Cardiovascular effects of arginine vasotocin, atrial natriuretic peptide, and epinephrine in freshwater eels

1995 ◽  
Vol 268 (5) ◽  
pp. R1273-R1280 ◽  
Author(s):  
G. Y. Oudit ◽  
D. G. Butler
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cardiovascular Effects ◽  
Aortic Pressure ◽  
Arginine Vasotocin ◽  
Systemic Resistance ◽  
Pressor Responses ◽  
Freshwater Eels ◽  
Positive Chronotropic Effect ◽  
Atrial Natriuretic

The effects of 150 ng/kg iv injections of arginine vasotocin (AVT), eel atrial natriuretic peptide (ANP), and epinephrine (Epi) on the cardiovascular dynamics of resting freshwater eels, Anguilla rostrata were studied. Injection of AVT into the caudal vein significantly increased cardiac output (CO) from 15.3 to 23.6 ml.min-1.kg-1 primarily by increasing stroke volume. Mean dorsal aortic pressure (PDA) also increased. Estimated branchial shunting (2.54 ml.min-1.kg-1) was elevated by 130% because of an increased proportion of CO, indicating a vasoconstriction of the branchial arterioarterial pathway. In contrast, Epi reduced the fraction of CO perfusing the arteriovenous pathway. Epi also produced a positive chronotropic effect, increased CO and systemic vasoconstriction, resulting in a vasopressor response. These changes occurred earlier than those of AVT and ANP. Pressor responses triggered by AVT and Epi preceded the increases in CO. Injections of 150 and 200 ng/kg ANP caused a reduction in PDA due to a decrease in CO (and SV) but failed to modulate systemic resistance. The change in CO was the primary contributor to the pressor (and depressor) responses elicited by the three hormones.

scholarly journals Renal and Cardiovascular Effects of Atrial Natriuretic Peptide in Fetal Sheep

1989 ◽  
Vol 26 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Barbara Y Hargrave ◽  
Harriet S Iwamoto ◽  
Abraham M Rudolph
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cardiovascular Effects ◽  
Fetal Sheep ◽  
Atrial Natriuretic

Renal effects of atrial natriuretic peptide in a marine elasmobranch

1990 ◽  
Vol 258 (5) ◽  
pp. R1201-R1206 ◽  
Author(s):  
S. Benyajati ◽  
S. D. Yokota
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Aortic Pressure ◽  
Renal Effects ◽  
Physiological Dose ◽  
Excretion Rates ◽  
Solute Excretion ◽  
Mammalian Peptide ◽  
Mean Aortic Pressure ◽  
Atrial Natriuretic

The effects of atrial natriuretic peptide on the renal function of the spiny dogfish (Squalus acanthias) in seawater were evaluated. A synthetic mammalian peptide, atriopeptin II (2 micrograms/kg), was injected intravascularly into unanesthetized, unrestrained fish prepared for renal clearance studies. The aortic pressure, glomerular filtration rate (GFR), urine flow rate (V), and urinary excretion of sodium, potassium, and total osmolytes were continuously monitored. Atriopeptin II significantly decreased mean aortic pressure (-12%), GFR (-40%), V (-66%), and the absolute excretion rates of sodium (-47%), potassium (-43%), and total osmolytes (-44%). However, the renal effects of atriopeptin II were temporally dissociated from the vasodepressor effect. Mean aortic pressure decreased quickly and returned to control values approximately 2 h after injection, whereas GFR did not decrease significantly until the third hour after injection. The decreases in renal water and solute excretion in response to atriopeptin could be accounted for by the decrease in GFR, since there were no significant changes in fractional water or solute excretion. Similar decreases in GFR were observed during constant infusions of a lower physiological dose of the peptide (80 pg.kg-1.min-1). The observed antidiuretic and antinatriuretic effect of synthetic atriopeptin in the dogfish contrasts with its putative role as a hormone mediating hypervolemic regulation.

Role of endogenous atrial natriuretic peptide in volume expansion diuresis and natriuresis of the Pekin duck

1994 ◽  
Vol 140 (1) ◽  
pp. 85-90 ◽  
Author(s):  
D A Gray
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Polyclonal Antibodies ◽  
Physiological Role ◽  
Arginine Vasotocin ◽  
Pekin Duck ◽  
Plasma Parameters ◽  
Atrial Natriuretic

Abstract Polyclonal antibodies raised in a rabbit against avian atrial natriuretic peptide (ANP) were shown to reduce circulating endogenous ANP levels in Pekin ducks by more than 90%, and were subsequently used to investigate the role of this peptide in volume expansion diuresis and natriuresis. Conscious birds, undergoing a steady-state diuresis and natriuresis maintained by an i.v. infusion of hypotonic saline at a rate of 0·7 ml/min, responded to ANP antiserum (anti-ANP) with an immediate 30% reduction in urine flow rate and sodium excretion which lasted for about 30 min. Plasma arginine vasotocin levels were not changed by anti-ANP whereas circulating angiotensin II concentrations increased immediately following the administration of anti-ANP. Serum from non-immunized normal rabbits produced no changes in the renal and plasma parameters monitored. The results show that the high circulating levels of endogenous ANP associated with volume expansion promote renal salt and fluid excretion and thus have a major physiological role in avian volume homeostasis. Journal of Endocrinology (1994) 140, 85–90

Cardiovascular effects of intracoronary atrial natriuretic peptide administration in man

1990 ◽  
Vol 120 (2) ◽  
pp. 308-315 ◽  
Author(s):  
Howard C. Herrmann ◽  
Andrew D. Rosenthal ◽  
Carol A. Davis
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cardiovascular Effects ◽  
Atrial Natriuretic

Endothelin acts as a paracrine regulator of stretch-induced atrial natriuretic peptide release

1995 ◽  
Vol 269 (5) ◽  
pp. R1093-R1098 ◽  
Author(s):  
J. P. Skvorak ◽  
S. J. Nazian ◽  
J. R. Dietz
Keyword(s):  
High Pressure ◽  
Control System ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cardiovascular Effects ◽  
Competitive Inhibitor ◽  
Dependent Manner ◽  
Direct Recording ◽  
Peptide Release ◽  
Atrial Natriuretic

Several lines of evidence suggest a paracrine regulatory role for endothelin (ET) in the release of atrial natriuretic peptide (ANP). To investigate this possibility, we used the ET A-type receptor (ETA-R) competitive inhibitor cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123) in isolated perfused atria to determine the effect of endogenously produced ET on the release of ANP. Initially, we found that high pressure (8-10 mmHg) increased the mean ANP secretion rate by 117.3 +/- 21.2% (P < 0.05). Next, we found that at high pressure 50 nM of exogenously applied ET significantly augmented the stretch-induced release of ANP (P < 0.05) and that this response could be significantly attenuated in a dose-dependent manner by 1 and 3 microM BQ-123 (P < 0.05). These experiments proved the efficacy of the inhibitor in our model. Subsequently, we found that the stretch-induced release of ANP was significantly reduced to 51.5 +/- 13.0 and 22.3 +/- 11.8% by 1 and 3 microM BQ-123, respectively (P < 0.05). Because the perfused atria model eliminates systemic cardiovascular effects, allows control and direct recording of the intra-atrial pressure, and preserves the potential endothelium-myocyte control system, we conclude that the stretch-induced release of ANP is partially regulated by ET and that the ET is locally produced and constitutes a paracrine control system.

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