Volume-homeostatic mechanisms in humans during a 12-h posture change

1993 ◽  
Vol 75 (1) ◽  
pp. 349-356 ◽  
Author(s):  
P. Norsk ◽  
C. Stadeager ◽  
L. B. Johansen ◽  
J. Warberg ◽  
P. Bie ◽  
...  

On one day six male subjects underwent an upright seated (SEAT) study, and on another day they were subjected to a head-down tilt of 3 degrees (HDT). Compared with SEAT, HDT induced prompt increases in central venous pressure (CVP) from -0.5 +/- 0.8 to 8.3 +/- 0.3 mmHg (P < 0.001) and in arterial pulse pressure of 8–18 mmHg (P < 0.001). CVP stabilized after 6 h at levels 2.4–2.8 mmHg below the peak value. Simultaneously, renal sodium excretion gradually increased over the initial 5 h of HDT and stabilized at a level approximately 125 mumol/min over that of SEAT (P < 0.001). Urine flow rate and solute free water clearance increased during the initial 2–6 h of HDT (P < 0.001) but returned to the level of SEAT thereafter. We concluded that CVP is slightly reduced over 12 h of HDT and that a clear temporal dissociation exists between renal sodium and water handling. We suggest that the combined effect of the sustained suppressions of plasma renin activity and plasma aldosterone and norepinephrine concentrations constitutes a mechanism of the increase in renal sodium excretion.

1975 ◽  
Vol 38 (6) ◽  
pp. 1038-1044 ◽  
Author(s):  
M. Epstein ◽  
D. S. Pins ◽  
M. Miller

Since previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant relative central hypervolemia induced by water immersion to the neck causes a profound natriuresis and a suppression of the renin-aldosterone system, it was of interest to assess whether the diuresis induced by immersion was mediated by an analogous inhibition of ADH. The effects of water immersion on renal water handling and urinary ADH excretion were assessed in 10 normal male subjects studied following 14 h of overnight dehydration on two occasions, control and immersion. The conditions of seated posture and time of day were identical. During control ADH persisted at or above prestudy values. Immersion resulted in a progressive decrease in ADH excretion from 80.1 plus or minus 7 (SEM) to 37.3 plus or minus 6.3 muU/min (P smaller than 0.025). Cessation of immersion was associated with a marked increase in ADH from 37.3 +/- 6.3 muU/min to 176.6 +/- 72.6 muU/min during the recovery hour (P smaller than 0.05). Concomitant with these changes urine osmolality decreased significantly beginning as early as the initial hour of immersion from 1044 +/- 36 to 542 +/- 66 mosmol/kg H2O during the final hour of immersion (P smaller than 0.001). Recovery was associated with a significant mean increase in Uosm of 190 +/- 40 mosmol/kg H2O over the final hour of immersion (P smaller than 0.001). The suppression of ADH occurred without concomitant changes in plasma tonicity. These studies are consistent with the suggestion that in hydrated subjects undergoing immersion suppression of ADH release contributes to the enhanced free water clearance, which has been previously documented.


1989 ◽  
Vol 256 (5) ◽  
pp. F780-F786
Author(s):  
L. Groban ◽  
T. J. Ebert ◽  
D. U. Kreis ◽  
M. M. Skelton ◽  
D. M. Van Wynsberghe ◽  
...  

The effects of incremental exogenous alpha-human atrial natriuretic factor (ANF) infusion (10 and 25 ng.kg-1. min-1) on the cardiovascular, renal, and hormonal systems were examined in 22 healthy males. Successive 45-min infusions of ANF increased plasma levels five- and ninefold from a basal 42 +/- 5 pg/ml (P less than 0.01 and P less than 0.001). Hemodynamic responses provoked by ANF consisted solely of progressive reductions in central venous pressure (CVP) (P less than 0.05). Heart rate and mean arterial pressure were unaltered. Plasma renin activity, aldosterone, and vasopressin were not modified by either dose of ANF. However, plasma norepinephrine increased 32% during the 10-ng.kg-1.min-1 infusion (P less than 0.05) and remained elevated during the higher dose of ANF. Renal function was unaltered by the 10-ng.kg-1.min-1 infusion of ANF when compared with base line and placebo responses. The 25-ng.kg-1. min-1 infusion of ANF increased sodium excretion 100% from base line (P less than 0.05), whereas potassium excretion decreased 47% (P less than 0.05). Urine output increased significantly from 7.7 +/- 0.6 to 12.5 +/- 0.7 ml/min (P less than 0.05). These responses were not observed in the placebo group or in an additional group of four volunteers who received a continuous low-dose infusion of ANF (10 ng.kg-1.min-1) for two consecutive 45-min periods. Neither dose of ANF altered creatinine clearance or free water clearance. The data indicate that fivefold elevations (physiological levels) of plasma ANF do not influence renal or hormonal function.(ABSTRACT TRUNCATED AT 250 WORDS)


1991 ◽  
Vol 260 (1) ◽  
pp. R82-R89
Author(s):  
M. G. Ervin ◽  
R. Castro ◽  
D. J. Sherman ◽  
M. G. Ross ◽  
J. F. Padbury ◽  
...  

