Renal responses to central vascular expansion are suppressed at night in conscious primates

1980 ◽  
Vol 239 (4) ◽  
pp. F343-F351 ◽  
Author(s):  
David A. Kass ◽  
Frank M. Sulzman ◽  
Charles A. Fuller ◽  
Martin C. Moore-Ede
Keyword(s):  
Sodium Excretion ◽  
Time Course ◽  
Venous Pressure ◽  
Urine Osmolality ◽  
Air Pressure ◽  
Saimiri Sciureus ◽  
Arterial Blood ◽  
Body Positive ◽  
Renal Responses ◽  
Diurnal Regulation

Renal and hemodynamic responses to central vascular volume expansion induced by 4 h of continuous lower bodv positive air pressure (LBPP) were examined in conscious, chair-restrained squirrel monkeys in a light/dark (12:12) cycle. LBPP (30 mmHg) during both day (1200–1600) and night (0000–0400) induced similar 4 cmH2O stable increases in central venous pressure (P < 0.001), rises in heart rate of 25 beat/min (P < 0.001), and small transient elevations in mean arterial blood pressure. In contrast, while daytime LBPP induced a significant increase in urine flow (V) from 2.12 ± 0.31 to 3.5 ± 0.42 ml/h (P < 0.05), and sodium excretion (UNaV) from 71.1 ± 14 to 271.2 ± 37 μeq/h (P < 0.001), there was a marked nocturnal inhibition of the response to LBPP, with no significant increases in V or UNaV. Urine osmolality decreased by more than 50% at both times of pressure exposure; potassium excretion was not significantly affected by either exposure, and drinking was suppressed during daytime LBPP. Comparisons of the time course and diurnal regulation of the urinary responses suggest that several separate efferent control pathways are involved. volume regulation; sodium excretion; squirrel monkey (Saimiri sciureus); lower body positive air pressure; circadian rhythms; Henry-Gauer reflex Submitted on October 29, 1979 Accepted on April 10, 1980

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep

2009 ◽  
Vol 297 (1) ◽  
pp. R185-R193 ◽  
Author(s):  
Robert Frithiof ◽  
Rohit Ramchandra ◽  
Sally Hood ◽  
Clive May ◽  
Mats Rundgren
Keyword(s):  
Creatinine Clearance ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sodium Excretion ◽  
Venous Pressure ◽  
Sodium Concentration ◽  
Ang Ii ◽  
Arterial Blood ◽  
Renal Sodium Excretion ◽  
Conscious Sheep

The contribution of the paraventricular nucleus of the hypothalamus (PVN) in mediating cardiovascular, renal, hormonal, and sympathetic nerve responses to increased cerebrospinal fluid (CSF) [Na+] was investigated in conscious sheep. Intracerebroventricular hypertonic NaCl (0.5 mol/l, 20 μl/min for 60 min) increased arterial blood pressure [AP; +13.4 (sd 2.0) mmHg, P < 0.001] and central venous pressure [CVP; +2.8 (sd 1.3) mmHg, P < 0.001], but did not significantly change heart rate or cardiac output ( n = 6). Elevated CSF [Na+] also lowered plasma ANG II levels [−3.3 (sd 1.6) pmol/l, P = 0.004] and increased creatinine clearance [+31.5 (sd 32.7) ml/min, P = 0.03] and renal sodium excretion [+9.2 (sd 9.2) mmol/h, P = 0.003]. Lidocaine injection (1 μl, 2%) into the PVN prior to the ICV infusion had no apparent effect per se, but it abolished the AP, CVP, creatinine clearance, and ANG II responses to hypertonic NaCl, as well as reducing the increase in renal sodium excretion ( n = 6). Subsequent studies were performed in conscious sheep with chronically implanted electrodes for measurement of renal sympathetic nerve activity (RSNA). The effects of ICV hypertonic NaCl on AP and RSNA were measured before and after PVN-injection of glycine (250 nmol in 500 nl artificial CSF). ICV NaCl increased AP and decreased RSNA ( P < 0.001). These effects were significantly reduced by glycine ( P = 0.02–0.001, n = 5). Saline injected into the PVN ( n = 5) or lidocaine injected outside the PVN ( n = 6) had no effect on the response to ICV hypertonic NaCl. These results indicate that the PVN is an important mediator of cerebrally induced homeostatic responses to elevated sodium concentration/hyperosmolality.

