central nervous system, although bradykinin did not cause a release of ADH from the isolated preparation (10). Furthermore, there is no data which suggests that the amines stimulated directly the neurohypophysis to increase the ADH release.

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“…In animals (Schmitt et al, 1981) or in man (Kimura et al, 1986), the natriuretic and diuretic effect of frusemide produces a decrease in plasma volume similar to the one observed after haemorrhage. As a consequence, AVP secretion is considerably enhanced by baroreceptors, mechanoreceptors (Ledsome et al, 1985), the renin-angiotensin system (Bonjour & Malvin, 1970) and the a-adrenergic system (Kimura et al, 1980;Paller & Linas, 1984;Brunner et al, 1983). …”

Section: Effects Of Lignocaine On Arginine-vasopressin Serum Levelsmentioning

confidence: 99%

Effect of lignocaine on arginine‐vasopressin plasma levels: baseline or induced by frusemide

Gariépy¹,

Larose²,

Bailey³

et al. 1992

British J Pharmacology

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1 To assess whether or not lignocaine influences baseline and frusemide-induced (5 mg kg-') plasma concentrations of arginine-vasopressin (AVP), 2 groups of rabbits received an infusion of lignocaine (130 fig min'-kg-') for 6 h. Lignocaine-induced changes in AVP plasma concentrations were substantiated by measurement of diuresis and natriuresis and hepatic plasma flow, by means of an infusion of indocyanine green (ICG) (249 fg min' kg-'). 2 Baseline plasma AVP levels were 4.9 ± 0.9 pg ml-' (+ s.e.), and following lignocaine, these values were reduced to 0.7 ± 0.1 pg ml-I (P<0.01). Frusemide increased AVP levels to 134.1 ± 73.6 pg ml' (P <0.05) and lignocaine totally prevented this increase, e.g. mean AVP levels of 2.7 pg ml-'. 3 Lignocaine enhanced baseline diuresis secondary to an increase in free water clearance; none of the experimental conditions affected the diuresis and natriuresis induced by frusemide. 4 Frusemide reduced the hepatic plasma flow and this decrease was not reversed by the infusion of lignocaine.5 It is concluded that in healthy rabbits lignocaine reduces baseline secretion of AVP and its antidiuretic effect; in addition, lignocaine prevents the rise in AVP induced by frusemide.

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Stimulation of ADH release by the renin-angiotensin system

Cited by 274 publications

References 0 publications

Plasma Renin Activity Related to Sodium Balance, Renal Function and Urinary Vasopressin in the Newborn Infant

Plasma Renin Activity Related to Sodium Balance, Renal Function and Urinary Vasopressin in the Newborn Infant

Antidiuresis of Centrally Administered Amines and Peptides and Release of Antidiuretic Hormone from Isolated Rat Neurohypophysis

Effect of lignocaine on arginine‐vasopressin plasma levels: baseline or induced by frusemide

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