Atrial natriuretic factor increases splenic microvascular pressure and fluid extravasation in the rat

Sultanian, Richard; Deng, Yiming; Kaufman, Susan

doi:10.1111/j.1469-7793.2001.0273b.x

Cited by 33 publications

(37 citation statements)

References 30 publications

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“…Our future studies will be directed toward addressing this question and specifically toward elucidating the role of renal endothelial ANP effects. Within the spleen, ANP stimulates fluid extravasation into the lymphatic system by raising intrasplenic microvascular pressure (30). ANP causes vasoconstriction in the splenic vasculature (of veins more than of arteries) by an endothelium-independent mechanism, mediated by GC-A (31).…”

Section: Discussionmentioning

confidence: 99%

“…Changes in capillary endothelial permeability seem not to be involved. The splenic capillary beds have a discontinuous endothelium (32) and are freely permeable to plasma proteins (33); i.e., there is no colloid osmotic gradient across the capillary wall to oppose fluid efflux, and modest increases in splenic microvascular hydraulic pressure are able to induce a significant increase in fluid extravasation (30). Thus, although the spleen is an important site of ANP-induced fluid extravasation, this action of ANP is not mediated by the endothelium and therefore is unlikely to be compromised in EC GC-A KO mice.…”

Section: Discussionmentioning

confidence: 99%

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Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide

Sabrane¹,

Kruse²,

Fabritz³

et al. 2005

J. Clin. Invest.

146

148

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Atrial natriuretic peptide (ANP), via its vasodilating and diuretic effects, has an important physiological role in the maintenance of arterial blood pressure and volume. Its guanylyl cyclase-A (GC-A) receptor is highly expressed in vascular endothelium, but the functional relevance of this is controversial. To dissect the endothelium-mediated actions of ANP in vivo, we inactivated the GC-A gene selectively in endothelial cells by homologous loxP/Tie2-Cre-mediated recombination. Notably, despite full preservation of the direct vasodilating effects of ANP, mice with endothelium-restricted deletion of the GC-A gene (EC GC-A KO) exhibited significant arterial hypertension and cardiac hypertrophy. Echocardiographic and Doppler flow evaluations together with the Evan's blue dilution technique showed that the total plasma volume of EC GC-A KO mice was increased by 11-13%, even under conditions of normal dietary salt intake. Infusion of ANP caused immediate increases in hematocrit in control but not in EC GC-A KO mice, which indicated that ablation of endothelial GC-A completely prevented the acute contraction of intravascular volume produced by ANP. Furthermore, intravenous ANP acutely enhanced the rate of clearance of radio-iodinated albumin from the circulatory system in control but not in EC GC-A KO mice. We conclude that GC-A-mediated increases in endothelial permeability are critically involved in the hypovolemic, hypotensive actions of ANP.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide

Sabrane¹,

Kruse²,

Fabritz³

et al. 2005

J. Clin. Invest.

146

148

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“…Increased splenic microvascular pressure 67 Fluid extravasation from the splenic vasculature into the lymphatic system 67 …”

Section: Effects In the Spleenmentioning

confidence: 99%

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

Kühn

2003

Circulation Research

240

164

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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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“…To discriminate between the roles of the NP A and NP B receptors, A71915 was used to selectively block NP A receptors. 19,20 A71915 is a structural analog of ANP 19 with a binding affinity to rat NP A receptors only 22 times less potent than native rat ANP . 21 …”

mentioning

confidence: 99%

Guanylyl Cyclase Receptors Mediate Cardiopulmonary Vagal Reflex Actions of ANP

Thomas

Woods

2003

Hypertension

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Abstract-Atrial natriuretic peptide (ANP) potentiates vagal cardiopulmonary reflexes due to chemosensory (BezoldJarisch [B-J] reflex) or mechanosensory (ramp baroreflex) activation. The ANP receptor mediating these actions is unknown. We examined the role of particulate guanylyl-cyclase (pGC) receptors in ANP-induced enhancement of cardiopulmonary vagal reflexes. Cardiopulmonary baroreceptor reflex function was assessed by bradycardic responses to ramp blood pressure rises after rapid intravenous methoxamine (100 g/kg bolus dose). The B-J reflex was evoked by 3 intravenous doses of serotonin (1 to 10 g/kg). In conscious, chronically instrumented rats (nϭ9), these tests were performed on each animal during randomized infusions of rat ANP (150 ng/kg per minute IV), saline (270 L/h IV), the pGC receptor antagonist HS-142-1 (3 mg/kg IV), or combined HS-142-1ϩANP treatment. 4,5 There are 3 known natriuretic peptide receptor subtypes: A (NP A ), B (NP B ), and C (NP C ). 8 Most of the well-known biological actions, such as vasodilation and natriuresis, of the natriuretic peptides occur subsequent to stimulating the production of the second-messenger cyclic guanosine 3Ј 5Ј-monophosphate (cGMP), through particulate guanylylcyclase (pGC)-coupled receptors (the NP A and NP B receptors). The NP C receptor fulfills the role of a clearance receptor for the 3 natriuretic peptides. 9 In addition, while not having guanylylcyclase activity, this receptor has been reported to influence 3 signal-transducing systems: phospholipase C, adenylyl cyclase, and calcium channels. 9 The NP C receptor is proposed to be a physiological regulator of activities such as adrenergic transmission, renin and progesterone secretion, and platelet aggregation. 9 Although there is a growing body of literature linking natriuretic peptide receptors to the more widely known cardiovascular and renal actions of ANP, BNP, and CNP, 10 -15 the nature of the natriuretic peptide receptors involved in the HR reflex activities of these hormones has not been studied or reported in the literature. Since BNP and CNP share with ANP the ability to enhance reflex bradycardic responses, 4,5 a common receptor may mediate these effects. In the present studies, the contribution from the guanylyl cyclase receptors to the cardiopulmonary vagal baroreflex and chemoreflex (Bezold-Jarisch [B-J]) actions of ANP was investigated. HS-142-1 was used to selectively antagonize the NP A ϩNP B guanylyl cyclase-coupled (pGC) receptors. 16 HS-142-1 is a polysaccharide microbial product isolated from the culture broth of Aureobasidium species. 16 HS-142-1 blocks the vasodilator and renal effects of exogenously administered ANP and BNP and also reverses the changes resulting from augmented endogenous production of ANP and BNP. 10,17,18 Although HS-142-1 can exclude a role for the non-guanylyl cyclase receptor NP C , 16 this compound does not distinguish between subclasses of the pGC natriuretic peptide receptors.

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Atrial natriuretic factor increases splenic microvascular pressure and fluid extravasation in the rat

Cited by 33 publications

References 30 publications

Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide

Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide

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

Guanylyl Cyclase Receptors Mediate Cardiopulmonary Vagal Reflex Actions of ANP

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