Stimulation of duodenal bicarbonate secretion after blood volume expansion — An effect mediated by atrial natriuretic peptide?

1988 ◽  
Vol 22 (4) ◽  
pp. 411
Author(s):  
C. Jönson ◽  
L. Fändriks ◽  
A. Pettersson
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Bicarbonate Secretion ◽  
Blood Volume Expansion ◽  
Duodenal Bicarbonate Secretion ◽  
Stimulation Of ◽  
Atrial Natriuretic

Plasma release of atrial natriuretic peptide in response to blood volume expansion

1986 ◽  
Vol 109 (1) ◽  
pp. 9-13 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Christofides ◽  
S. R. Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Colloidal Solution ◽  
Venous Pressure ◽  
Molecular Size ◽  
Rat Plasma ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

ABSTRACT The response of plasma atrial natriuretic peptide (ANP) concentration to acute intravascular volume expansion was measured in ten male Wistar rats. An infusion of 3 ml polygelene colloidal solution at 37 °C over 45 s produced peak venous pressure rises of 1·5cm water. A highly significant (P<0·001) rise of immunoreactive plasma ANP from 24·4 ± 2·2 (mean ± s.e.m.) pmol/l to a peak of 70·0±10·5 pmol/l occurred within 2·5 min. Plasma ANP concentrations had virtually returned to basal levels (32·7 ± 2·7 pmol/l) 30 min after this acute volume load. A further infusion of 10 ml polygelene colloidal solution in 2 min produced peak venous pressure rises of 10 cm water and caused a dramatic and significant (P< 0·001) increase of plasma ANP concentration to a peak of 534·8 ± 38·5 pmol/l, occurring 7·5 min after infusion. The plasma ANP concentration had fallen but remained above basal levels 30 min later (137·2 ± 26·4 pmol/l). Similar results were obtained using an identical protocol but with whole rat blood instead of polygelene solution as the volume-expanding agent. Gel column chromatography suggested that the majority of the immunoreactive ANP in rat plasma was of similar molecular size to rat α-ANP(1–28). These results support the hypothesis that blood volume expansion is a potent stimulus for the release of ANP into plasma. J. Endocr. (1986) 109, 9–13

scholarly journals Role of Atrial Natriuretic Peptide in the Response to Blood Volume Expansion in the Weanling Rat

1990 ◽  
Vol 27 (4) ◽  
pp. 396-400 ◽  
Author(s):  
Robert L Chevalier ◽  
Barbara Thornhill ◽  
R Ariel Gomez ◽  
Nancy V Ragsdale ◽  
Michael J Peach ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

Vasopressin and atrial natriuretic peptide release in cardiopulmonary denervated dogs

1990 ◽  
Vol 258 (3) ◽  
pp. R704-R710 ◽  
Author(s):  
Y. Shiraishi ◽  
S. Fujimura ◽  
M. Handa ◽  
T. Kimura ◽  
K. Ota ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Change ◽  
Volume Expansion ◽  
Ringer Solution ◽  
Late Period ◽  
Blood Volume Expansion ◽  
Peptide Release ◽  
Atrial Natriuretic

To assess the effect of cardiopulmonary denervation on the release of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP), either hemorrhage (1.0 ml.kg-1.min-1, for 40 min) or an infusion of 3% dextran in lactated Ringer solution (RL) (3% dextran in RL, 1.0 ml.kg-1.min-1, for 40 min) was carried out in chronic cardiopulmonary denervated (CPD, n = 7) and sham-operated (SO, n = 7) dogs under anesthesia. Plasma AVP increased significantly in both groups during hemorrhage, but its rise was significantly attenuated in CPD dogs. Plasma ANP decreased similarly during hemorrhage in both groups. An infusion of 3% dextran in RL decreased significantly plasma AVP during its whole period in SO dogs, but AVP release was only suppressed in the late period in SO dogs. Plasma ANP increased significantly during its infusion in both groups. These results indicate that cardiopulmonary denervation may attenuate the release of AVP in response to either hemorrhage or blood volume expansion but may not affect the release of ANP in response to the blood volume change. Moreover, a large increase in plasma ANP may attenuate the release of AVP.

Atrial natriuretic peptide in brain and pituitary gland

1997 ◽  
Vol 77 (2) ◽  
pp. 465-515 ◽  
Author(s):  
J. Gutkowska ◽  
J. Antunes-Rodrigues ◽  
S. M. McCann
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Brain Stem ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Body Fluid ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis ◽  
The Right ◽  
Atrial Natriuretic

The data reviewed establish the presence and important role in body fluid homeostasis of brain atrial natriuretic peptide (ANP) in all vertebrate-species examined. The peptide is localized in neurons in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation, and its receptors are located in regions that contain the peptide. Most, if not all, of the actions of ANP are mediated by activation of particulate guanylyl cyclase with generation of guanosine 3',5'-cyclic monophosphate, which mediates its actions in brain as in the periphery. Although atrial stretch releases ANP from cardiac myocytes, the experiments indicate that the response to acute blood volume expansion is markedly reduced after elimination of neural control. Volume expansion distends baroreceptors in the right atria, carotid-aortic sinuses, and kidney, altering afferent input to the brain stem and hence the hypothalamus, resulting in stimulation via ANPergic neurons in the hypothalamus of oxytocin release from the neurohypophysis that circulates to the right atrium to stimulate ANP release. The ANP circulates to the kidney and induces natriuresis. Atrial natriuretic peptide also induces vasodilation compensating rapidly for increased blood volume by increased vascular capacity. Atrial natriuretic peptide released into hypophysial portal blood vessels inhibits release of adrenocorticotropic hormone (ACTH), thereby decreasing aldosterone release and enhancing natriuresis. Furthermore, the ANP neurons inhibit AVP release leading to diuresis and decreased ACTH release. Activation of hypothalamic ANPergic neurons via volume expansion also inhibits water and salt intake. These inhibitory actions may be partially mediated via ANP neurons in the olfactory system altering salt taste. Atrial natriuretic peptide neurons probably also alter fluid movement in the choroid plexus and in other brain vascular beds. Therefore, brain ANP neurons play an important role in modulating not only intake of body fluids, but their excretion to maintain body fluid homeostasis.

Atrial natriuretic peptide in multiple system atrophy

1996 ◽  
Vol 271 (4) ◽  
pp. R1047-R1053
Author(s):  
M. Bevilacqua ◽  
G. Norbiato ◽  
V. Righini ◽  
L. Castelli ◽  
A. Rogolino ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Multiple System Atrophy ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Plasma Osmolality ◽  
Type A ◽  
Type B ◽  
Blood Volume Expansion ◽  
Osmotic Load

Central nervous system feedback loops centered on hypothalamic neurons control atrial natriuretic peptide (ANP). We evaluated the ANP response to arterial hypotension, isotonic blood volume expansion, and increase in plasma osmolality in 14 patients with multiple system atrophy (MSA). Seven of the patients were characterized by a lack of vasopressin response to hypotension (MSA type B), suggesting chronic sinoaortic denervation, and seven by a preserved response (MSA type A). Orthostatic hypotension decreased ANP in controls and type A patients, whereas ANP in type B was not affected. Isotonic saline infusion increased ANP and diuresis in controls and type A patients, whereas it did not affect ANP in type B. Osmotic load increased plasma osmolality and vasopressin in controls and MSA patients and ANP in controls and type A but not in type B patients. In MSA patients with altered afferent control of vasopressin, ANP secretion is not stimulated by blood volume expansion, osmotic load, or blood pressure, suggesting that afferent excitatory control plays a role in the release of ANP.

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