Acute saline loading in normal and bilaterally atrial-resected conscious dogs

1988 ◽  
Vol 255 (1) ◽  
pp. H144-H152
Author(s):  
A. W. Cowley ◽  
P. R. Anderas ◽  
M. M. Skelton
Keyword(s):  
Arterial Pressure ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Water Excretion ◽  
Volume Load ◽  
Saline Loading ◽  
Before And After ◽  
Level 3 ◽  
The Central Nervous System

Acute isotonic saline volume loads (400 ml) were intravenously administered to conscious, renal-denervated dogs before and after bilateral removal of the atrial free walls and atrial appendages to determine the role of atrial-mediated hormonal factors in the renal excretory response. In one group of dogs (n = 11), the volume was given in 10 min; in another group (n = 5), the volume was given in 30 min while arginine vasopressin (AVP) was infused to maintain plasma AVP at a fixed, normal level (3 pg/ml). Sodium and water excretion, mean arterial pressure, and plasma hormone levels were determined before and for 5 h after volume loads. Atrial resection resulted in a 40-50% reduction of sodium and water excretion in both groups during the first 2 h after volume expansion. The blunted renal excretory responses could not be explained by differences in arterial pressure, renal sympathetic nerve activity, or by hormonal differences of plasma immunoreactive atrial natriuretic factor (iANP), plasma AVP, plasma renin activity, or plasma aldosterone. Plasma iANP was not significantly increased by the volume load in either the normal or atrial-resected state. Atrial-resected dogs exhibited normal plasma levels of iANP. The data indicate the presence of an unidentified diuretic and natriuretic substance, which is released with volume expansion from either the cardiac atria or via the central nervous system, and that the release of this factor is removed by atrial resection.

Saline diuresis and natriuresis in unanesthetized dogs: a missing atrial factor?

1992 ◽  
Vol 263 (3) ◽  
pp. H792-H797
Author(s):  
A. W. Cowley ◽  
A. G. Brice ◽  
M. M. Skelton
Keyword(s):  
Plasma Renin ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Cardiac Denervation ◽  
Volume Load ◽  
Before And After ◽  
Intravenous Saline ◽  
Renal Nerve Activity ◽  
The Central Nervous System

Recent studies in our laboratory indicated that a blunted (40–50%) renal excretory response to isotonic intravenous saline loads occurred in conscious, renal-denervated dogs after 70% of the atrial mass was removed. The blunted responses could not be explained by differences in the responses of arterial pressure, renal nerve activity, or by measured changes of plasma immunoreactive atrial natriuretic peptide (iANP), arginine vasopressin (AVP), plasma renin activity (PRA), or aldosterone (Aldo). The present study was designed to determine whether the central nervous system (CNS) was the source of an unidentified substance, which could account for the blunting of the urine excretory response seen in the atrial-resected dogs. Renal denervation was performed in all dogs to eliminate alterations in efferent renal sympathetic nerve activity derived from reflexes activated during volume expansion. Cardiac denervation (CDX) was used to eliminate sensory cardiac afferent nerve activity to the CNS. A group of five renal-denervated dogs was given an isotonic volume load (400 ml/30 min) before and after complete CDX. Plasma AVP was fixed at normal plasma levels of 3 pg/ml by continuous intravenous infusion. Na and H2O excretion were not different in renal-denervated dogs compared with combined renal and cardiac denervation during the 5 h after the saline load. Plasma AVP and Aldo were unchanged with the volume loads, although PRA rose gradually over the 5 h after the saline loads. Plasma iANP increased transiently in the combined renal and cardiac-denervated state rising from a control of 65–120 pg/ml at the end of the load period.(ABSTRACT TRUNCATED AT 250 WORDS)

Dominance of colloid osmotic pressure in renal excretion after isotonic volume expansion

1991 ◽  
Vol 261 (4) ◽  
pp. H1214-H1225 ◽  
Author(s):  
A. W. Cowley ◽  
M. M. Skelton
Keyword(s):  
Arterial Pressure ◽  
Osmotic Pressure ◽  
Whole Blood ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Renal Perfusion ◽  
Colloid Osmotic Pressure ◽  
Urine Excretion ◽  
Water Excretion ◽  
Plasma Arginine