Initial renal responses of nonhuman primate to immersion and intravascular volume expansion

1980 ◽  
Vol 48 (2) ◽  
pp. 243-248 ◽  
Author(s):  
T. V. Peterson ◽  
J. P. Gilmore ◽  
I. H. Zucker
Keyword(s):  
Nonhuman Primate ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Renal Plasma Flow ◽  
Water Immersion ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Water Excretion ◽  
Arterial Blood ◽  
Renal Responses

Experiments were performed in anesthetized Macaca fascicularis monkeys to determine if the initial renal responses of these animals to head-out vertical water immersion and isoncotic, isotonic volume expansion are similar, especially with regard to the onset of any changes in solute or water excretion. Significant increases in urine flow, sodium excretion, and osmolar clearance occurred after 10 min of immersion but not until 30 min after volume expansion. Potassium excretion increased during immersion but decreased after volume expansion. Mean arterial blood pressure increased after 30 min of immersion but was unchanged after volume expansion. Indices of vascular filling, central venous pressure in the immersed animals and left ventricular end-diastolic pressure in the volume-expanded animals, increased immediately after the intervention. Effective renal plasma flow increased in both groups but glomerular filtration rate was not consistently elevated. These results suggest that, in the nonhuman primate, immersion and volume expansion exert their renal effects through different afferent and/or efferent mechanisms and should not be considered as similar volume stimuli.

Volume expansion during NOS substrate donation with l-arginine: regulatory offsetting of renal response?

2002 ◽  
Vol 282 (4) ◽  
pp. R1149-R1155 ◽  
Author(s):  
Jens Lundbæk Andersen ◽  
Niels C. F. Sandgaard ◽  
Peter Bie
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Free Water ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Ang Ii ◽  
Free Water Clearance ◽  
Arterial Blood

The responses to infusion of nitric oxide synthase substrate (l-arginine 3 mg · kg−1 · min−1) and to slow volume expansion (saline 35 ml/kg for 90 min) alone and in combination were investigated in separate experiments. l-Arginine left blood pressure and plasma ANG II unaffected but decreased heart rate (6 ± 2 beats/min) and urine osmolality, increased glomerular filtration rate (GFR) transiently, and caused sustained increases in sodium excretion (fourfold) and urine flow (0.2 ± 0.0 to 0.7 ± 0.1 ml/min). Volume expansion increased arterial blood pressure (102 ± 3 to 114 ± 3 mmHg), elevated GFR persistently by 24%, and enhanced sodium excretion to a peak of 251 ± 31 μmol/min, together with marked increases in urine flow, osmolar and free water clearances, whereas plasma ANG II decreased (8.1 ± 1.7 to 1.6 ± 0.3 pg/ml). Combined volume expansion and l-arginine infusion tended to increase arterial blood pressure and increased GFR by 31%, whereas peak sodium excretion was enhanced to 335 ± 23 μmol/min at plasma ANG II levels of 3.0 ± 1.1 pg/ml; urine flow and osmolar clearance were increased at constant free water clearance. In conclusion, l-arginine 1) increases sodium excretion, 2) decreases basal urine osmolality, 3) exaggerates the natriuretic response to volume expansion by an average of 50% without persistent changes in GFR, and 4) abolishes the increase in free water clearance normally occurring during volume expansion. Thus l-arginine is a natriuretic substance compatible with a role of nitric oxide in sodium homeostasis, possibly by offsetting/shifting the renal response to sodium excess.

Renal responses to prolonged central volume expansion in conscious primates

1982 ◽  
Vol 242 (6) ◽  
pp. F649-F656
Author(s):  
D. A. Kass ◽  
M. C. Moore-Ede
Keyword(s):  
Volume Expansion ◽  
Urine Osmolality ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Normal Range ◽  
Hormonal Responses ◽  
Body Positive ◽  
Central Volume ◽  
Renal Responses ◽  
Sodium And Potassium

