ANP inhibits Na+-H+ antiport in proximal tubular brush border membrane: Role of dopamine

Winaver, Joseph; Burnett, John C.; Tyce, Gertrude M.; Douša, Thomas P.

doi:10.1038/ki.1990.323

Cited by 63 publications

(43 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Based on previous studies, the chief sites of ANP action were thought to be in glomeruli, IMCD, and CCD (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)24). Although ANP inhibits Na and fluid reabsorption in IMCD and CCD, which can contribute substantially to the natriuresis and diuresis of ANP, the results of micropuncture studies (7,14,33) (6,12,(34)(35)(36). Our present data completely agree with these data.…”

Section: Discussionsupporting

confidence: 81%

Effects of atrial natriuretic peptide and vasopressin on chloride transport in long- and short-looped medullary thick ascending limbs.

Nonoguchi¹,

Tomita²,

Marumo³

1992

J. Clin. Invest.

View full text Add to dashboard Cite

Recent studies have suggested a selective effect of atrial natriuretic peptide (ANP) in regulating NaCI reabsorption in juxtamedullary nephrons. We examined (a) functional differences between medullary thick ascending limbs from long and short loops of Henle (IMAL and sMAL, respectively) and (b) the interaction of ANP and arginine vasopressin (AVP) on Cltransport (Ja) in these two segments. AVP-, glucagon-, and calcitonin-stimulated cAMP accumulation was higher in IMAL than in sMAL. 10-10 M AVP increased Ja in IMAL but not in sMAL. ANP-stimulated cGMP production was higher in IMAL than in sMAL. 10' and 10-M ANP inhibited AVP-

show abstract

Section: Discussionsupporting

confidence: 81%

Effects of atrial natriuretic peptide and vasopressin on chloride transport in long- and short-looped medullary thick ascending limbs.

Nonoguchi¹,

Tomita²,

Marumo³

1992

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…This may have resulted in enhanced renin release due to decreased sodium delivery to the macula densa ( 31 ) and further activation of aldosterone. Indeed, ANP has been demonstrated to reduce proximal tubule sodium reabsorption via a dopamine mediated mechanism (30). In the current study, proximal tubule sodium handling was indirectly determined by lithium clearance, as supported by previous studies which have demonstrated the validity of lithium clearance as an accurate method of estimating whole kidney proximal tubular sodium reabsorption ( 17,18).…”

Section: Discussionsupporting

confidence: 79%

“…The reduction in sodium excretion and the blunted natriuretic response to volume expansion in the ELVD-APPX group are consistent with the effects of ANP to enhance sodium excretion via known renal tubular effects (29,30) and by opposing the antinatriuretic effects of the RAAS. The physiological mechanism responsible for activation of the RAAS and sodium retention in the absence of elevation of ANP can only be speculated.…”

Section: Discussionsupporting

confidence: 68%

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Stevens¹,

Burnett²,

Kinoshita³

et al. 1995

J. Clin. Invest.

115

View full text Add to dashboard Cite

Asymptomatic or early left ventricular dysfunction in humans is characterized by increases in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS). We previously reported a canine model of early left ventricular dysfunction (ELVD) produced by rapid ventricular pacing and characterized by an identical neurohumoral profile and maintenance of the natriuretic response to volume expansion (VE). To test the hypothesis that elevated endogenous ANP suppresses the RAAS and maintains sodium excretion in ELVD, we assessed the effects of antagonism of ANP on cardiorenal and neurohumoral function in ELVD. Chronic ANP suppression was produced by bilateral atrial appendectomies before the production of ELVD by rapid ventricular pacing (ELVD-APPX, n = 5). This group was compared with a separate group with ELVD and intact atrial appendages (ELVD-INTACT, n = 8). ELVD-APPX was characterized by lower circulating ANP (50±11 vs. 158±37 pg/ml, P < 0.05), activation of plasma renin activity (PRA) (9.4±2.4 vs. 0.6±0.4 ng/ml per h, P < 0.05) and aldosterone (36.4±12.5 vs. 2.5±0.0 ng/dl, P < 0.05) when compared to ELVD-INTACT. In comparison to the ELVD-INTACT group, sodium excretion was decreased before and during VE in the ELVD-APPX group. Acute ANP antagonism was produced by administration of the particulate guanylate cyclase coupled natriuretic peptide receptor antagonist, HS-142-1, to seven conscious dogs with ELVD and intact atrial appendages (ELVD-INTACT). HS-142-1 decreased plasma concentrations and renal generation of the ANP second messenger, cGMP, and was associated with activation of PRA and sodium retention with enhanced tubular sodium reabsorption. These data support a significant role for elevated endogenous ANP in the maintenance of sodium excretion

show abstract

“…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. During continuous infusion of HS-142-1, since PRA changed in proportion to the urinary sodium excretion rate, decreased sodium delivery to the macula densa may enhance renin secretion.…”

Section: Plasma Hormonal Changesmentioning

confidence: 99%

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

et al. 1998

View full text Add to dashboard Cite

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...

show abstract

ANP inhibits Na+-H+ antiport in proximal tubular brush border membrane: Role of dopamine

Cited by 63 publications

References 24 publications

Effects of atrial natriuretic peptide and vasopressin on chloride transport in long- and short-looped medullary thick ascending limbs.

Effects of atrial natriuretic peptide and vasopressin on chloride transport in long- and short-looped medullary thick ascending limbs.

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

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

Contact Info

Product

Resources

About