Circulating epinephrine alters atrial natriuretic factor (ANF) and arginine vasopressin (AVP) secretion, and all three hormones influence renal function. To quantify the relationships among fetal plasma epinephrine levels, fetal ANF and AVP secretion, and fetal renal function, six chronically catheterized fetal lambs (132 +/- 1 days gestation) received successive 40-min epinephrine infusions (0.1, 0.4, and 1.8 micrograms.min-1.kg-1). The second epinephrine infusion dose evoked significant increases in urine flow (V; 0.7 +/- 0.2 to 1.2 +/- 0.2 ml/min), free water clearance (CH2O; 0.3 +/- 0.1 to 0.7 +/- 0.1 ml/min), glomerular filtration rate (GFR; 3.9 +/- 0.7 to 5.4 +/- 0.8 ml/min), fractional water excretion (V/CH2O; 19 +/- 3 to 25 +/- 2%), mean arterial pressure (MAP; 45 +/- 3 to 51 +/- 4 mmHg), and a 94% increase in plasma ANF levels. A fourfold increase in the infusion dose significantly increased osmolar clearance (0.3 +/- 0.1 to 0.6 +/- 0.1 ml/min), sodium excretion (28 +/- 8 to 53 +/- 13 mueq/min), and plasma AVP levels (2.4 +/- 0.5 to 6.4 +/- 2.4 pg/ml) with no additional effect on V, CH2O, GFR, V/GFR, MAP, or plasma ANF levels. Urine osmolality and fractional sodium excretion did not change in response to epinephrine infusion. Our results demonstrate that epinephrine infusion stimulates fetal ANF secretion and to a lesser extent AVP secretion and significantly influences fetal renal function.


1988 ◽  
Vol 74 (2) ◽  
pp. 137-143 ◽  
Author(s):  
M. Bernardi ◽  
Rossana De Palma ◽  
F. Trevisani ◽  
R. Malatesta ◽  
M. Baraldini ◽  
...  

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.


1991 ◽  
Vol 69 (8) ◽  
pp. 1196-1203 ◽  
Author(s):  
Dorothea E. Blandford ◽  
Donald D. Smyth

Previous studies have demonstrated a diuretic effect of clonidine at low intrarenal infusion rates with a natriuretic effect being observed at high infusion rates (≥3 μg∙kg−1∙min−1). The natriuresis at high infusion rates may have been secondary to increased renal prostaglandin production. We therefore evaluated the effects of indomethacin (a cyclooxygenase inhibitor) on the response to cionidine in the anesthetized rat. Intrarenal infusions of saline (vehicle) or clonidine (0.1, 0.3, 1, and 3 μg∙kg−1∙min−1) were examined both in the presence and absence of pretreatment with indomethacin (5 mg/kg, i.p.). Clonidine produced a dose-related increase in urine volume and free water clearance at 0.3, 1, and 3 μg∙kg−1∙min−1 as compared with the vehicle group. Sodium excretion and osmolar excretion were increased only at the highest infusion rate investigated. Following indomethacin pretreatment, clonidine produced a greater increase in urine volume at each infusion rate investigated. The indomethacin pretreatment also resulted in a potentiation of the natriuretic effect of clonidine at all infusion rates. Interestingly, this was associated with an increase in osmolar clearance but not free water clearance. These effects of indomethacin were reversed by infusion of prostaglandin E2. An infusion of prostaglandin E2 attenuated the indomethacin-induced increase in both urine flow rate and sodium excretion, indicating that the effects of indomethacin were mediated by prostaglandin inhibition. These results suggest that endogenous prostaglandin production attenuates the renal effects of clonidine, and as well, that in the presence of α2-adrenoceptor stimulation, prostaglandin E2 mediates an antidiuretic and antinatriuretic effect.Key words: clonidine, indomethacin, prostaglandin E2, diuresis, natriuresis.


