Atrial natriuretic factor inhibits vasopressin-stimulated osmotic water permeability in rat inner medullary collecting duct.

Nonoguchi, Hiroshi; Sands, Jeff M.; Knepper, Mark A.

doi:10.1172/jci113742

Cited by 110 publications

(61 citation statements)

References 43 publications

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“…Cyclic GMP, the intracellular mediator of NO, has direct effects on tubular transport. 10 ' 11 Alternatively, L-NA treatment could have altered tubular transport by decreasing renal medullary blood flow, which may indirectly influence tubular sodium and water transport by reducing renal interstitial fluid pressure 9 or by altering the renal cortical-medullary solute gradient. 12 Because there were no significant effects on glomerular filtration rate, fractional sodium or water excretion, or urine osmolality in the present study, it is difficult to determine the mechanism of the sodium and water retention.…”

Section: Discussionmentioning

confidence: 99%

Role of nitric oxide in renal papillary blood flow and sodium excretion.

1992

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Renal medullary interstitial infusion of A^'-nitro-L-arginine (120 fig/hr, n=7) decreased papillary blood flow to 71 ±5% of control without altering outer cortical flow. Before A' G -nitro-L-arginine infusion, interstitial acetylcholine administration (200 jtg/hr) increased cortical and papillary blood flow to 134±6% and 113±2% of control, respectively. After JV G -nitro-L-arginine administration, the vasodilator response to acetylcholine was abolished. In clearance experiments, renal medullary infusion of A' G -nitro-L-arginine (120 /tg/hr, n=l) significantly decreased total renal blood flow by 10%, renal interstitial fluid pressure by 23%, sodium excretion by 34%, and urine flow by 39% without altering glomerular filtration rate, fractional sodium and water excretion, blood pressure, or urine osmolality. These data indicate that selective inhibition of nitric oxide in the renal medullary vasculature reduces papillary blood flow, which is associated with decreased sodium and water excretion. We conclude that nitric oxide exerts a tonic influence on the renal medullary circulation. 7 These data suggest that the renal medulla produces NO, which may exert a paracrine influence on tubular or vascular function in this portion of the kidney.In the present studies, a nonpressor dose of the NO inhibitor JV G -nitro-L-arginine (L-NA) was infused directly into the renal medullary interstitium of anesthetized rats to determine if NO inhibition in the renal medulla would selectively reduce inner medullary blood flow. The effects of a selective reduction of inner medullary blood flow on renal interstitial fluid pressure and sodium and water excretion were then examined. Methods Surgical PreparationExperiments were performed on 24 male SpragueDawley rats purchased from SASCO, Inc., Madison, Wis.

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Section: Discussionmentioning

confidence: 99%

Role of nitric oxide in renal papillary blood flow and sodium excretion.

1992

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“…Vasodilatation 68 Modulation of endothelial permeability 69 Central Nervous System Effects Modulation of sympathetic activity 70,71 Inhibition of arginine vasopressin secretion 47,72 Diminished salt appetite and water drinking 47,60 Effects on blood pressure/volume-regulating regions in the brain 47,60 than do ANP-deficient mice. Whereas BNP-deficient mice do not have hypertension or cardiac hypertrophy, they are susceptible to cardiac fibrosis.…”

Section: Vascular Effectsmentioning

confidence: 99%

Structure, Regulation, and Function of Mammalian Membrane Guanylyl Cyclase Receptors, With a Focus on Guanylyl Cyclase-A

Kühn

2003

Circulation Research

241

161

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Abstract-Besides soluble guanylyl cyclase (GC), the receptor for NO, there are at least seven plasma membrane enzymes that synthesize the second-messenger cGMP. All membrane GCs (GC-A through GC-G) share a basic topology, which consists of an extracellular ligand binding domain, a short transmembrane region, and an intracellular domain that contains the catalytic (GC) region. Although the presence of the extracellular domain suggests that all these enzymes function as receptors, specific ligands have been identified for only three of them (GC-A through GC-C). GC-A mediates the endocrine effects of atrial and B-type natriuretic peptides regulating arterial blood pressure and volume homeostasis and also local antihypertrophic actions in the heart. GC-B is a specific receptor for C-type natriuretic peptide, having more of a paracrine function in vascular regeneration and endochondral ossification. GC-C mediates the effects of guanylin and uroguanylin on intestinal electrolyte and water transport and on epithelial cell growth and differentiation. GC-E and GC-F are colocalized within the same photoreceptor cells of the retina and have an important role in phototransduction. Finally, the functions of GC-D (located in the olfactory neuroepithelium) and GC-G (expressed in highest amounts in lung, intestine, and skeletal muscle) are completely unknown. This review discusses the structure and functions of membrane GCs, with special emphasis on the physiological endocrine and cardiac functions of GC-A, the regulation of hormone-dependent GC-A activity, and the relevance of alterations of the atrial natriuretic peptide/GC-A system to cardiovascular diseases. (Circ Res. 2003;93:700-709.)

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“…Aldosterone de®ciency is therefore characterized by hyponatraemia. Atrial natriuretic peptide (ANP) inhibits sodium reabsorption, increases glomerular ®ltra-tion rate (GFR) and reduces water permeability in the collecting duct, giving rise to a natriuresis and a diuresis (Nonoguchi et al, 1988;Shiragy et al, 1988). In clinical practice, however, high plasma concentrations of natriuretic peptide rarely cause hyponatraemia, though the syndrome of cerebral salt wasting, which is characterized by hypovolaemic hyponatraemia and natriuresis, has been associated with elevated plasma atrial and brain natriuretic peptide concentrations (Yamanoto et al, 1987;Berendes et al, 1997).…”

Section: Control Of Sodium Balancementioning

confidence: 99%