Hemodynamic and renal effects of low-dose infusions of atrial peptide in awake dogs

Bie, Peter; Wang, B. C.; Leadley, Robert J.; Goetz, K. L.

doi:10.1152/ajpregu.1988.254.2.r161

Cited by 36 publications

(31 citation statements)

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“…Bie et al (26) reported that the comparable rise in plasma ANP to the present study gave rise to an increase in urinary Na' excretion (less than 2-fold) in euhydrated conscious dogs. Weidman et a/.…”

Section: Discussionsupporting

confidence: 76%

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

Inoue

Kimura

Ota

et al. 1990

J Neuroendocrinology

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Effect of atrial natriuretic peptide (ANP) on the vasopressin response to osmotic stimulation (Experiment I) as well as to hemorrhage (Experiment II) was investigated in anesthetized dogs. Moreover, cardiovascular function and renal water and electrolyte excretion were studied. In Experiment I , 2.5 M NaCI, containing 0.02 pg.kg ' of ANP, was infused intravenously at a rate of 0.2 ml.kg-'. min ' after one bolus injection of 0.75 pg.kg ' ANP (HSA group). In the control group, 2.5 M NaCl alone (HS group) was infused.The infusion was continued for 75 min. In Experiment 11, 0.15 M NaCI, containing the identical dose of ANP to Experiment I (HA group), or 0.15 M NaCl alone (H group) was infused intravenously during bleeding at a rate of 1 ml.kg-'.min ' for 40 min. In Experiment I, infused ANP suppressed the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and attenuated ANP release and a rise in arterial and central venous pressures in response to plasma volume expansion, without the enhanced natriuresis. In Experiment I I , infused ANP neither impaired t h e vasopressin response to bleeding nor potentiated a fall in mean arterial pressure and central venous pressure.In conclusion, ANP at physiological and/or supraphysiological range may suppress the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and to hemorrhage. In addition, ANP given intravenously may attenuate ANP release and a rise in blood pressure without any natriuresis.It has recently been postulated that there is a direct relationship between the release of atrial natriuretic peptide (ANP) and that of vasopressin (AVP), and this mutual relationship may be important in the regulation of body fluid.AVP has been reported to stimulate ANP release in in vivo and in vitw studies (1-3). On the contrary, the central and peripheral administrations of ANP have been shown to attenuate AVP release in euhydration as well as the AVP response to dehydration, hemorrhage and osmotic stimulation in animals (4-9) and human subjects (10. 1 I). Furthermore. ANP was found to attenuate AVP release produced by angiotensin I1 (12). In in vitro studies, moreover, ANP has been reported to stimulate AVP release in small doses, and in large doses, to attenuate the release of AVP (13).On the other hand, it has been documented that peripheral administration of ANP has no effect on AVP release in rats, sheep and man ( 5 , 14-18). Furthermore, AVP release has been shown to increase in response to hypertonic saline given iv. despite a marked rise in ANP release (1 9).Thus, it is still uncertain whether a rise in plasma ANP within physiological and/or supraphysiological range really affects AVP release in response to osmotic and hemorrhagic stimuli.In the present study, therefore, effects of ANP (iv) on AVP release elicited by hypertonic saline and hemorrhagic shock were investigated. Hypertonic saline infusion and continuous bleeding were carried out in ancsthetizcd dogs. In addition. renal water...

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Section: Discussionsupporting

confidence: 76%

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

Inoue

Kimura

Ota

et al. 1990

J Neuroendocrinology

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“…It has also been reported that highdose ANF infusion in normovolemic animals induces only modest natriuresis. 3 The suppressed natriuresis in response to high-dose ANF infusions may similarly have resulted from the chloride-mediated feedback mechanism, in which a decreased tubular chloride concentration after acute ANF natriuresis may have prevented further natriuresis by inhibiting binding of ANF to its receptor.…”

Section: Misono Chloride-mediated Feedback Control Of Anf Receptormentioning

confidence: 99%

“…1,2 For example, infusion of ANF in normovolemic animals to mimic endogenous ANF increase on a high-salt diet fails to induce comparable natriuresis. 3 In edematous disease states such as congestive heart failure, 4,5 nephrotic syndrome, 5 and liver cirrhosis, 6 plasma ANF levels are elevated, yet sodium is retained. In addition, transgenic animals overexpressing ANF, with plasma ANF levels elevated 10-fold or more, maintain normal salt excretion.…”

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confidence: 99%

Atrial Natriuretic Factor Binding to Its Receptor Is Dependent on Chloride Concentration