Urinary and hormonal responses to prolonged central vascular volume expansion induced by 4 days of continuous lower body positive air pressure (LBPP) were examined in conscious, chair-acclimatized squirrel monkeys. The initial 12 h of exposure to LBPP (20 mmHg) induced a marked natriuresis, diuresis, kaliuresis, and decrease in urine osmolality. During the subsequent 4 days of LBPP stimulation, the acute natriuresis gradually declined by 75%, whereas potassium excretion completely returned to control rates after 24 h. In contrast, the diuresis and decrease in osmolality persisted, although there were significant circadian variations in urine flow (as well as sodium and potassium excretion) produced by a marked nocturnal suppression of renal responses to LBPP. Plasma aldosterone and potassium concentration both decreased acutely following LBPP initiation; however, aldosterone levels subsequently returned to normal range during continued LBPP exposure, whereas plasma potassium remained low until the pressure stimulus was terminated. These results indicated that prolonged central volume expansion induced both a sustained natriuresis and diuresis; however, chronic adaptation limited net fluid and electrolyte losses through the first 24 h of LBPP exposure. The loss of potassium appeared to be a consequence of the initial diuresis and natriuresis induced by LBPP, rather than being directly mediated by aldosterone.

Continuous blood densitometry: fluid shifts after graded hemorrhage in animals

1986 ◽  
Vol 250 (3) ◽  
pp. H342-H350 ◽  
Author(s):  
H. Hinghofer-Szalkay
Keyword(s):  
Time Course ◽  
Venous Pressure ◽  
Relative Volume ◽  
Fluid Replacement ◽  
Whole Body ◽  
Arterial Blood ◽  
Fluid Shifts ◽  
Transvascular Fluid Shifts ◽  
Arterial Plasma ◽  
Erythrocyte Density

To evaluate rapid fluid shifts after graded hemorrhage in splenectomized animals, four pigs and two dogs were bled 15-23 ml/kg body wt in steps of 2.2-6.0 ml/kg. Arterial blood density (BD), mean arterial pressure (MAP), and central venous pressure (CVP) were recorded continuously, and arterial plasma density (PD) and hematocrit (Hct) were determined from blood samples. Erythrocyte density was computed from PD, BD, and Hct. Starting with stable control conditions, MAP, CVP, and BD fell from the beginning of hemorrhage. Each blood withdrawal was followed by an immediate and rapid decrease in BD, even at the lowest (less than 3 ml/kg) initial blood losses. The time course of BD change mirrored that of the volume replacement, with time constants of 3.0-9.6 min and amplitudes depending on the magnitude of the relative volume loss. The PD decrease was significant (P less than 0.01) after 5.4 +/- 0.7 ml/kg hemorrhage. At 15 ml/kg blood loss the mean PD and BD had dropped by 0.99 +/- 0.15 and 2.42 +/- 0.26 g/l, respectively, and Hct had dropped by 2.40 +/- 0.47 units. Calculations suggest that either the inward-shifted fluid has a higher density than normal ultrafiltrate and/or there is a rise of the whole-body-to-large vessel Hct (F cell ratio). The rapid fluid replacement ranged from 5.8 +/- 0.8 to 10.6 +/- 2.0% of the initial plasma volume, or one-fifth to one-third of the lost volume with a 20% hemorrhage. Transvascular fluid shifts can be monitored with continuous high-precision blood densitometry.

Changes in plasma catecholamines in response to reflex modulation of sympathetic vasoconstrictor tone by cardiopulmonary receptors

1985 ◽  
Vol 68 (5) ◽  
pp. 503-510 ◽  
Author(s):  
Guido Grassi ◽  
Cecilia Gavazzi ◽  
Andrea M. Cesura ◽  
Giovanni B. Picotti ◽  
Giuseppe Mancia
Keyword(s):  
Vascular Resistance ◽  
Time Course ◽  
Venous Pressure ◽  
Plasma Catecholamines ◽  
Plasma Noradrenaline ◽  
Reflex Modulation ◽  
Arterial Blood ◽  
Cardiopulmonary Receptors ◽  
Forearm Vascular Resistance ◽  
Stimulation Of

