Diuretic and natriuretic action of rat atrial natriuretic peptide (6–33) administered intracerebroventricularly in rats

Israel, A; Barbella, Yarisma

doi:10.1016/0361-9230(86)90108-5

Cited by 33 publications

(9 citation statements)

References 14 publications

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“…The dose of a-hANP used in the present study was 78 pmol/ kg, almost comparable to the one used in their study. Furthermore, Israel & Barbella (1986) re¬ ported that rat ANP given intracerebroventricularly (82-410 pmol) produces a dose-related in¬ crease in urinary sodium and potassium excre¬ tions in rats. Therefore, the present results are well in line with their observation, and the slight difference observed in the diuretic responses may be due mainly to the difference in the molecular struc¬ ture of ANP, as well as in experimental proce¬ dures.…”

Section: Discussionmentioning

confidence: 97%

“…Furthermore, ANP is shown peripherally to inhibit dehydration-and haemor¬ rhage-induced AVP release in rats (Samson 1985a) and, at high doses, to attenuate AVP release from the isolated rat posterior pituitary gland (Januszewicz et al 1985). Moreover, intraventricular administration of ANP has been re¬ ported to induce a diuresis and natriuresis in rats (Fitts et al 1985;Israel & Barbella 1986).Therefore, ANP in the central nervous system is suspected to play an important role in the regulation of body fluid, but whether intracerebroventricular administration of ANP affects ar¬ terial blood pressure and the release of AVP, ANP, renin, and aldosterone and how it influences natriuresis and diuresis still remain questionable. The present study was undertaken to investi¬ gate the central effects of ANP on renal function, blood pressure and heart rate, PRA, plasma aldo¬ sterone concentration, and plasma AVP and ANP concentrations in anaesthetized dogs.…”

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Effects of centrally administered atrial natriuretic peptide on renal functions

Miyake¹,

Kimura²,

Matsui³

et al. 1987

Acta Endocrinologica

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In order to assess the effects of centrally administered atrial natriuretic peptide (ANP) on renal water and electrolytes handling, arterial blood pressure, plasma vasopressin, renin activity, aldosterone, and ANP concentrations, synthetic \g=a\-human ANP (\g=a\-hANP) was administered intracerebroventricularly at a dose of 2.6 pmol \m=.\ kg\ m=-\ 1 \m=.\ min\m=-\1 for 30 min in pentobarbitalanaesthetized dogs (N = 6). In the control study (N = 6), artificial cerebrospinal fluid was infused. Intracerebroventricular administration of \g=a\-hANPincreased significantly urine flow from 178 \m=+-\37 to 303 \m=+-\43 \g=m\l/min (mean \ m=+-\sem), sodium excretion from 27.3 \ m=+-\8.9 to 54.4 \m=+-\10.5, \ g=m\ mol / mi n, potassium excretion from 16.1 \m=+-\3.7 to 24.0 \m=+-\ 5.1 \ g=m\ mol / mi n, and osmolar and negative free water clearances, accompanied by a significant rise in renal blood flow from 77.0 \m=+-\14.6 to 94.9 \m=+-\16.9 ml/min. Whereas glomerular filtration rate fell significantly, blood pressure and heart rate did not change.Plasma ANP, aldosterone, and PRA did not change significantly during the experiment, but plasma AVP were slightly but significantly decreased from 52 \m=+-\11 to 34 \m=+-\6 nmol/l. On the other hand, these parameters showed no changes in the control study, except a significant fall in glomerular filtration rate and a significant rise in PRA. Thus, it has been confirmed that ANP centrally brings about diuresis, natriuresis, and kaliuresis via some unknown mechanisms independent of the release of these hormones.It is well known that there is a peptide hormone in the mammalian atrium (atrial natriuretic peptide, ANP), which is released in response to the expan¬ sion of extracellular fluid volume, resulting in natriuresis and vaso relaxation (De Bold 1986).More recently, it has been reported that ANP is also present in the central nervous system in rats (David et al. 1985;Morii et al. 1985;Saper et al. 1985;Tanaka et al. 1984) and its content in these areas is decreased in response to dehydration (Samson 1985b). Furthermore, ANP is shown peripherally to inhibit dehydration-and haemor¬ rhage-induced AVP release in rats (Samson 1985a) and, at high doses, to attenuate AVP release from the isolated rat posterior pituitary gland (Januszewicz et al. 1985). Moreover, intraventricular administration of ANP has been re¬ ported to induce a diuresis and natriuresis in rats (Fitts et al. 1985;Israel & Barbella 1986).Therefore, ANP in the central nervous system is suspected to play an important role in the regulation of body fluid, but whether intracerebroventricular administration of ANP affects ar¬ terial blood pressure and the release of AVP, ANP, renin, and aldosterone and how it influences natriuresis and diuresis still remain questionable. The present study was undertaken to investi¬ gate the central effects of ANP on renal function, blood pressure and heart rate, PRA, plasma aldo¬ sterone concentration, and plasma AVP and ANP concentrations in anaesthetized dogs. Materials and MethodsExperim...

