Angiotensin II and atrial natriuretic factor receptor interactions at the blood-brain barrier

Grammas, Paula; Giacomelli, F; Bessert, Denise; Wiener, Joseph

doi:10.1016/0006-8993(91)91191-3

Cited by 13 publications

(4 citation statements)

References 23 publications

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“…As described previously, this peptide increases the permeability of BBB via cGMP-PKG pathway (Grammas et al, 1991;Sarker and Fraser, 2002;Vigne and Frelin, 1992). It is therefore reasonable that there are some differences in the ANP effect on tissue water in brains and other organs, such as lungs.…”

Section: Anp Effect On Brain Edema Formationmentioning

confidence: 86%

“…Recent experimental studies in vitro showed that ANP increased the permeability of brain capillaries via the cGMP-PKG pathway (Grammas et al, 1991;Sarker and Fraser, 2002;Vigne and Frelin, 1992). It is therefore possible that ANP administration may exacerbate brain edema formation found in brain injuries, as based upon the vasogenic mechanism, and this may be enhanced by the preexistence of critical damage in the blood brain barrier (BBB).…”

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confidence: 99%

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Differential Effects of Atrial Natriuretic Peptide on the Brain Water and Sodium after Experimental Cortical Contusion in the Rat

Fukui

Fazzina

Amorini

et al. 2003

J Cereb Blood Flow Metab

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Summary:Atrial natriuretic peptide (ANP) plays an important role in the regulation of water and sodium in the body via cyclic GMP (cGMP) pathway. Although ANP has been shown to be protective in cerebral ischemia or intracerebral hemorrhage, its role in traumatic brain injury (TBI) has yet to be elucidated. We herein assessed ANP effects on brain water and sodium in TBI. Controlled cortical impact (3 mm depth, 6 m/sec) was used to induce an experimental cortical contusion in rats. Continuous administration of ANP 0.2 (n ‫ס‬ 6) or 0.7 g/kg/24 h (n ‫ס‬ 6), cGMP analogue (8-Bromo-cGMP) 0.1 (n ‫ס‬ 5) or 0.3 mg/kg/24 h (n ‫ס‬ 5), or vehicle (n ‫ס‬ 6) was begun 15 minutes after injury, using a mini-osmotic pump implanted into the peritoneal cavity. At 24 hours after injury, ANP significantly exacerbated brain edema in the injured hemisphere in a dose-dependent manner while it reduced brain sodium concentrations in both hemispheres. These ANP effects could be mimicked by a cGMP analogue. In the second series (n ‫ס‬ 20), BBB integrity was assessed by evaluating the extravasation of Evans blue dye. ANP or cGMP analogue significantly worsened BBB disruption in the injured hemisphere at 24 hours after injury. These findings suggest that ANP administration exacerbates brain edema after the experimental cortical contusion in rats, possibly because of an increase in the BBB permeability via cGMP pathway, whereas it reduces brain sodium levels.

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Section: Anp Effect On Brain Edema Formationmentioning

confidence: 86%

mentioning

confidence: 99%

Differential Effects of Atrial Natriuretic Peptide on the Brain Water and Sodium after Experimental Cortical Contusion in the Rat

Fukui

Fazzina

Amorini

et al. 2003

J Cereb Blood Flow Metab

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“…These natriuretic peptides also have high affinities for the NPR‐C clearance receptor, which has been associated with inhibition of adenylyl cyclase (Hempel et al 1998). Natriuretic peptides have been shown to increase the permeability of cerebral and peripheral microvessels (Huxley et al 1987; Vigne & Frelin, 1992) and to increase cGMP levels in brain microvessels (Grammas et al 1991). In the present series of experiments, both ANP and CNP increased permeability in a dose‐dependent manner (Fig.…”

Section: Discussionmentioning

confidence: 99%

The role of guanylyl cyclases in the permeability response to inflammatory mediators in pial venular capillaries in the rat

