Effects of centrally administered atrial natriuretic peptide on renal functions

Abstract

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...

Central Effects of Atrial Natriuretic Peptide on Plasma Catecholamines, Vasopressin, Renin and Beta-Endorphin and on Renal Excretory Functions in the Dog

“…It is likely that suppression of AVP release by atrial natriuretic peptide is markedly enhanced when vasopressinergic system is activated by other stimuli {Iitake et Januszewicz, Thibault, Garcia, Gutkowska, Genest and Cantin 1986). A weak and delayed inhibition of plasma AVP concentration was observed in acute experiments on anaesthetized dogs in which ANP was infused into the lateral ventricle at a rate similar to that applied in the present study (Shoji et al 1987). The resting level of AVP in the latter study was elevated by a factor of 10 presumably owing to anesthesia and brain surgery (Simon-Operman, Gray, Szczepanska-Sadowska and Simon 1983).…”

The renal and vascular effects of central angiotensin II and atrial natriuretic factor in the anaesthetized rat.

“…The diuretic action of central ANF differed, however, from that of ANF in the periphery, as this was not associated with a natriuresis (Maack, Camargo, Kleiert, Laragh & Atlas, 1985), as also described in the conscious rat and sheep (Fitts et al 1985;Lee et al 1987). None the less, central administration of human ANF in pentobarbitoneanaesthetized dogs infused i.v.with 09 % NaCl has been shown to produce a diuresis and natriuresis (Shoji, Kimura, Matsui, Ota, litake, Inoue, Yasujima, Abe & Yoshinaga, 1987), a discrepancy which might be due to differences in experimental protocol and/or the molecular structure of the ANF used.…”

Intracerebroventricular Anp(1–28) Has No Obvious Effects on Renal Blood Flow and Function in Conscious Sheep

“…The doses of ANP used in the present study (25 and 85 pmol/ min) would therefore be expected to have elevated CSF ANP far above normal levels. Control experiments with intravenous administration of the same amounts of ANP were not performed, but ICV infusions of similar doses of the peptide in dogs (Shoji et al 1987) and sheep (Cameron et al 1990) did not cause any change in plasma immunoreactive ANP concentration.…”

“…This is also supported by several reports on accepted 5 January 1994. effects of central administration of different ANP peptides on water and sodium turnover (Samson et al 1987;Parkes et al 1988;Weisinger et al 1992). However, large doses are apparently needed when the peptide is administered intracerebroventricularly (ICV; Samson et al 1987), and reports on effects on, for instance, arginine vasopressin (AVP) release (Iitake et al 1986;Sczepanska-Sadowska et al 1990) and renal Na excretion are inconsistent (Shoji et al 1987;Rohmeiss et al 1991). Very few studies seem to have looked into possible centrally mediated effects of ANP on renal haemodynamics, but an increase in effective renal plasma flow has been reported in dogs (Shoji et al 1987).…”

“…However, large doses are apparently needed when the peptide is administered intracerebroventricularly (ICV; Samson et al 1987), and reports on effects on, for instance, arginine vasopressin (AVP) release (Iitake et al 1986;Sczepanska-Sadowska et al 1990) and renal Na excretion are inconsistent (Shoji et al 1987;Rohmeiss et al 1991). Very few studies seem to have looked into possible centrally mediated effects of ANP on renal haemodynamics, but an increase in effective renal plasma flow has been reported in dogs (Shoji et al 1987). Therefore, it was of interest to study whether ICV ANP influences renal water and electrolyte excretion, AVP release and renal blood flow in conscious sheep.…”