Studies were carried out in unanesthetized dogs to determine the relative importance of neural, endocrine, and colloid osmotic pressure (COP) in the diuretic and natriuretic responses associated with volume expansion. Renal excretory responses to 30-min intravenous infusions of isotonic saline (400 ml) or whole blood (100 ml) were compared while various controllers of sodium and water excretion were either eliminated or held constant. Dogs were studied in the normal state; with plasma arginine vasopressin (AVP) fixed by intravenous infusion; with bilateral renal denervation and plasma AVP fixed; renal denervated with plasma AVP, angiotensin II, aldosterone, atrial natriuretic factor fixed; and renal denervated with these same hormones fixed and with renal arterial pressure servo-controlled at a constant level. Normal uncontrolled dogs increased sodium and water excretion nearly fourfold by the end of the saline load and excreted 85% of the load within 5 h. Urine excretion was minimally affected when the various neural and endocrine controllers were fixed or eliminated. There were no changes of mean arterial pressure with the saline volume loads, but COP fell 2.5 mmHg. Equivalent expansion of the blood volume (100 ml) with whole blood in which COP was unchanged resulted in nearly no increase of urine excretion in renal-denervated dogs with plasma hormones fixed and renal perfusion pressure held constant. We conclude that the rapid diuresis and natriuresis following isotonic volume expansion is predominantly a result of plasma protein dilution and a reduction of COP.

Effect of volume expansion on pressor response to angiotensin II in pregnant ewes

1981 ◽  
Vol 240 (6) ◽  
pp. H908-H913
Author(s):  
S. Matsuura ◽  
R. P. Naden ◽  
N. F. Gant ◽  
C. R. Parker ◽  
C. R. Rosenfeld
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Response Curves ◽  
Pregnant Sheep ◽  
Before And After ◽  
Near Term

Vascular refractoriness to infused angiotensin II (AII) characterizes normal human and ovine pregnancy. To ascertain whether the refractoriness in the gravid ewe is mediated by either endogenous plasma concentrations of renin and AII or vasomotor reflexes, effects of acute volume expansion (VE) on the pressor response to AII were studied in chronically instrumented nonpregnant and near-term pregnant sheep. Dose-response curves describing the pressor response (delta BP) were determined before and after infusions of 1.0 1 of isotonic saline (NS) or 0.5 1 of 10% dextran (D). In nonpregnant sheep, hematocrit (Hct) and plasma renin activity (PRA) fell in all animals after NS (n = 7) and D (n = 6) (P less than 0.005). After VE with NS and D, delta BP increased at each dose of AII (P less than 0.05). The pressor response to AII in pregnant sheep was not altered by NS although decreases in Hct and PRA were comparable to those in nonpregnant sheep. Baroreceptor responses were not altered. Vascular refractoriness to infused AII in pregnant sheep is not due primarily to changes in plasma concentrations of renin-AII but more likely to another factor, vessel wall refractoriness. In this respect, the ewe is similar to the human.

High-NaCl diets increase natriuretic and diuretic responses in salt-resistant but not salt-sensitive SHR

1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Isotonic Saline ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.

Fluid retention after oral loading with water or saline in camels

1992 ◽  
Vol 262 (5) ◽  
pp. R915-R920 ◽  
Author(s):  
S. Benlamlih ◽  
K. Dahlborn ◽  
R. Z. Filali ◽  
J. Hossaini-Hilali
Keyword(s):  
Body Weight ◽  
Plasma Proteins ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
The Body ◽  
Plasma Aldosterone Concentration ◽  
Excess Water ◽  
Saline Loading ◽  
Long Time

When dehydrated camels are offered water they drink volumes of water exceeding their body water loss during the water deprivation period. The excess water is excreted during 2-4 days. To investigate the ability to retain fluid in the body, normohydrated camels were loaded with water or isotonic saline (0.1 l/kg body wt) by esophageal tube. After water loading plasma osmolality decreased and a water diuresis was seen, but it took 3 days until the body weight returned to prehydration level. Plasma aldosterone concentration (PAC) increased, but plasma renin activity (PRA) and plasma atrial natriuretic peptide (ANP) concentration did not change. After the saline loading plasma osmolality increased and total plasma proteins and hematocrit decreased. Renal Na excretion increased 4 h after the saline load, but the magnitude of the natriuresis was small, and the camels had not regained their body weight 6 days after the load. PAC and PRA decreased after saline loading, while plasma ANP concentration did not change. These data show that camels are able to retain excess water within the body and to tolerate blood hyposmolality for a relatively long time. With saline the retention of fluid lasts even longer despite an attenuation of PAC.