Sarker

Fraser

2002

The Journal of Physiology

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Inflammatory mediators have a role in the formation of cerebral oedema and there is evidence that cGMP is an important signal in vascular permeability increase. We have investigated the role and the source of cGMP in mediating the permeability response to acutely applied bradykinin and the histamine H2 agonist dimaprit on single cerebral venular capillaries, by using the single vessel occlusion technique. We found that 8‐bromo‐cGMP applied acutely resulted in a small and reversible permeability increase with a log EC50−7.2 ± 0.15 m. KT 5823, the inhibitor of cGMP‐dependent protein kinase, abolished the permeability responses to both bradykinin and dimaprit, while zaprinast, an inhibitor of type 5 phosphodiesterase, potentiated the response to bradykinin. On the other hand, l‐NMMA blocked the response to dimaprit, but not that to bradykinin. Inhibitors of soluble guanylyl cyclase, LY 85353 and methylene blue, also inhibited the permeability response to dimaprit, but not bradykinin. The permeability responses to the natriuretic peptides ANP and CNP were of similar magnitude to that of bradykinin with log EC50−10.0 ± 0.33 m and −8.7 ± 0.23 m, respectively. The natriuretic peptide receptor antagonist HS‐142–1 blocked permeability responses to bradykinin as well as to ANP, and leukotriene D4 blocked the responses to CNP and bradykinin, but not to dimaprit. In conclusion, the histamine H2 receptor appears to signal via cGMP that is generated by a NO and soluble guanylyl cyclase, while bradykinin B2 receptor also signals via cGMP but through particulate guanylyl cyclase.

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“…It has been known that during ischemic stroke ANP increases permeability of brain capillaries and it's expression is increased in glial cells surrounding the ischemic core [26][27][28]. Even though NPs were shown to increase capillary permeability in ischemic stroke and intracranial hemorrhage, ANP is able to reduce the size of brain areas affected with edema in those conditions [29,30].…”

Section: Natriuretic Peptides and Their Functionmentioning

confidence: 99%

Natriuretic peptides in brain physiology

Sinđić

Dobrivojević

Hirsch

2011

Translational Neuroscience

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Natriuretic peptides (NPs) regulate salt and water homeostasis by inducing natriuresis and diuresis in the kidney. These actions in addition to those via the heart and vascular system play important roles in the regulation of blood pressure. In the central nervous system NPs play a significant role in neuronal development, synaptic transmission and neuroprotection. Currently, six different human NPs have been described: atrial natriuretic peptide (ANP), urodilatin (URO, renal natriuretic peptide), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) as well as guanylin and uroguanylin. ANP, URO and BNP activate the natriuretic peptide receptor A (NPR-A or guanylate cyclase A (GC-A)) while CNP activates natriuretic peptide receptor B (NPR-B or guanylate cyclase B (GC-B)). Guanylin and uroguanylin are known to activate guanylate cyclase C (GC-C). The receptors GC-A, GC-B, and GC-C are widely expressed in the human body. Currently, GC-B and CNP seems to have the highest expression in central nervous system compared to other NPs and their receptors. All known NPs generate intracellular cyclic GMP (cGMP) by activating their specific guanylate cyclase receptors. Subsequently, cGMP is able to activate protein kinase I or II (PKG I or II) and/or directly regulate transmembrane proteins such as ion channels, transporters and pumps. NPs also bind to the natriuretic peptide receptor C (also called clearance receptor NPR-C) which is a major pathway for the degradation of NPs and has no guanylate cyclase activity. In this review we will focus on new insights regarding the physiological effects of NPs in the brain, especially specific areas of their signaling pathways in neurons and glial cells.

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Angiotensin II and atrial natriuretic factor receptor interactions at the blood-brain barrier

Cited by 13 publications

References 23 publications

Differential Effects of Atrial Natriuretic Peptide on the Brain Water and Sodium after Experimental Cortical Contusion in the Rat

Differential Effects of Atrial Natriuretic Peptide on the Brain Water and Sodium after Experimental Cortical Contusion in the Rat

The role of guanylyl cyclases in the permeability response to inflammatory mediators in pial venular capillaries in the rat

Natriuretic peptides in brain physiology

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