Neurohumoral modulators and sodium balance in experimental heart failure

1993 ◽  
Vol 264 (4) ◽  
pp. H1187-H1193 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Av Fistula ◽  
Before And After ◽  
High Output Heart Failure

The acute and chronic interactions of the renal nerves, atrial natriuretic factor (ANF), and mineralocorticoids for the regulation of sodium balance were examined in dogs with an arteriovenous (AV) fistula and the syndrome of high-output heart failure (HOHF) (n = 6). After the AV fistula and bilateral renal denervation, the animals avidly retained sodium for 5-7 days and then regained sodium balance for the subsequent 3 wk. This compensation was associated with the sustained elevations of plasma ANF and the normalization of plasma renin. Subsequent administration of deoxycorticosterone acetate (DOCA) for 10 days produced consistent sodium retention despite additional elevations in plasma ANF. All of these responses were similar to previous studies in AV fistula dogs with intact renal nerves. In a separate part of the study, the renal actions of acute synthetic ANF infusions were examined in these renal-denervated AV fistula dogs before and after DOCA. In the pre-DOCA experiments, ANF infusions at 15, 30, and 100 ng.kg-1.min-1 produced dose-related increases in urinary sodium excretion and significant elevations in creatinine clearance. In the presence of DOCA, urinary sodium excretion was markedly attenuated during identical ANF infusions. The composite results suggest that mineralocorticoids have an important modulatory role for the regulation of sodium balance in experimental HOHF. However, compared with earlier studies in compensated AV fistula dogs with intact renal nerves, the present studies demonstrate that blockade of efferent renal sympathetic nerve activity can restore the natriuretic expression of acute elevations in circulating ANF.

Influence of captopril on fluid and electrolyte balances and adrenocortical responses during sodium deprivation in the rat

1983 ◽  
Vol 98 (2) ◽  
pp. 211-NP ◽  
Author(s):  
Annette McKeever ◽  
J. A. Oliver ◽  
I. W. Henderson ◽  
Warwick Mosley
Keyword(s):  
Sodium Excretion ◽  
Enzyme Inhibitor ◽  
Gastric Lavage ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Zona Glomerulosa ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Deficient Diet ◽  
Angiotensin I Converting Enzyme

An angiotensin I-converting enzyme inhibitor (captopril) was given by gastric lavage at a dose of 30 mg/kg body weight per day to Long–Evans rats for a 13-day period during which they received a sodium-deficient diet. This regime was preceded by a 3-day period during which measurements were made on the animals on a sodium-replete dietary intake. Control sodium-deprived rats showed increased plasma renin activities, increased peripheral aldosterone concentrations and reduced urinary sodium excretion; they maintained positive sodium balance and the zona glomerulosa of the adrenal cortex hypertrophied. Captopril-treated sodium-deprived rats failed to reduce urinary sodium excretion sufficiently and entered a period of marked and sustained negative sodium balance. Peripheral aldosterone concentrations after 12 days of sodium deprivation in the presence of captopril treatment were similar to those of sodium-replete rats. The adrenocortical zona glomerulosa of the captopril-treated rats did not increase in size and regressive changes were noted.

Captopril enhances renal responsiveness to ANF in dogs with compensated high-output heart failure

1992 ◽  
Vol 262 (3) ◽  
pp. R509-R516 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson
Keyword(s):  
Heart Failure ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Systemic Hemodynamic ◽  
Av Fistula ◽  
High Output Heart Failure ◽  
Converting Enzyme Inhibition ◽  
Control Infusion ◽  
High Output

The systemic hemodynamic, hormonal, and renal effects of chronic angiotensin-converting enzyme inhibition (CEI) with captopril and the responses to synthetic atrial natriuretic factor (ANF) infusions in the presence and absence of captopril were examined in normal dogs (n = 6) and in dogs with an arteriovenous (AV) fistula and compensated high-output heart failure (n = 6). This experimental model is characterized by normalization of the circulating renin-angiotensin-aldosterone system (RAAS) and persistent elevations in central filling pressures and plasma ANF. In both normal and AV-fistula dogs, oral captopril for 1 wk at 35 mg.kg-1.day-1 in three divided doses produced progressive reductions in arterial and atrial pressures (P less than 0.05), plasma ANF (P less than 0.05), and aldosterone (P less than 0.05). After 1-2 days of a modest increase in urinary sodium excretion (UNaV) (P less than 0.05), all of the dogs regained and maintained sodium balance during captopril administration. On the 8th day of the captopril regimen, synthetic ANF was infused at 15 and 30 ng.kg-1.min-1 for 75-min periods each. Control infusion experiments were performed in the same animals before captopril administration. The normal dogs exhibited dose-related elevations in UNaV (P less than 0.05) that were not augmented with captopril (P greater than 0.05). In contrast, in the AV-fistula dogs the observed renal unresponsiveness to synthetic ANF in the control experiments was reversed with chronic CEI, and ANF-induced UNaV achieved levels comparable to those obtained in the normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Hormonal determinants of sodium excretion in rats with experimental high-output heart failure