scholarly journals Lack of an effect of collecting duct-specific deletion of adenylyl cyclase 3 on renal Na+ and water excretion or arterial pressure

2014 ◽  
Vol 306 (6) ◽  
pp. F597-F607 ◽  
Author(s):  
Wararat Kittikulsuth ◽  
Deborah Stuart ◽  
Alfred N. Van Hoek ◽  
James D. Stockand ◽  
Vladislav Bugaj ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Adenylyl Cyclase ◽  
Collecting Duct ◽  
Urine Volume ◽  
Physiological Role ◽  
Plasma Renin ◽  
Water Restriction ◽  
Water Excretion ◽  
And Control

cAMP is a key mediator of connecting tubule and collecting duct (CD) Na+ and water reabsorption. Studies performed in vitro have suggested that CD adenylyl cyclase (AC)3 partly mediates the actions of vasopressin; however, the physiological role of CD AC3 has not been determined. To assess this, mice were developed with CD-specific disruption of AC3 [CD AC3 knockout (KO)]. Inner medullary CDs from these mice exhibited 100% target gene recombination and had reduced ANG II- but not vasopressin-induced cAMP accumulation. However, there were no differences in urine volume, urinary urea excretion, or urine osmolality between KO and control mice during normal water intake or varying degrees of water restriction in the presence or absence of chronic vasopressin administration. There were no differences between CD AC3 KO and control mice in arterial pressure or urinary Na+ or K+ excretion during a normal or high-salt diet, whereas plasma renin and vasopressin concentrations were similar between the two genotypes. Patch-clamp analysis of split-open cortical CDs revealed no difference in epithelial Na+ channel activity in the presence or absence of vasopressin. Compensatory changes in AC6 were not responsible for the lack of a renal phenotype in CD AC3 KO mice since combined CD AC3/AC6 KO mice had similar arterial pressure and renal Na+ and water handling compared with CD AC6 KO mice. In summary, these data do not support a significant role for CD AC3 in the regulation of renal Na+ and water excretion in general or vasopressin regulation of CD function in particular.

α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 307s-309s ◽  
Author(s):  
A. Morganti ◽  
Carla Sala ◽  
Anna Palermo ◽  
Lucia Turolo ◽  
A. Zanchetti
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Test Dose ◽  
Blocking Agent ◽  
Renin Activity ◽  
Renin Release ◽  
Arterial Blood ◽  
Before And After

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.

Systemic inhibition of nitric oxide and prostaglandins in volume-induced natriuresis and hypertension

1998 ◽  
Vol 274 (1) ◽  
pp. R175-R180 ◽  
Author(s):  
James D. Krier ◽  
Juan Carlos Romero
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Significant Elevation ◽  
Synthesis Inhibition ◽  
Anesthetized Dogs ◽  
Change Map

Nitric oxide (NO) synthesis inhibition with N G-nitro-l-arginine methyl ester (l-NAME) (10 μg ⋅ kg−1 ⋅ min−1iv), cyclooxygenase inhibition with meclofenamate (Meclo; 5 mg/kg iv bolus), and combination of drugs (l-NAME+Meclo) were used to investigate the roles of NO and prostaglandins (PG) in the hemodynamic and natriuretic responses to isotonic saline volume expansion (VE; 5% body wt over 60 min) in anesthetized dogs. Before VE,l-NAME ( n = 6), Meclo ( n = 6), andl-NAME+Meclo ( n = 6) produced significant increments in mean arterial pressure (MAP) of 12 ± 2, 15 ± 3, and 17 ± 3 mmHg, respectively. VE did not change MAP in Meclo-treated dogs, but produced a significant elevation in the control dogs (14 ± 6 mmHg), inl-NAME-treated dogs (17 ± 6 mmHg), and in dogs pretreated withl-NAME+Meclo (12 ± 5 mmHg). VE alone induced marked natriuretic responses in the control (38 ± 9 to 562 ± 86 μmol/min),l-NAME (31 ± 9 to 664 ± 65 μmol/min), and Meclo groups (41 ± 10 to 699 ± 51 μmol/min). However, this natriuretic response was attenuated in dogs pretreated with l-NAME+Meclo (12 ± 4 to 185 ± 52 μmol/min). These results indicate that 1) blockade of both NO and PGs has significant diminishing effects on volume-induced natriuresis, 2) NO blockade alone impairs volume-induced natriuresis in a manner that requires further increases in MAP to restore the natriuresis, and 3) PG blockade alone does not curtail volume-induced natriuresis.