1978 ◽  
Vol 45 (5) ◽  
pp. 786-790 ◽  
Author(s):  
I. H. Zucker ◽  
J. P. Gilmore

The present investigation evaluated the renal and hemodynamic responses to head-out water immersion in dogs. Dogs were immersed in the vertical (seated) position in a 34 degrees C bath. Urine flow (V), osmolar clearance (Cosm), free water clearance (CH2O), sodium excretion (UNa+V), potassium excretion (UK+V), GFR, effective renal plasma flow (ERPF), central venous pressure (CVP), and cardiac output (CO) all increased significantly during immersion. This response was unchanged by bilateral cervical vagotomy or by deoxycorticosterone acetate and antidiuretic hormone administration. The control values of these dogs were low and indicated a state of peripheral vascular pooling which was readjusted to normal by the immersion maneuver. The renal and hemodynamic values during the period of immersion were similar to values of a group of dogs which were recumbent in air. Furthermore, when the latter group of dogs were tilted head down 19 degrees, there was no further increase in any of the measured parameters. These data are consistent with the view that water immersion in the upright dog simply redistributes blood volume back to that level seen in the recumbent dog, a position which is more natural for this species.


1978 ◽  
Vol 235 (1) ◽  
pp. H29-H33 ◽  
Author(s):  
A. L. Mark ◽  
F. M. Abboud ◽  
A. E. Fitz

We evaluated effects of the low- and high-pressure baroreceptors on plasma renin activity (immunoassay) using graded lower body suction (LBS) in six healthy men. LBS at -10 and -20 mmHg for 10 min decreased central venous pressure without changing arterial pressure and thereby presumably reduced low- but not high-pressure baroreceptor inhibition of renin release. LBS at these levels produced forearm vasoconstriction, but did not increase renin. LBS at -40 mmHg decreased central venous and arterial pulse pressure and thus reduced both low- and high-pressure baroreceptor inhibition. LBS at this level produced forearm vasoconstriction and tachycardia and increased renin from 2.1 +/- 0.4 (mean +/- SE to 7.4 +/- 1.4 ng.ml-1.h-1 (P less than 0.05). In summary, reduction in low-pressure baroreceptor inhibition in humans did not increase renin in the presence of physiological tonic inhibition from high-pressure baroreceptors. Increases in renin did not occur until there was combined reduction of high- and low-pressure baroreceptor inhibition on plasma renin activity.


1990 ◽  
Vol 258 (6) ◽  
pp. R1424-R1430 ◽  
Author(s):  
F. Tajima ◽  
S. Sagawa ◽  
J. Iwamoto ◽  
K. Miki ◽  
B. J. Freund ◽  
...  

The present study was undertaken to determine the relative influence of the action of the central nervous system on the mechanism of water-immersion-induced diuresis by comparing physiological responses of quadriplegic (QP) and normal subjects. After overnight fasting seven male QP subjects with complete cervical cord transections (C5-C8) and six normal men were tested before, during, and after 3 h of head-out immersion (HOI) in thermoneutral water (34.5-35.0 degrees C). The reversible increase in urine flow and the total urine volume (309 +/- 53 ml in 3 h) in QP subjects were comparable with that of the normal subjects (318 +/- 96 ml in 3 h). While osmolal excretion was increased in QP subjects, its magnitude was less when compared with that of normal subjects. Instead, the increased urine flow in QP subjects was characterized by increased glomerular filtration rate (GFR) and free water clearance, in contrast to a predominantly osmotic diuresis with no changes in GFR in the normal subjects. The HOI elevated (P less than 0.05) systolic pressure only in QP subjects, whereas the increase in cardiac output was the same in both groups. While plasma renin activity and aldosterone responses to HOI in QP subjects were comparable with those of normal individuals, plasma atrial natriuretic factor (ANF) in QP subjects was twofold higher (P less than 0.05) during HOI, and the approximately threefold increase in ANF (P less than 0.05) in QP subjects due to HOI was the same as that of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)


2001 ◽  
Vol 281 (2) ◽  
pp. R459-R467 ◽  
Author(s):  
Anders Gabrielsen ◽  
Peter Bie ◽  
Niels Henrik Holstein-Rathlou ◽  
Niels Juel Christensen ◽  
Jørgen Warberg ◽  
...  

To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 ± 0.03 (mean ± SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis ( P < 0.05 for all) compared with seated control. Compared with control subjects ( n = 9), ANG II, Aldo, and ANP concentrations were increased ( P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 ± 16 vs. 88 ± 15 μmol/min and 0.42 ± 0.18 vs. 0.68 ± 0.12% (mean ± SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed ( P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased ( P < 0.05) to the level of control subjects (108 ± 34 μmol/min and 0.70 ± 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.


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