Evidence for a humoral factor modifying the renal response to blood volume expansion in the rat

1969 ◽  
Vol 47 (4) ◽  
pp. 377-386 ◽  
Author(s):  
J. W. Pearce ◽  
H. Sonnenberg ◽  
A. T. Veress ◽  
U. Ackermann
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Regulatory Mechanism ◽  
Humoral Factor ◽  
Plasma Sodium ◽  
Acute Administration ◽  
Albumin Solution ◽  
Salt Loading ◽  
Renal Response ◽  
Blood Volume Expansion

In this study, designed to examine the interaction of mechanisms regulating renin secretion with those producing "volume diuresis and natriuresis", rats depleted of renin by chronic salt-loading and desoxycorticosterone (DOCA) administration (DOCA rats) showed exaggerated responses to iso-oncotic blood volume expansion. Conversely, chronically salt-deficient rats (NaD rats), known to have high renin levels, showed very depressed responses to expansion. Isovolemic cross-circulation of DOCA and NaD rats, including exchange of the animals' blood with bovine albumin solution in a reservoir, largely restored the renal response of NaD rats to subsequent infusion from the reservoir without altering responsiveness of the DOCA rats. Changes in plasma sodium, hematocrit value, and vascular pressures following cross-circulation were not different from those which followed exchange without cross-circulation in control experiments. In the latter, the renal response of NaD rats remained depressed, a finding not altered by acute administration of DOCA. The modification of response in cross-circulated NaD rats was therefore attributed to transfer of a humoral factor which interacted with the volume regulatory mechanism. Such a factor could be anti-renin, or alternately, a humoral effector, the level of which was critically increased in NaD rats before expansion.

Effect of Vagotomy on the Renal Response to Blood Volume Expansion in the Rat

1972 ◽  
Vol 50 (5) ◽  
pp. 463-466 ◽  
Author(s):  
A. T. Veress ◽  
J. W. Pearce
Keyword(s):  
Blood Volume ◽  
Whole Blood ◽  
Volume Expansion ◽  
Vagal Afferents ◽  
Reflex Inhibition ◽  
Vagus Nerves ◽  
Vasopressin Release ◽  
Renal Response ◽  
Blood Volume Expansion ◽  
Cervical Vagotomy

Bilateral cervical vagotomy in the rat reduces the diuretic but not the natriuretic response to vascular expansion by infusion of whole blood. The attenuation of volume diuresis is similar to that observed in rats with intact vagus nerves but receiving an infusion of pitressin as well as the vascular expansion. The findings are consistent with the Gauer–Henry reflex, which attributes volume diuresis in part to reflex inhibition of vasopressin release, but imply that vagal afferents are not involved in volume natriuresis.

Cardiac output and renal excretion rates during acute blood volume expansion in rats

1978 ◽  
Vol 234 (1) ◽  
pp. H21-H27 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Volume Expansion ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Plasma Protein Concentration ◽  
Renal Response ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

Selected central vascular parameters and renal excretion rates were monitored in anesthetized rats after acute, isohemic blood volume expansion by 33 percent. The infusate was an equilibrated mixture of animals' own blood and isotonic, isoncotic (6 percent) bovine albumin. Expansion increased mean arterial pressure by 35 percent, mean central venous pressure (CVP) by 850 percent, cardiac output (CO) by 56 percent, hematocrit (Hct) by 25 percent, plasma protein concentration (Ppr) by 25 percent, renal excretion rates of volume by 4,400 percent, of sodium by 2,800 percent, and of potassium by 360 percent of the respective preinfusion value. Hct and Ppr measurements suggested that 15 min after the end of the infusion, only 33 percent of infused volume remained within the circulation and that there was little further change in this during the remainder of the experiment. At the end of the elevated renal response, CVP and CO alone had returned to control values. Renal excretion rates were highly correlated with CO, but they were delayed by 2-5 min with respect to it. The results suggest that the renal response to acute volume expansion does not primarily control blood volume. Cardiac output may be the controlled variable in the response.

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