Evidence for a dopaminergic mechanism for the diuretic and natriuretic action of centrally administered atrial natriuretic factor

Israel, A; Torres, Marysabel; Barbella, Yarisma

doi:10.1007/bf00711416

Cited by 13 publications

(3 citation statements)

References 35 publications

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“…There are several reports indicating that the natriuretic effect of ANP requires the presence of dopamine 1 like receptors, (24)(25)(26)(27)(28). It has also been shown that the inhibitory effect of ANP on the Na ϩ ,H ϩ exchanger and on Na ϩ ,K ϩ ATPase are at least partially mediated via dopamine 1 like receptors (29,30).…”

Section: Reprintsmentioning

confidence: 95%

Mechanisms by Which Intrarenal Dopamine and Anp Interact to Regulate Sodium Metabolism

Brismar

Holtbäck

Aperia

2000

Clinical and Experimental Hypertension

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Maintenance of a normal blood pressure requires a precise and fine-tuned regulation of salt metabolism. This is accomplished by a bidirectional regulation of renal tubular sodium transporters by natriuretic and antinatriuretic hormones. Dopamine, produced in the renal proximal tubular cells, plays an important role in this interactive system. Dopamine inhibits the activity of Na+,K+ ATPase as well as of many important sodium influx pathways in the nephron. These effects of dopamine are particularly pronounced in situation of sodium loading. There is an abundance of evidence suggesting that the natriuretic effects of ANP are to a large extent mediated via renal dopamine 1 like receptors. The renal tubular dopamine 1 like receptors are, under basal conditions, mainly located intracellularly. ANP and its second messenger, cGMP, cause a rapid translocation of the dopamine 1 like receptors to the plasma membrane. This phenomenon may explain how ANP and dopamine act in concert to regulate sodium metabolism. Regulation of sodium metabolism and blood pressure is critically dependent on a normal function of the renal dopamine system. Hence, abnormalities in the interaction between dopamine and ANP may predispose to hypertension.

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Section: Reprintsmentioning

confidence: 95%

Mechanisms by Which Intrarenal Dopamine and Anp Interact to Regulate Sodium Metabolism

Brismar

Holtbäck

Aperia

2000

Clinical and Experimental Hypertension

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“…The possible involvement of brain dopaminergic systems in the diuresis and natriuresis induced by AV3Vinjected ANP was investigated by Israel et al (241). The diuretic and natriuretic actions of injection of ANP in the third ventricle were inhibited in animals with central sympathectomy.…”

Section: Dopaminementioning

confidence: 99%

Neuroendocrine Control of Body Fluid Metabolism

Antunes‐Rodrigues

Castro

Elias

et al. 2004

Physiological Reviews

401

310

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Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+ receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

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“…This hypothesis is supported by preclinical evidence showing that centrally acting natriuretic peptides require the integrity of central dopaminergic system function to mediate natriuresis. 9 Haloperidol, for example, can increase the level of central natriuretic peptides and induce natriuresis. 10 We are aware of the speculative nature of our argument, but other causes for CSWS in our patient could be ruled out.…”

Section: Commentmentioning

confidence: 99%

Cerebral Salt-Wasting Syndrome in a Patient With Neuroleptic Malignant Syndrome

Lenhard¹,

Külkens²,

Schwab³

2007

Arch Neurol

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Background: Hyponatremia associated with neuroleptic malignant syndrome has thus far been described as a syndrome of inappropriate secretion of antidiuretic hormone. Objectives: To ascertain and describe the role of cerebral salt-wasting syndrome as the cause of hyponatremia in a patient with neuroleptic malignant syndrome. Patient: A psychotic patient being treated with olanzapine presenting with sopor, muscle rigidity, polyuria, tachycardia, pyrexia, and severe hyponatremia. Methods: Serial serological examinations of plasma tonicity (sodium level and osmolality), brain natriuretic peptide, and antidiuretic hormone were performed, and sodium excretion and urine osmolality were determined from 24-hour urine collection. In addition, markers for rhabdomyolysis were monitored. Results: The patient shows clear symptoms of cerebral salt-wasting syndrome in association with neuroleptic malignant syndrome, characterized by severe hyponatremia, volume depletion, and elevated brain natriuretic peptide but normal antidiuretic hormone levels. Cerebral saltwasting syndrome improved under dantrolene sodium treatment and concomitant fluid and sodium replacement. Conclusion: Hyponatremia in patients with neuroleptic malignant syndrome might more likely reflect cerebral salt-wasting syndrome than a syndrome of inappropriate secretion of antidiuretic hormone as an additional aspect of autonomic dysregulation caused by antidopaminergic drugs.

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Evidence for a dopaminergic mechanism for the diuretic and natriuretic action of centrally administered atrial natriuretic factor

Cited by 13 publications

References 35 publications

Mechanisms by Which Intrarenal Dopamine and Anp Interact to Regulate Sodium Metabolism

Mechanisms by Which Intrarenal Dopamine and Anp Interact to Regulate Sodium Metabolism

Neuroendocrine Control of Body Fluid Metabolism

Cerebral Salt-Wasting Syndrome in a Patient With Neuroleptic Malignant Syndrome

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