1. The effects of selective deactivation and stimulation of cardiopulmonary receptors on plasma noradrenaline (radioenzymatic method) were studied in nine normotensive subjects by reducing and increasing central venous pressure for 20 min via lower body suction and leg-raising manoeuvres that did not alter arterial blood pressure and heart rate. 2. Deactivation of cardiopulmonary receptors was accompanied by a rise in plasma noradrenaline that achieved a peak within 5 min (91.8 ± 22%, mean ± se) and was then sustained. Stimulation of cardiopulmonary receptors was accompanied by a fall in plasma noradrenaline (−16.6 ± 3.4%) that levelled off at the second minute and was then sustained. 3. On average the increase and the reduction in plasma noradrenaline had a time course and a magnitude similar to the increase (80.5 ± 10.5%) and the reduction (−28.4 ± 5%) in forearm vascular resistance (derived from plethysmographic flow measurement) concomitantly caused by cardiopulmonary receptors. Furthermore, analysis of individual data showed that changes in plasma noradrenaline and forearm vascular resistance were linked by a positive relationship (r = 0.64). 4. Thus the cardiopulmonary receptor reflex can produce rapid, marked and sustained changes in both plasma noradrenaline and forearm vasomotor tone. This is in sharp contrast with the previously observed inability of the carotid baroreflex to alter both these humoral and haemodynamic variables. Taken together these findings support the hypothesis that sympathetic tone to skeletal muscle is an important determinant of the concentration of plasma noradrenaline in blood.

Role of hemodilution on renal responses to water immersion in humans

1995 ◽  
Vol 269 (5) ◽  
pp. R1068-R1076 ◽  
Author(s):  
L. B. Johansen ◽  
P. Bie ◽  
J. Warberg ◽  
N. J. Christensen ◽  
P. Norsk
Keyword(s):  
Lower Extremity ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Venous Pressure ◽  
Colloid Osmotic Pressure ◽  
Central Venous ◽  
Fluid Shifts ◽  
Capillary Bed ◽  
Renal Responses

The present experiments were designed to elucidate 1) the role of the lower extremity capillary bed in decreasing plasma colloid osmotic pressure (COP) during immersion of humans (n = 8) for 6 h, and 2) the extent to which the natriuresis of water immersion is triggered by this decrease in COP. Irrespective of the depth, COPs were very similar during the immersion procedures, varying between 25.3 +/- 0.5 and 26.4 +/- 0.6 mmHg, which was significantly lower than during control (28.3 +/- 0.3 and 28.6 +/- 0.3 mmHg). During neck immersion, central venous pressure rose instantly by approximately 12 mmHg (P < 0.05) and remained elevated. Only a transient, marginal increase (1.6 +/- 0.7 mmHg) occurred during hip immersion. Cumulated sodium excretion during seated control, hip immersion, and neck immersion, respectively, differed significantly (30 +/- 5, 45 +/- 5, and 101 +/- 6 mmol). It is concluded that the decrease in COP during immersion is primarily due to fluid shifts occurring in the capillary bed of the legs and that this may account for up to 25% of the immersion-induced increase in renal sodium excretion.

Effect of increased intracardiac and arterial pressure on plasma vasopressin in humans

1984 ◽  
Vol 246 (5) ◽  
pp. H647-H651 ◽  
Author(s):  
S. R. Goldsmith ◽  
A. W. Cowley ◽  
G. S. Francis ◽  
J. N. Cohn
Keyword(s):  
Heart Rate ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Water Restriction ◽  
Lower Body Positive Pressure ◽  
Arterial Blood ◽  
Body Positive ◽  
Cardiopulmonary Receptors

The effects of loading cardiopulmonary and sinoaortic baroreceptors on plasma arginine vasopressin (AVP) levels were examined in 18 healthy young adults after a mild water restriction. Cardiopulmonary receptors were acutely loaded by volume expansion which increased central venous pressure (CVP) from 4.7 +/- 1.9 to 7.3 +/- 2.2 mmHg but did not change mean arterial blood pressure (MAP). Both receptor groups were acutely loaded by applications of lower body positive pressure, which induced a comparable increase in CVP and, in addition, raised MAP from 85 +/- 6.7 to 93 +/- 6.8 mmHg (P less than 0.001). There was evidence of reflex activation as forearm blood flow and heart rate increased during volume expansion while the increase in heart rate was blocked during lower body positive pressure. Neither intervention significantly altered the control AVP level of 4.6 +/- 1.4 pg/ml. An investigation of more prolonged stimulation of cardiopulmonary receptors was carried out using 1 h of head-down tilt. Again, despite increases in CVP (5.1 +/- 1.3 to 9.0 +/- 1.4 mmHg, P less than 0.005), AVP (5.7 +/- 2.4 pg/ml) did not decrease. MAP did not change during head-down tilt. There were no changes in osmolality throughout any of the studies. AVP levels in humans are therefore not responsive to moderate isosmotic loading of the cardiopulmonary and sinoaortic baroreceptors under conditions of mild water restriction.

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

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