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Section: Discussionmentioning

confidence: 97%

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Effects of centrally administered atrial natriuretic peptide on renal functions

Miyake¹,

Kimura²,

Matsui³

et al. 1987

Acta Endocrinologica

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“…In addition to very high numbers of ANF receptors, it contains also very high concentrations of A II receptors and this organ has been shown to be the main brain target site for circulating A II [28,43]. The presence of ANF receptors in the SFO sug gests that this structure could mediate some of the postulated central actions of the circulating peptide, such as inhibition of thirst [I, 26,32], inhibition of vasopressin release [14], inhibi tion of salt appetite [7[, diuresis [15] and a fall in blood pres sure [17]. Since these actions oppose those of A II, a local antagonism between these two peptides was postulated to exist in the SFO [41].…”

Section: Discussionmentioning

confidence: 99%

Atrial Natriuretic Peptides in Brain Nuclei of Rats with Inherited Diabetes insipidus (Brattleboro Rats)

Bahner¹,

Geiger²,

Palkóvits

et al. 1990

Neuroendocrinology

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The concentration of atrial natriuretic peptides (ANF) was measured radioimmunologically in 18 selected microdissected brain areas of rats with inherited diabetes insipidus (Brattleboro rats) and their control rats (Long-Evans rats). In 7 brain areas known to be involved in the regulation of fluid homeostasis or blood pressure (subfornical organ, organum vasculosum lamina terminalis, periventricular preoptic nucleus, perifornical nucleus, nucleus of the solitary tract, tegmentum pontis, arcuate nucleus) ANF concentration was significantly changed. After restoration of antidiuresis with the V₂ receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP) ANF levels of Brattleboro rats adapted at least partly to those of the control rats in all brain areas except the subfornical organ. Furthermore, ANF was then significantly changed in the supraoptic and paraventricular nuclei of DDAVP-treated diabetes insipidus rats. These data show that the central ANF system is sensitive for changes in electrolyte and fluid homeostasis.

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“…6 Like peripheral nervous system ANF, CNS ANF appears to contribute to the regulation of body sodium and intravascular volume. Intracerebroventricular administration of ANF produces natriuresis and diuresis 7 ; CNS-administered ANF inhibits the release of arginine vasopressin 8 and the intake of salt 9 and water. 10 High sodium intake reduces the brain ANF content, 11 and dehydration reduces the hypothalamic ANF content in rats.…”

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Cerebrospinal fluid atrial natriuretic factor in intracranial disease.

Diringer

Kirsch

Ladenson

et al. 1990

Stroke

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We tested the hypothesis that the concentration of atrial natriuretic factor in the cerebrospinal fluid is an indicator of brain injury in patients with intracranial disease. Atrial natriuretic factor concentration was measured in 72 samples of cerebrospinal fluid from 28 patients with intraventricular drains and in nine samples from outpatient controls undergoing diagnostic lumbar puncture. Levels were correlated with diagnosis; systemic fluid administration; concentration of atrial natriuretic factor in the plasma; intracranial pressure; sodium, glucose, and protein concentrations, osmolality, and cell count in the cerebrospinal fluid; sodium concentration in the serum; and hemodynamics. Atrial natriuretic factor concentration was highest in cerebrospinal fluid from patients with intracerebral hematoma, followed by those with obstructive hydrocephalus and subarachnoid hemorrhage (19±2, 13±3, and 8±2 pg/ml, respectively); atrial natriuretic factor concentration was <4 pg/ml in the controls. Patients treated with fluid restriction had significantly higher atrial natriuretic factor levels than those receiving maintenance or high-volume fluids (16±3, 8 ± 2 , 1 0 ± l pg/ml, respectively). The concentration of atrial natriuretic factor in the plasma was significantly elevated in patients with intracerebral hematoma and subarachnoid hemorrhage (155 ±38 and 92 ±20 pg/ml, respectively) and did not correlate with fluid administration or the concentration of atrial natriuretic factor in the cerebrospinal fluid. Neither cerebrospinal fluid nor plasma concentrations of atrial natriuretic factor correlated with intracranial pressure; cerebrospinal fluid sodium, glucose, or protein concentrations, osmolality, or cell count; serum sodium concentration; or hemodynamics. We conclude that the concentration of atrial natriuretic factor in the cerebrospinal fluid is a nonspecific indicator of brain injury. Cerebrospinal fluid levels of atrial natriuretic factor may be elevated in response to dehydration therapy. Elevated plasma levels of atrial natriuretic factor suggest a central mechanism modulating cardiac release. (Stroke 1990;21:1550-1554)

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Diuretic and natriuretic action of rat atrial natriuretic peptide (6–33) administered intracerebroventricularly in rats

Cited by 33 publications

References 14 publications

Effects of centrally administered atrial natriuretic peptide on renal functions

Effects of centrally administered atrial natriuretic peptide on renal functions

Atrial Natriuretic Peptides in Brain Nuclei of Rats with Inherited Diabetes insipidus (Brattleboro Rats)

Cerebrospinal fluid atrial natriuretic factor in intracranial disease.

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