Effects of a three-day head-down tilt on renal and hormonal responses to acute volume expansion

1999 ◽  
Vol 277 (5) ◽  
pp. R1444-R1452 ◽  
Author(s):  
Pierre Mauran ◽  
Saïd Sediame ◽  
Anne Pavy-Le Traon ◽  
Alain Maillet ◽  
Alain Carayon ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Upright Position ◽  
Hormonal Responses ◽  
Water Load ◽  
Time Control ◽  
Supine Posture ◽  
Baseline Values

To clarify whether exposure to 6° head-down tilt (HDT) leads to alterations in body fluid volumes and responses to a saline load similar to those observed during space flight we investigated eight healthy subjects during a 4-day, 6° HDT and during a time-control ambulatory period with cross-over. Compared with the ambulatory period, HDT was associated with greater urinary excretion of water and sodium (UV, UNaV) from 0 to 12 h (cumulated UV 1,781 ± 154 vs. 1,383 ± 170 ml, P < 0.05; cumulated UNaV 156 ± 14 vs. 117 ± 9 mmol, P < 0.05), and with higher plasma atrial natriuretic factor (ANF) at 4 h. Hemoglobin and hematocrit increased over the first 24 h, and blood and plasma volumes were decreased after 48 h of HDT ( P< 0.05). Plasma renin activity (PRA) and aldosterone did not differ between the two groups. With prolongation of HDT, UV and UNaV returned close to baseline values. On the fourth HDT day, a 30-min infusion of 20 ml/kg isotonic saline was performed, while a large oral water load maintained a high urine output. The ambulatory period experiment was done with the subjects in the acute supine posture. Sodium excreted within 4 h of loading was 123 ± 8 mmol during HDT vs. 168 ± 16 mmol during the ambulatory period ( P < 0.05). The increase in plasma ANF and decrease in PRA were greater during HDT than during the ambulatory period (ANF 30 ± 5 vs. 13 ± 4 pg/ml, P < 0.05; PRA −1.4 ± 0.4 vs. −0.5 ± 0.2 ng ⋅ ml−1 ⋅ h−1, P < 0.05). Our data suggest that after a 3-day HDT period, thoracic volume receptor loading returns to the level seen in the upright position, leading to blunted responses to volume expansion, compared with acute supine control.

Influence of Volume Expansion on Renal Diluting Capacity in the Rat

1974 ◽  
Vol 46 (3) ◽  
pp. 331-345
Author(s):  
M. Martinez-Maldonado ◽  
G. Eknoyan ◽  
W. N. Suki
Keyword(s):  
Volume Expansion ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Free Water ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption ◽  
Water Excretion ◽  
Hypotonic Saline

1. The functional capacity of Henle's loop was examined during hypotonic, isotonic and hypertonic extracellular fluid volume expansion. To eliminate a possible role of antidiuretic hormone (ADH) in the alteration of free water excretion, rats with congenital diabetes insipidus were used. The infusion of hypotonic saline resulted in a progressive rise in free water clearance (CH2O) throughout the range of urine flow (V) attained. Similar results were obtained in rats treated chronically with deoxycorticosterone acetate (DOCA). The infusion of isotonic saline (sodium chloride, 154 mmol/l) produced an initial rise in CH2O until V represented 10% of the filtered load, after which CH2O appeared to reach a plateau. The limitation of CH2O was more marked when hypertonic saline was infused. Medullary and papillary non-urea solute (NUS) concentration rose progressively with the increasing concentration of the saline solution infused. 2. The greater fractional sodium excretion (FENa) after acute isotonic and hypertonic volume expansion is probably the result of inhibition of sodium reabsorption in the collecting duct, although inhibition in the ascending limb cannot be entirely excluded. The depression of CH2O as a function of V seen during acute isotonic or hypertonic volume expansion can be attributed in part to enhanced water back-diffusion from the collecting duct consequent to the increasing medullary and papillary interstitial NUS concentration, even in the absence of ADH. 3. Chronic expansion of extracellular fluid volume by DOCA administration did not modify the response to hypotonic saline infusion.

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