Contribution of ANP to plasma protein escape during VE: effects of thiorphan and atrial appendectomy

1996 ◽  
Vol 271 (3) ◽  
pp. R610-R618
Author(s):  
V. L. Tucker

The effects of endopeptidase inhibition and right atrial appendectomy (AA) on plasma immunoreactive atrial natriuretic peptide (irANP) concentrations and extravascular accumulation of 131I-labeled bovine serum albumin (CBSA) during volume expansion (VE) were examined in pentobarbital sodium-anesthetized rats (n = 5 per group). Compared with controls, infusion of isoncotic albumin (30 ml/kg) increased central venous pressure (CVP) by 5.5 mmHg, plasma irANP by 7-fold, and CBSA in multiple tissues by 1.6- to 4-fold (P < or = 0.05). Inhibition of ANP metabolism with thiorphan (40 mg/kg) had no effect in control animals but increased plasma irANP (+118%) and CBSA (+30-100%) compared with VE alone (P < or = 0.05). Likewise, interference with ANP release by AA reduced plasma irANP (-80%) and CBSA (-30 to -80%) response to VE in parallel (P < or = 0.05). The peak increase in CVP during VE was not affected by either of these manipulations. It is concluded that endogenous ANP increases plasma protein extravasation independent of volume and pressure disturbances during acute intravascular expansion.

1996 ◽  
Vol 271 (3) ◽  
pp. R601-R609 ◽  
Author(s):  
V. L. Tucker

The relationship between plasma immunoreactive atrial natriuretic peptide (irANP) and radiolabeled albumin clearance (CBSA) in multiple tissues after graded volume stimuli was examined. To obtain a pure volume stimulus, pentobarbital sodium-anesthetized rats (5 or 6 per group) were equilibrated with a reservoir of blood by a femoral arteriovenous shunt, and volume expansion (VE) was produced by adjusting reservoir outflow. Peak increases in central venous pressure (CVP) during VE equal to 2 and 4% of the body weight over 5 min were 3.6 +/- 0.2 and 7.0 +/- 0.3 mmHg, and plasma irANP levels measured at 40 min post-VE were elevated 1.9- and 4.1-fold above baseline, respectively. Graded increases in CBSA measured between 5 and 35 min post-VE occurred in selective tissues, including intestine, visceral fat, lung, and muscle (P < or = 0.05). In separate animals, the level of VE was maintained after 2% VE by slower administration of an additional 2% VE for the remaining 30 min. This resulted in a more sustained CVP elevation and larger increases in irANP levels and CBSA compared with either 2 or 4% VE. Furthermore, equations derived from previous work in this laboratory involving intravenous administration of ANP predicted the magnitude of CBSA elevation during maintained VE. These findings support a role for ANP in regulating transcapillary protein distribution during acute intravascular expansion.


2006 ◽  
Vol 46 (2) ◽  
pp. 276-285 ◽  
Author(s):  
Sigrid Schuh-Hofer ◽  
Mandana Tayefeh ◽  
Uwe Reuter ◽  
Ulrich Dirnagl ◽  
Guy Arnold

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.


1988 ◽  
Vol 254 (4) ◽  
pp. R699-R705
Author(s):  
B. A. Benjamin ◽  
C. H. Metzler ◽  
T. V. Peterson

The purpose of this study is to determine whether chronic removal of atrial appendages alters renal response to volume expansion in the conscious monkey. Chronic bilateral atrial appendectomy (ATX) was performed in six animals. Six additional animals served as sham-operated controls. Monkeys were studied 1-2 wk after chronic surgery. The protocol consisted of three consecutive 10-min urine collections followed by 20% ischemic blood volume expansion (VE) and 120 min of post-VE measurements. In sham animals, VE caused an increase in plasma atrial natriuretic peptide (ANP) levels (48 +/- 7 pg/ml to a peak of 108 +/- 34 pg/ml). Urine flow increased from 0.43 +/- 0.07 to 1.07 +/- 0.24 ml/min, sodium excretion increased from 17.9 +/- 2.6 to 74.9 +/- 12.0 mu eq/min, and fractional sodium excretion increased from 0.67 +/- 0.10 to 2.43 +/- 0.28%. ATX attenuated the increase in ANP (34 +/- 8 pg/ml to a peak of 38 +/- 9 pg/ml) in four of six animals. In these animals, renal response to VE was significantly attenuated. Urine flow increased from 0.21 +/- 0.05 to 0.30 +/- 0.01 ml/min, sodium excretion increased from 19.3 +/- 6.02 to 37.8 +/- 5.05 mu eq/min, and fractional sodium excretion increased from 0.79 +/- 0.08 to 1.43 +/- 0.17%. Renal response of two ATX animals with normal increases in atrial natriuretic factor was similar to the sham group. Effect of volume expansion on mean arterial pressure, central venous pressure, and renal hemodynamics was not altered by ATX. These findings demonstrate that bilateral atrial appendectomy in the monkey attenuates the increase in ANP and reduces renal response to VE.


2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
A Hunfeld ◽  
D Segelcke ◽  
M Andriske ◽  
F Paris ◽  
X Zhu ◽  
...  

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Anika Hunfeld ◽  
Daniel Segelcke ◽  
Ingo Bäcker ◽  
Badreddine Mecheri ◽  
Kathrin Hemmer ◽  
...  

Cephalalgia ◽  
1991 ◽  
Vol 11 (4) ◽  
pp. 165-168 ◽  
Author(s):  
Maria Gabriella Buzzi ◽  
Michael A Moskowitz

Neurogenic plasma extravasation, endothelial cell activation (increase in vesicle number and vacuole formation), platelet aggregation and adhesion, and mast cell degranulation occur selectively in postcapillary venules of the dura mater following electrical trigeminal ganglion stimulation, and are mediated by release of neuropeptides from perivascular unmyelinated C fibres. Pre-treatment with the antimigraine drugs dihydroergotamine and sumatriptan, two drugs that bind with high affinity to 5-HT1B/1D receptors, markedly attenuated plasma protein extravasation induced by electrical trigeminal ganglion stimulation. Trigeminal stimulation increased plasma calcitonin gene-related peptide levels in rat superior sagittal sinus. Pre-treatment with dihydroergotamine and, to a lesser extent, sumatriptan, attenuated this increase. Both drugs reduced morphological changes in post-capillary venules and mast cells within dura mater following electrical trigeminal ganglion stimulation. Plasma protein extravasation was selectively blocked in dura mater (but not in extracranial tissues) by pre-treatment with those receptor agonists showing a rank order of potency suggesting a 3-HT1B/1D interaction (5-CT > 5-BT > DHE > sumatriptan > 8-OH-DPAT). Pre-treatment with 5-HT2 and 5-HT3 antagonists was not effective. Taken together, these data are consistent with the interpretation that putative 5-HT-1B/1D receptors located on sensory fibres are coupled to inhibition of peptide release and blockade of neurogenic inflammation. An important therapeutic action of ergot alkaloids and sumatriptan in migraine headaches is so defined.


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