Increased Aldosterone Secretion in Dogs With Right-Sided Congestive Heart Failure and in Dogs With Thoracic Inferior Vena Cava Constriction

The current studies were designed to investigate the functional significance of elevated endogenous atrial natriuretic factor (ANF) in acute congestive heart failure (CHF). Integrated cardiorenal and endocrine function were measured in three models of acute low-output congestive heart failure with comparably reduced cardiac output (CO) and mean arterial pressure (MAP). Acute CHF was produced by rapid right ventricular pacing (group I, n = 5) which decreases CO and increases atrial pressures and plasma ANF. In group II, n = 5, thoracic inferior vena caval constriction (TIVCC) was produced to decrease venous return and CO but without increases in atrial pressure or plasma ANF. In group III, n = 5, TIVCC was performed and exogenous ANF infused to achieve plasma concentrations observed in acute CHF. In acute CHF with increases in endogenous ANF, sodium excretion (UNaY), renal blood flow (RBF), plasma renin activity (PRA), and plasma aldosterone (PA) were maintained despite decreases in CO and MAP. In contrast, TIVCC with similar reductions in CO and MAP but without increases in ANF resulted in decreases in UN2V and RBF and increases in PRA and PA. Exogenous administration of ANF in TIVCC to mimic levels in acute CHF prevented sodium retention, renal vasoconstriction, and activation of renin and aldosterone. These studies demonstrate that endogenous ANF serves as an important physiologic volume regulator in acute CHF to maintain sodium excretion and possibly participate in the suppression of activation of the reninangiotensin-aldosterone system despite the stimulus of arterial hypotension.

Section: Methods Ofmeasurementsupporting

confidence: 93%

“…The RAAS contributes importantly to the regulation of fluid and electrolyte balance and in the pathogenesis of congestive heart failure (20,21). Systemic hypotension is a potent stimulus for activation of this vasoconstrictive-sodium retaining system.…”

Section: Methods Ofmeasurementmentioning

confidence: 99%

Role of endogenous atrial natriuretic factor in acute congestive heart failure.

Me¹,

Miller²,

Edwards³

et al. 1989

“…Constriction of the supradiaphragmatic inferior vena cava is a well documented stimulus to increase of aldosterone secretion (1,6). The results of this procedure in 11 normal dogs are shown in Table V.…”

Section: Methodsmentioning

confidence: 99%

Increase in Aldosterone Secretion by Carotid Artery Constriction in the Dog and Its Prevention by Thyrocarotid Arterial Junction Denervation *

Bartter¹,

Mills²,

Gann³

1960

Although it has been shown that the vagus nerves may carry impulses mediating decreases in the rate of aldosterone secretion (1), no equivalent pathway has been demonstrated which might mediate increases in aldosterone secretion. Because of evidence that aldosterone secretion may be increased by some function of a decreased intravascular volume (2), and the evidence cited above that this increase is not dependent upon the integrity of intrathoracic vagal receptors (1), the present experiments were designed to investigate the role of receptors located in the arterial system. METHODSAcute experiments were performed on mongrel dogs under pentobarbital anesthesia. The lumboadrenal veins were cannulated (3) and blood samples were collected intermittently for determination of aldosterone by Mills, Casper and Bartter's modification (1) of the method of Neher and Wettstein (4). This method has an absolute sensitivity of 0.1 ,ug of aldosterone. Losses during extraction and chromatography were determined on every sample by adding C,4-cortisone to each specimen before extraction and counting the cortisone region on the final chromatogram after development of the soda fluorescence. The mean recovery rate was 42 ± 9 per cent (SD). The overall sensitivity, considering the amount of the sample taken for analysis and the recovery rate, was 0.5 ,ug per hour. The final value was corrected for all losses by dividing each observed value by the rate of recovery of that sample. Thus, the only variable altering reproducibility is that of measurement of the soda fluorescence on paper. The technique used was that described by Ayres, Simpson and Tait (5) who found that, in measuring 0.5 Ag of aldosterone diacetate, the standard error was 0.01 and the standard errors for measurement of 2, 4, and 8 ,ug were, respectively, 0.17, 0.43, and 0.73. In experiments in this laboratory, the standard error for measurement of 1 ,ug of cortisone was found to be 0.04. Aldosterone secretion was stimulated by supradiaphragmatic inferior vena cava constriction (6) in 29 experiments. In 22 studies the stimulus was bilateral con-

“…The chronic caval dog has been widely used by Davis and associates (3,(6)(7)(8)) as a reasonable model in which to study the pathophysiology of edema. These authors, and others (4,9) have demonstrated that the development of sodium retention in this preparation cannot be correlated with depression of glomerular filtration (GFR) or renal plasma flow (RPF), increased renal venous pressure, altered renal nerve activity, or increased secretion of antidiuretic hormone (ADH) or adrenal cortical hormones.…”

Section: Introductionmentioning

confidence: 99%

Effects of Acute Volume Expansion and Altered Hemodynamics on Renal Tubular Function in Chronic Caval Dogs

Levy¹

1972

A B S T R A C T It is well established that dogs with chronic partial constriction of the thoracic inferior vena cava develop sodium retention, ascites, and respond poorly to acute saline loading. A group of such chronic caval dogs, and a group of normal controls were studied during hydropenia, and again after acute saline loading by clearance and recollection xnicropuncture techniques. After volume expansion, the caval dogs excreted 52 ImEq/ min per kidney of sodium compared with 370 MEq/min per kidney for the normal controls. During hydropenia and after the saline infusions, single nephron filtration rates, fractional reabsorption of sodium within the proximal tubule, and proximal delivery of filtrate to the distal nephron were comparable in both groups of dogs.Micropuncture of distal tubular segments confirmed that the loop of Henle was the major site for salt and water retention in the expanded caval dogs. Alteration of intrarenal hemodynamics by vasodilating one kidney and elevating systemic arterial blood pressure induced a normal natriuretic response in the saline-loaded caval dogs. Proximal tubular function remained unchanged and the loop of Henle appeared to be the major site responsive to these hemodynamic maneuvers. These same experiments in saline-loaded control dogs had no effect on function of the proximal or distal nephron and did not increase urinary excretion of sodium or water.These experiments provide evidence that the loop of Henle is the major site for sodium retention in volumeexpanded chronic caval dogs excreting minimal amounts of sodium.This report was published in part in abstract form in Clin.