Misono

2000

Circulation Research

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Abstract-Although considerable evidence indicates a role for atrial natriuretic factor (ANF) in renal salt regulation, other studies have found a lack of natriuretic response to high-plasma ANF under certain physiological and pathophysiological conditions. The mechanism for this apparent insensitivity to ANF is unknown. In the present study, it was found that ANF binding to its receptor requires the presence of chloride and occurs in a chloride concentration-dependent manner. ANF binding was measured using the purified recombinant hormone-binding domain of the ANF receptor in the presence of 0.1 mol/L NaCl or other selected salt. High specific binding was detected in the presence of NaCl, KCl, or NH 4 Cl. However, binding was undetectable when the salt was replaced with NaHCO 3 , CH 3 COONa, or CH 3 COONH 4 , indicating that binding requires the presence of chloride. Chloride dependence was also found with the native receptor in bovine adrenocortical membrane preparations. ANF binding to the recombinant protein was chloride concentration-dependent over a range from 0.05 to 10 mmol/L, and a half-maximum binding was attained at Ϸ0.6 mmol/L equivalent chloride concentration.Competitive-binding assays at several fixed concentrations of NaCl showed that lowering chloride concentration caused a decrease in maximum binding but did not alter K d values, suggesting that a loss of chloride turns off ANF binding rather than reducing affinity for ANF. Saturation-binding studies showed that excess ANF cannot overcome loss of binding caused by low chloride. Chloride-dependent ANF-receptor binding may function as a feedback-control mechanism regulating the ANF-receptor action and, hence, renal sodium excretion.

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“…4 The increased PRA may be due to continuous relief from the direct suppression by ANP. 19 Furthermore, ANP acts within the kidney to increase GFR 6,20,21 and to decrease proximal sodium and water reabsorption via both inhibition of angiotensin-stimulated transport and a dopamine mediated mechanism. 22,23 The administration of HS-142-1 may decrease sodium delivery to macula densa.…”

Section: Plasma Hormonal Changesmentioning

confidence: 99%

“…Pharmacological doses of ANP increased excretion of water and sodium, associated with a significant increase in GFR. 6,20 Bolus administration of HS-142-1 reduced urine flow rate and urinary sodium excretion rate in advanced HF. 4 Furthermore, we observed the tendency to a decrease in urine flow rate and urinary sodium excretion rate following bolus administration of HS-142-1 in early-stage HF.…”

Section: Changes In Renal Functionsmentioning

confidence: 99%

Short-Term and Long-Term Inhibition of Endogenous Atrial Natriuretic Peptide in Dogs With Early-Stage Heart Failure

et al. 1998

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n congestive heart failure, neurohormonal factors such as the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system are activated, and the RAAS activation may lead to deterioration of heart failure (HF) due to the vasoconstrictive and volume-retaining effects. 1 Atrial natriuretic peptide (ANP) demonstrates increased secretion in proportion to the severity of HF, and may act to counterbalance the adverse effects of the RAAS through its direct vasodilatory action, inhibition of the excessive release of renin and aldosterone, and by its direct diuretic and natriuretic effects. [2][3][4] As reported in the Study of Left Ventricular Dysfunction (SOLVD), early-stage HF is characterized by an increase in circulating ANP without activation of the RAAS or body fluid retention. 5 Considering these hormonal profiles and the body fluid balance, ANP may be one of the principal factors inhibiting the activation of the RAAS and body fluid retention in early-stage HF. However, in advanced HF the intracardiac pressure increases, volume overload develops, and the RAAS activates in spite of the fact that the plasma ANP level remains elevated above basal values. Elevated plasma ANP in advanced HF may not be as effective as expected. In addition, the responsiveness to exogenous ANP decreases in renin suppression or renal excretion in advanced HF. 6 Thus the decreased responsiveness to endogenous ANP may play a part in the pathogenesis of vasoconstriction, activation of the RAAS and body fluid retention in HF. However, it has not been demonstrated experimentally whether hyporesponsiveness to ANP is directly related to the progression of HF.We and others have attempted to clarify the role of endogenous ANP in HF through short-term inhibition of ANP activity using an ANP receptor antagonist, HS-142-1. 4,[7][8][9][10][11] However, the influence of long-term inhibition of endogenous ANP activity by an ANP receptor antagonist in established HF, in which ANP has previously exerted an effect, has not been determined. We assumed that longterm inhibition of endogenous ANP activity in early-stage HF provokes the progression to advanced HF. It is important to examine how long-term inhibition of endogenous ANP affects cardiorenal and neurohormonal factors in early-stage HF in order to clarify the exact role of ANP in the progression from early-stage to advanced HF.The objective of the present study is to clarify whether endogenous ANP inhibits the deterioration of early-stage HF by investigating the effects of long-term suppression of endogenous ANP activity by HS-142-1 in dogs with earlystage HF. Furthermore, since it is expected that the longterm inhibition of endogenous ANP will cause the activation of various substances that affect vascular tone, hormonal secretion and renal functions, we compared the differences in the effects of short-term and long-term inhibition, and determined the direct and indirect influences of the suppression of endogenous ANP in early-stage HF. Short-Term and Long-Term Inhibition of Endoge...

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Hemodynamic and renal effects of low-dose infusions of atrial peptide in awake dogs

Cited by 36 publications

References 0 publications

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

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

Atrial Natriuretic Factor Binding to Its Receptor Is Dependent on Chloride Concentration

Short-Term and Long-Term Inhibition of Endogenous Atrial Natriuretic Peptide in Dogs With Early-Stage Heart Failure

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