Role of guanylyl cyclase receptors for CNP in salt secretion by shark rectal gland

1997 ◽  
Vol 273 (4) ◽  
pp. R1400-R1406 ◽  
Author(s):  
Mark Gunning ◽  
Richard J. Solomon ◽  
Franklin H. Epstein ◽  
Patricio Silva
Keyword(s):  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Competitive Inhibitor ◽  
Systemic Circulation ◽  
Rectal Gland ◽  
Saline Solutions ◽  
Salt Secretion

The role of C-type natriuretic peptide (CNP) and its guanylyl cyclase-linked receptors in mediating salt secretion by the rectal gland of the spiny dogfish shark ( Squalus acanthias) was investigated using HS-142–1, a competitive inhibitor of the binding of natriuretic peptides to their guanylyl cyclase receptors. CNP binds to receptors and activates guanylyl cyclase in rectal gland membranes in a way that is inhibited by HS-142–1. Guanylyl cyclase activation in rectal gland membranes is far more sensitive to CNP than to atrial natriuretic peptide, whereas the reverse is true for membranes derived from mammalian (rabbit) renal collecting duct cells. HS-142–1 inhibited the stimulatory effect of CNP on ouabain-inhibitable oxygen consumption by rectal gland tubules. In explanted rectal glands continuously perfused with blood from intact donor sharks, HS-142–1 inhibited the increase in salt secretion normally provoked by infusing isotonic saline solutions into the donor animal. These results strongly support the view that CNP released into the systemic circulation in response to volume expansion mediates the secretion of chloride by the rectal gland via receptors linked to guanylyl cyclase.

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.

scholarly journals Phosphodiesterase inhibitors correct resistance to natriuretic peptides in rats with Heymann Nephritis.

1996 ◽  
Vol 7 (4) ◽  
pp. 582-593
Author(s):  
J P Valentin ◽  
W Z Ying ◽  
L A Sechi ◽  
K T Ling ◽  
C Qiu ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Phosphodiesterase Inhibitors ◽  
Contralateral Kidney ◽  
Heymann Nephritis

Experimental nephrotic syndrome is characterized by abnormal sodium metabolism, reflected in a blunted natriuretic response both to volume expansion and to infused atrial natriuretic peptide (ANP). The studies presented here examined the relationships among plasma ANP concentration and urinary sodium (VNaV) and cyclic GMP excretion (UcGMPV) in vivo, and the responsiveness of isolated glomeruil and inner medullary collecting duct (IMCD) cells to ANP and urodilatin (renal natriuretic peptide; RNP) in vitro in rats with Heymann nephritis, an immunologically mediated model of nephrotic syndrome. Nine to 14 days after Ip injection of anti-Fx1A antiserum, rats were proteinuric and had a blunted natriuretic response to intravenous infusion of isotonic saline (2% body weight, given over 5 min). Thirty min after the onset of the infusion, plasma ANP concentration was increased to the same extent in both normal and nephritic rats, compared with their respective hydropenic controls. Despite this increase, UcGMPV was significantly less in nephritic rats after the saline infusion. Accumulation of cGMP by isolated glomeruil and IMCD cells from nephritic rats after incubation with ANP and RNP was also significantly reduced, compared with normal rats. This difference was not related to differences in either density or affinity of renal ANP receptors, but was abolished when accumulation of cGMP was measured in the presence of 10(-3) M isobutylmethylxanthine or Zaprinast, two different inhibitors of cyclic nucleotide phosphodiesterases (PDE). Infusion of Zaprinast into one renal artery in nephritic rats normalized both the natriuretic response to volume expansion and the increase in UcGMPV from the infused, but not the contralateral, kidney. Furthermore, cGMP-PDE activity was increased in IMCD cell homogenates from nephritic compared with normal rats (388 +/- 32 versus 198 +/- 93 pmol/min per mg protein, P < 0.03). These results indicate that blunted volume expansion natriuresis accompanied by cellular resistance to ANP in vitro occurs in an immunologic model of renal injury. The resistance is not related to an alteration in ANP release or binding to its renal receptors, but is suppressed by PDE inhibitors and is associated with increased renal cGMP. PDE activity, thus suggesting that enhanced cGMP-PDE activity may account for resistance to the natriuretic actions of ANP observed in vivo. This defect may represent the intrinsic sodium transport abnormality linked to sodium retention in nephrotic syndrome.

scholarly journals Role of Natriuretic Peptide Receptor Guanylyl Cyclase-A in Myocardial Infarction Evaluated Using Genetically Engineered Mice

Hypertension ◽  
2005 ◽  
Vol 46 (2) ◽  
pp. 441-447 ◽  
Author(s):  
Michio Nakanishi ◽  
Yoshihiko Saito ◽  
Ichiro Kishimoto ◽  
Masaki Harada ◽  
Koichiro Kuwahara ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Genetically Engineered ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Genetically Engineered Mice

Role of atrial natriuretic peptide in natriuresis in volume-expanded rats

1987 ◽  
Vol 253 (6) ◽  
pp. R877-R882
Author(s):  
K. Kaneko ◽  
K. Okada ◽  
S. Ishikawa ◽  
T. Kuzuya ◽  
T. Saito
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Critical Role ◽  
Hormone Secretion ◽  
Isotonic Saline ◽  
Fold Increase ◽  
Urinary Sodium Excretion ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Atrial Natriuretic

Continuous intravenous infusion of rat atrial natriuretic peptide (rANP) was carried out for 60 min in urethan-anesthetized rats. Plasma rANP (PANP) levels during 0, 12.5, and 50 ng/min rANP infusion reached 20.9 +/- 3.4, 61.2 +/- 12.3, and 228 +/- 30.6 pg/ml, respectively. Urinary sodium excretion (UNaV) remained unchanged during the 0 and 12.5 ng/min rANP infusion. In contrast, the 50 ng/min rANP infusion resulted in a 5.6-fold increase in UNaV without significant changes in plasma aldosterone levels and glomerular filtration rate. Isotonic saline infusion (116 microliter/min for 60 or 120 min) caused a significant increase in UNaV. UNaV in an experimental model of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was 5.0 times greater than in control animals. PANP levels in 60- or 120-min saline-infused and SIADH rats were 46.3 +/- 6.7, 39.0 +/- 9.0, and 35.6 +/- 3.2 pg/ml, respectively. These values were significantly higher than control values but failed to achieve a level at which natriuresis occurred during the infusion of rANP. These results suggest that endogenous ANP may not play a critical role in the induction of acute natriuresis in volume-expanded states, although it could be partially involved in such a natriuretic response.

Sign in / Sign up

Export Citation Format

Share Document