Effects of autonomic stimulation on plasma immunoreactive atrial natriuretic peptide in the anesthetized rabbit

1987 ◽  
Vol 65 (4) ◽  
pp. 532-537 ◽  
Author(s):  
A. J. Rankin ◽  
N. Wilson ◽  
J. R. Ledsome
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Vagus Nerve ◽  
Cardiac Myocytes ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Cervical Ganglion ◽  
Significant Change ◽  
The Right ◽  
Stimulation Of ◽  
Atrial Natriuretic

Infusions of norepinephrine led to a significant sevenfold increase in plasma immunoreactive atrial natriuretic peptide, while infusions of acetylcholine caused no significant change in the level of the peptide. Efferent stimulation of the right vagus nerve or right inferior cervical ganglion in anesthetized, vagotomized rabbits produced no significant changes in the immunoreactive atrial natriuretic peptide. The findings suggest that the mechanism by which norepinephrine releases immunoreactive atrial natriuretic peptide is not the result of a direct action on the cardiac myocytes.

Mechanisms for the release of atrial natriuretic peptide

1987 ◽  
Vol 65 (8) ◽  
pp. 1673-1679 ◽  
Author(s):  
A. J. Rankin
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Substantial Evidence ◽  
Humoral Factors ◽  
Disease States ◽  
Haemodynamic Changes ◽  
Stimulation Of ◽  
Atrial Natriuretic

In assessing the role that atrial natriuretic peptide (ANP) might have in the homeostasis of fluid volume and blood pressure, it is important to define the physiological and pathophysiological conditions that determine its release into the circulation. There is substantial evidence that ANP is released through atrial distension under a variety of conditions. There are also some indications that ANP may be released through humoral factors, although it is not clear whether this is a result of direct action on the myocytes or simply a result of ensuing haemodynamic changes. There is no evidence to suggest that ANP can be released through stimulation of efferent fibres innervating the atria, but it may be released as a result of changes in myocardial work and oxygen consumption. Plasma levels of ANP are elevated in several disease states and that release appears to be a result of the haemodynamic disturbances in those conditions.

Effects of homologous atrial natriuretic peptide on drinking and plasma ANG II level in eels

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Drinking Rate ◽  
Plasma Sodium Concentration ◽  
Atrial Natriuretic

The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.

Time course of release of atrial natriuretic peptide in the anaesthetized dog

1986 ◽  
Vol 64 (7) ◽  
pp. 1017-1022 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
A. J. Rankin ◽  
C. A. Courneya
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Time Course ◽  
Atrial Wall ◽  
Humoral Mechanism ◽  
Arterial Plasma ◽  
The Right ◽  
Atrial Receptors ◽  
Anaesthetized Dog ◽  
Atrial Natriuretic

In 12 chloralose anaesthetized dogs plasma concentration of immunoreactive atrial natriuretic peptide (IR-ANP) was measured using a radioimmunoassay. Plasma IR-ANP was 74 ± 4.8 pg/mL (mean ± SE) and increased by 39 ± 4.1 pg/mL when left atrial pressure was increased by 10 cm H2O during partial mitral obstruction. Observation of the time course of the changes in IR-ANP during atrial distension showed that IR-ANP was increased within 2 min of atrial distension and declined after atrial distension, with a half-time of 4.5 min. The time course of the changes in IR-ANP was unaffected by vagotomy or administration of atenolol. Maximum electrical stimulation of the right ansa subclavia failed to produce any change in IR-ANP. IR-ANP was higher in coronary sinus plasma than in femoral arterial plasma confirming that the heart was the source of the IR-ANP. The results support the hypothesis that IR-ANP is released from the heart by a direct effect of stretch of the atrial wall rather than by a neural or humoral mechanism involving a reflex from atrial receptors.

Adenosine modulates hypoxia-induced atrial natriuretic peptide release in fetal sheep

1995 ◽  
Vol 269 (1) ◽  
pp. H282-H287 ◽  
Author(s):  
D. A. Ogunyemi ◽  
B. J. Koos ◽  
C. P. Arora ◽  
L. C. Castro ◽  
B. A. Mason
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Fetal Hemoglobin ◽  
Blood Gases ◽  
Fetal Sheep ◽  
Control Value ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
The Right ◽  
Atrial Natriuretic

The effects of adenosine on atrial natriuretic peptide (ANP) secretion were determined in chronically catheterized fetal sheep (> 0.8 term). Adenosine was infused into the the right jugular vein for 1 h at 8 +/- 0.4 (5 fetuses), 160 +/- 8 (6 fetuses), and 344 +/- 18 micrograms.min-1.kg estimated fetal wt-1. Fetal arterial blood gases and pH were generally unaffected by adenosine, although mean arterial CO2 tension increased transiently by 2-5 Torr and pH fell progressively during the highest rate of infusion. During the intermediate and high infusion rates, fetal hemoglobin concentrations increased by 11-13% and mean fetal heart rate rose by 18% from a control value of approximately 167 beats/min. Mean arterial pressure was not affected during adenosine infusion. Adenosine significantly increased fetal plasma ANP levels, with maximum concentrations 1.80, 2.36, and 2.51 times greater than control means (142-166 pg/ml) for the respective infusion rates of 8, 160, and 344 micrograms.min-1.kg estimated fetal wt-1. In seven fetuses, reducing fetal arterial O2 tension by approximately 9-10 Torr from a control of 23 +/- 1.3 Torr increased plasma ANP concentrations approximately 2.4 times the control mean of 176 pg/min. Adenosine-receptor blockade with 8-(p-sulfophenyl)-theophylline reduced by 50% the maximum hypoxia-induced rise in plasma ANP concentrations. It is concluded that adenosine causes a dose-dependent rise in fetal plasma ANP concentrations and modulates fetal ANP release during hypoxia.

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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