Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation.

Ehrlich, Kelly; Fitts, Douglas A.

doi:10.1037/0735-7044.104.2.365

Cited by 47 publications

(17 citation statements)

References 37 publications

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“…Intracerebroventricular administration of synthetic ANP decreases the water intake of dehydrated rats (16)(17)(18), and neutralization of ANP with anti-ANP antiserum potentates water intake induced by water deprivation or angiotensin II injection (16,19). These findings suggest that endogenous ANP in rat brain antagonizes the action of angiotensin and plays an important role in the maintenance of drinking behavior.…”

Section: Resultsmentioning

confidence: 61%

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

Dubois

Kishimoto

Lillis

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Disruption of the atrial natriuretic peptide (ANP) receptor [guanylyl cyclase-A (GC-A)] gene yields mice with a salt-resistant form of hypertension, raising fundamental questions on the role of ANP in acute regulation of the kidney. Here, we show that water intake, food consumption, stool weight, urine volume, and sodium excretion are not significantly different between wild-type and GC-A null mice on standard rodent chow (0.7% NaCl) or a high-salt diet (8% NaCl). In conscious mice with an indwelling catheter, the infusion of a physiological saline solution containing 4% BSA resulted in a marked natriuresis͞diuresis in wild-type mice but no response in GC-A null animals. When physiological saline was given by gavage, however, the kidney response of wild-type and null mice was equivalent, raising the possibility that the gastrointestinal tract can directly regulate kidney function. However, administration of 0.9% saline through an intraperitoneal route also resulted in equal kidney responses in wild-type and null mice. When 0.9% NaCl lacking protein was infused i.v., wild-type and null mice both responded at the kidney level. Thus, GC-A appears dispensable for regulation of sodium͞water excretion in response to changes in dietary sodium concentration, but likely becomes critical in volume expansions where the isooncotic pressure remains constant, such as head-out immersion or the initial and correctable stages of congestive heart failure.

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Section: Resultsmentioning

confidence: 61%

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

Dubois

Kishimoto

Lillis

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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“…In mammals and birds, the SFO and OVLT are forebrain CVOs important for controlling drinking by systemic hormones (Takei, 1992;Fitzsimons, 1998). The SFO and OVLT are the target sites for circulating ANG II (Kobayashi and Takei, 1996;Ferguson and Bains, 1996;Fitzsimons, 1998), since local injection of femtomolar doses of ANG II into these sites induces drinking, and since local lesioning of these structures eliminates the dipsogenic effects of systemic injection of ANG II (Simpson and Routenberg, 1973;Takei, 1977;Ehrlich and Fitts, 1990;Schmid and Simon, 1992;Li and Ferguson, 1993). Further, the ANG II subtype 1 receptor (AT1) is localized in the SFO (Song et al, 1992) and ANG II enhances neuronal activities of SFO (Gutman et al, 1988;Hattori et al, 1988) in the rat.…”

Section: The Journal Of Experimental Biologymentioning

confidence: 99%

Area postrema, a brain circumventricular organ, is the site of antidipsogenic action of circulating atrial natriuretic peptide in eels

Tsukada

Nobata

Hyodo

et al. 2007

Journal of Experimental Biology

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SUMMARY Accumulating evidence indicates that circulating atrial natriuretic peptide(ANP) potently reduces excess drinking to ameliorate hypernatremia in seawater(SW) eels. However, the cerebral mechanism underlying the antidipsogenic effect is largely unknown. To localize the ANP target site in the brain, we examined the distribution of ANP receptors (NPR-A) in eel brain immunohistochemically using an antiserum specific for eel NPR-A. The immunoreactive NPR-A was localized in the capillaries of various brain regions. In addition, immunoreactive neurons were observed mostly in the medulla oblongata, including the reticular formation, glossopharyngeal-vagal motor complex, commissural nucleus of Cajal, and area postrema (AP). Trypan Blue, which binds serum albumin and does not cross the blood–brain barrier, was injected peripherally and stained the neurons in the AP but not other NPR-A immunopositive neurons. These histological data indicate that circulating ANP acts on the AP, which was further confirmed by physiological experiments. To this end, the AP in SW eels was topically destroyed by electric cauterization or were by chemical lesion of its neurons by kainic acid, and ANP (100 pmol kg–1) was then injected into the circulation. Both heat-coagulative and chemical lesions to the AP greatly reduced an antidipsogenic effect of ANP, but the ANP effect was retained in sham-operated eels and in those with lesions outside the AP. These results strongly suggest that the AP, a circumventricular organ without a blood–brain barrier, serves as a functional window of access for the circulating ANP to inhibit drinking in eels.

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“…These observations first suggest that not all actions ofNPs are directed toward a common physiological goal, and second indicate that such contrasting effects of these different NPs may be the result specific actions in different regions of the CNS. The studies of Erlich and Fitts (15), in which ANP administered directly into SFO inhibited ANG and dehydration-induced drinking, suggest this CVO, in which high densities ofNPR-A receptors are found, to be the site at which ANP exerts such inhibitory effects. This conclusion draws support both from the demonstration of increased numbers of ANP binding sites in SFO and choroid plexus following 4 d of water deprivation (18), and from the demonstrated ability of ANP to stimulate guanylyl cyclase activity in these regions (19).…”

Section: Roles In Control Of Fluid Intakementioning

confidence: 94%

“…One of the first physiological actions of ANP described was its ability to antagonize ANG actions within the SFO to induce drinking (15). A number of different in vitro single-unit recording studies have attempted to determine the effects of NPs on SFO neurons, but unfortunately have yielded contradictory results.…”

Section: Forebrain Neuronsmentioning

confidence: 99%

Natriuretic Peptide Actions in the Brain

Ferguson¹

1997

Natriuretic Peptides in Health and Disease

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Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation.

Cited by 47 publications

References 37 publications

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

Area postrema, a brain circumventricular organ, is the site of antidipsogenic action of circulating atrial natriuretic peptide in eels

Natriuretic Peptide Actions in the Brain

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