Inhibition of contraction of isolated lymphatic ducts by atrial natriuretic peptide

Atrial natriuretic peptide (ANP) potently relaxes blood vessels but its effect on lymphatic motility is unreported. We studied the effect of ANP, and the smooth muscle relaxing agent nitroprusside (NP), on isolated ovine mesenteric lymphatic ducts. Duct segments were mounted on a myograph, and noncumulative dose-response curves were obtained for the effect of ANP and NP on the rate and force of spontaneous (and norepinephrine-induced) duct contraction. Both ANP (threshold approximately 1 nM) and NP (threshold approximately 10 nM) in a dose-related fashion reduced the frequency and force of contraction of both spontaneously contracting and norepinephrine-stimulated duct segments. ANP may therefore affect interstitial fluid balance through its effect on lymphatic motility.

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Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽

10.1152/physiologyonline.1996.11.3.138 ◽

1996 ◽

Vol 11 (3) ◽

pp. 138-143 ◽

Cited By ~ 2

Author(s):

EM Renkin ◽

VL Tucker

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Volume ◽

Fluid Balance ◽

Interstitial Fluid ◽

Fluid Volume ◽

Interstitial Fluid Volume ◽

Atrial Natriuretic

Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.

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Variability of response to atrial natriuretic peptide and sodium nitroprusside in cultured vascular smooth muscle cells from three blood vessels

Critical Care Medicine ◽

10.1097/00003246-199409000-00017 ◽

1994 ◽

Vol 22 (9) ◽

pp. 1461-1464 ◽

Cited By ~ 2

Author(s):

LI-MING ZHANG ◽

MANUEL CASTRESANA ◽

WALTER H. NEWMAN

Keyword(s):

Smooth Muscle ◽

Atrial Natriuretic Peptide ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Sodium Nitroprusside ◽

Blood Vessels ◽

Natriuretic Peptide ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells ◽

Atrial Natriuretic

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EFFECT OF ATRIAL NATRIURETIC PEPTIDE (ANP) AND SODIUM NITROPRUSSIDE (SNP) ON cGMP IN SMOOTH MUSCLE CELLS CULTURED FROM THREE BLOOD VESSELS

Critical Care Medicine ◽

10.1097/00003246-199304001-00070 ◽

1993 ◽

Vol 21 (Supplement) ◽

pp. S162

Author(s):

Li-ming Zhang ◽

Manuel Castresana ◽

Walter Newman

Keyword(s):

Smooth Muscle ◽

Atrial Natriuretic Peptide ◽

Smooth Muscle Cells ◽

Sodium Nitroprusside ◽

Blood Vessels ◽

Natriuretic Peptide ◽

Muscle Cells ◽

Cells Cultured ◽

Atrial Natriuretic

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Regulation of atrial natriuretic peptide receptors in vascular smooth muscle cells: role of cGMP

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.264.6.h1753 ◽

1993 ◽

Vol 264 (6) ◽

pp. H1753-H1759 ◽

Cited By ~ 3

Author(s):

L. M. Zhang ◽

H. Tao ◽

W. H. Newman

Keyword(s):

Smooth Muscle ◽

Atrial Natriuretic Peptide ◽

Smooth Muscle Cells ◽

Natriuretic Peptide ◽

Muscle Cells ◽

Cell Types ◽

Response Curves ◽

Acute Response ◽

Anp Receptors ◽

Atrial Natriuretic

We tested the hypothesis that intracellular guanosine 3',5'-cyclic monophosphate (cGMP) regulates atrial natriuretic peptide (ANP) receptors. The effect of chronic exposure to ANP, sodium nitroprusside (SNP), and 8-bromo-cGMP (8-BrcGMP) on ANP receptors and cGMP formation was determined in guinea pig thoracic aorta smooth muscle cells (TASM) and in coronary artery smooth muscle cells (CASM). TASM express both the ANP-activated guanylyl cyclase (B-receptor) and the clearance receptor (C-receptor) and respond to ANP with increased cGMP. CASM exhibit only the ANP C-receptor. In TASM, 24-h treatment with 1 microM atriopeptin (AP) III [rat ANP-(103–126)] caused a sixfold increase in basal cGMP levels, which were unaltered in CASM. In AP III-treated TASM, maximal binding of 125I-labeled AP III (Bmax) was reduced 40% while affinity [dissociation constant (KD)] was unaltered. In CASM, Bmax and KD were not affected. In treated TASM, washed free of AP III, acute dose-response curves of cGMP to AP III were not different from that in untreated cells. In both TASM and CASM, basal cGMP levels were elevated and Bmax was decreased by 6-h treatment with SNP. SNP did not alter the acute response of cGMP to AP III. In both cell types, 8-BrcGMP for 6 h caused reduction in Bmax. These findings support the conclusion that elevated cGMP was necessary for ANP-induced downregulation of receptors. The unaltered responsiveness of cGMP to AP III suggests the B-receptor was not altered and the reduced Bmax was due to decreased C-receptor.

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