Stimulation of muscarinic M 2 receptors inhibits atrial natriuretic peptide-mediated relaxation in bovine tracheal smooth muscle

2002 ◽  
Vol 366 (4) ◽  
pp. 376-379 ◽  
Author(s):  
Tsutomu Nakahara ◽  
Motonari Yunoki ◽  
Akiko Mitani ◽  
Kenji Sakamoto ◽  
Kunio Ishii
Keyword(s):  
Smooth Muscle ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Tracheal Smooth Muscle ◽  
Stimulation Of ◽  
Atrial Natriuretic

Lidocaine potentiates atrial natriuretic peptide-induced relaxation of bovine tracheal smooth muscle

2001 ◽  
Vol 425 (2) ◽  
pp. 129-133
Author(s):  
Tsutomu Nakahara ◽  
Motonari Yunoki ◽  
Hiroshi Moriuchi ◽  
Kenji Sakamato ◽  
Kunio Ishii
Keyword(s):  
Smooth Muscle ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Tracheal Smooth Muscle ◽  
Atrial Natriuretic

Atrial natriuretic peptide accounts for increased cGMP in hypoxia-induced hypertensive rat lungs

1997 ◽  
Vol 272 (6) ◽  
pp. L1126-L1132 ◽  
Author(s):  
M. Muramatsu ◽  
R. C. Tyler ◽  
J. Gutkowska ◽  
J. R. Klinger ◽  
N. S. Hill ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Vascular Tone ◽  
Physiological Salt Solution ◽  
Hypertensive Rat ◽  
Rat Lungs ◽  
Stimulation Of ◽  
Atrial Natriuretic

Perfusate levels of nitric oxide (NO)-containing compounds and guanosine 3',5'-cyclic monophosphate (cGMP) are increased in hypoxia-induced hypertensive rat lungs. To test if increased cGMP was due to NO stimulation of soluble guanylate cyclase (sGC), we examined effects of inhibition of NO synthase with N omega-nitro-L-arginine (L-NNA) on perfusate accumulation of cGMP in physiological salt solution (PSS)-perfused hypertensive lungs isolated from rats exposed for 3-4 wk to hypobaric hypoxia. Because 200 microM L-NNA did not reduce cGMP, we next examined inhibitors of other pathways of stimulation of either sGC or particulate GC (pGC). Neither 5 microM Zn-protophorphyrin, an inhibitor of CO production by heme oxygenase, nor 10 mM aminotriazole, an inhibitor of H2O2 metabolism by catalase, reduced perfusate cGMP. However, an antiserum to atrial natriuretic peptide (ANP; 100 microliters antiserum/30 ml PSS), to inhibit ANP activation of pGC, completely prevented accumulation of the nucleotide. ANP antiserum was also more effective than L-NNA in reducing lung tissue cGMP. In contrast, L-NNA but not ANP antiserum increased resting vascular tone. These results suggested that whereas ANP determined perfusate and tissue levels of cGMP, NO regulated vascular tone. To test if perfusate cGMP reflected ANP stimulation of pGC in endothelial rather than smooth muscle cells, we examined effects of 10 microM Zaprinast, an inhibitor of cGMP hydrolysis in smooth muscle but not endothelial cells, and found no increase of cGMP in hypertensive lungs. ANP levels were not elevated in hypertensive lungs, and it is unclear by what mechanism the ANP-stimulated activity of pGC is increased in hypertensive pulmonary vascular endothelial cells.

Interaction between atrial natriuretic peptide and vasoactive intestinal peptide in guinea pig cecal smooth muscle

1995 ◽  
Vol 109 (4) ◽  
pp. 1105-1112 ◽  
Author(s):  
Hirotada Akiho ◽  
Yoshiharu Chijiiwa ◽  
Hiroaki Okabe ◽  
Naohiko Harada ◽  
Hajime Nawata
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Atrial Natriuretic Peptide ◽  
Vasoactive Intestinal Peptide ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic

Inhibition of contraction of isolated lymphatic ducts by atrial natriuretic peptide

1991 ◽  
Vol 260 (3) ◽  
pp. R610-R614 ◽  
Author(s):  
W. D. Anderson ◽  
T. J. Kulik ◽  
J. E. Mayer
Keyword(s):  
Smooth Muscle ◽  
Atrial Natriuretic Peptide ◽  
Blood Vessels ◽  
Natriuretic Peptide ◽  
Dose Response ◽  
Fluid Balance ◽  
Interstitial Fluid ◽  
Force Of Contraction ◽  
Response Curves ◽  
Atrial Natriuretic

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.

Atrial natriuretic peptide stimulates salt secretion by shark rectal gland by releasing VIP

1987 ◽  
Vol 252 (1) ◽  
pp. F99-F103 ◽  
Author(s):  
P. Silva ◽  
J. S. Stoff ◽  
R. J. Solomon ◽  
S. Lear ◽  
D. Kniaz ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Rectal Gland ◽  
Channel Blockers ◽  
Dogfish Shark ◽  
Local Release ◽  
Salt Secretion ◽  
Stimulation Of ◽  
Cardiac Peptides ◽  
Atrial Natriuretic

Salt secretion by the isolated perfused rectal gland of the spiny dogfish shark, Squalus acanthias, is stimulated by synthetic rat atrial natriuretic peptide (ANP II) as well as extracts of shark heart, but not by 8-bromo-cyclic guanosine 5'-monophosphate. Cardiac peptides have no effect on isolated rectal gland cells or perfused tubules, suggesting that stimulation requires an intact gland. The stimulation of secretion by ANP II is eliminated by maneuvers that block neurotransmitter release. These include: perfusion with procaine (10(-2) M), perfusion with high Mg2+ (9.5 mM) and low Ca2+ (0.5 mM) concentrations, and addition to the perfusate of the calcium channel blockers nifedipine (10(-6)M), diltiazem (5 X 10(-5)M), or verapamil (10(-4)M). Cardiac peptides stimulate the release of vasoactive intestinal peptide (VIP), known to be present in rectal gland nerves, into the venous effluent or perfused glands in parallel with their stimulation of salt secretion, but the release of VIP induced by ANP II is prevented by perfusion with procaine. Cardiac peptides thus appear to regulate rectal gland secretion by releasing VIP from neural stores within the gland. It is possible that other physiological effects of these hormones might be explained by an action to enhance local release of neurotransmitters.

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