1988 ◽  
Vol 254 (5) ◽  
pp. R776-R784 ◽  
Author(s):  
J. Winaver ◽  
A. Hoffman ◽  
J. C. Burnett ◽  
A. Haramati
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Plasma Aldosterone ◽  
Base Line ◽  
Sham Control ◽  
Renal Handling ◽  
High Output Heart Failure ◽  
High Output

The present study evaluates the inter-relationship between the alteration in atrial natriuretic factor (ANF) and the renal handling of Na in rats with chronic aortocaval (a-v) fistula, an experimental model of congestive heart failure. Balance studies in these animals showed two distinct patterns of Na excretion: some rats developed progressive Na retention [urinary sodium excretion (UNaV) less than 100 mueq/24 h], whereas others compensated and returned to normal Na balance (UNaV greater than 1,200 mueq/24 h). Base-line plasma ANF levels were equally elevated in Na-retaining and compensated rats with a-v fistula (588 +/- 70 vs. 621 +/- 114 pg/ml, P, NS). However, the response of the two groups to exogenous administration of synthetic rat ANF-(101-126) in incremental doses varied greatly. ANF infusion increased the fractional Na excretion (FENa) in compensated animals from 0.12 +/- 0.03 to 2.6 +/- 0.5%, whereas the rise in FENa in Na-retaining animals was markedly blunted (0.11 +/- 0.06 to 0.89 +/- 0.35%). A similar pattern of ANF action was observed on the glomerular filtration rate and urine flow. The blunted response to ANF in the Na-retaining animals was associated with a marked increase in plasma renin activity (PRA) (35.6 +/- 6.9 vs. 4.5 +/- 0.7 ng ANG I.ml-1.h-1 in sham control rats, P less than 0.05) and plasma aldosterone levels (729.3 +/- 28.2 vs. 42.6 +/- 18.4 ng/dl in sham control rats, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of renal denervation on postprandial sodium excretion in experimental heart failure

1994 ◽  
Vol 266 (5) ◽  
pp. R1599-R1604 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
R. A. Johnson ◽  
J. C. Simmons
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
High Salt ◽  
Renal Nerves ◽  
Av Fistula ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
Filtered Load ◽  
High Output

The hormonal, hemodynamic and renal excretory changes after an oral load of sodium were examined in renal-denervated dogs with an arteriovenous (AV) fistula and the syndrome of compensated high-output heart failure. After ingestion of a meal containing 125 meq of sodium, the total postprandial urinary sodium excretion and fractional sodium excretion were approximately twofold higher in the renal-denervated AV fistula dogs, compared with a control group with intact renal nerves (P < 0.05). The postprandial elevations in right atrial pressure, plasma atrial natriuretic factor, and filtered load of sodium were similar in the two groups (P > 0.05). Mean arterial pressure and plasma renin activity remained unchanged from baseline in the two subsets of animals (P > 0.05). In the renal-denervated AV fistula dogs, ingestion of a low-salt meal containing 2-3 meq of sodium produced elevations in creatinine clearance and filtered load of sodium of similar magnitude to the high-salt meal. However, the increases in sodium excretion and plasma atrial natriuretic factor were modest and inconsistent. These results demonstrate that the renal nerves play an important modulatory role for postprandial sodium metabolism after a high-salt meal in experimental compensated high-output heart failure. It is suggested that the renal nerves attenuate the expression of postprandial natriuretic mechanisms via a direct tubular mechanism of action.

Urinary Sodium Excretion and Proximal Tubule Reabsorption in Rats with High-Output Heart Failure

Nephron ◽  
1974 ◽  
Vol 12 (4) ◽  
pp. 261-274 ◽  
Author(s):  
Klaus O. Stumpe ◽  
B. Reinelt ◽  
C. Ressel ◽  
H. Klein ◽  
F. Krück
Keyword(s):  
Heart Failure ◽  
Proximal Tubule ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Output Heart Failure ◽  
High Output

Central effects of atrial natriuretic factor on renal salt excretion

1991 ◽  
Vol 261 (2) ◽  
pp. F354-F359 ◽  
Author(s):  
P. Rohmeiss ◽  
G. Demmert ◽  
T. Unger
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Nerves ◽  
Urinary Flow ◽  
Renal Nerve ◽  
Ureteral Catheter ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial natriuretic factor (ANF) has been localized in periventricular brain areas involved in cardiovascular and fluid control. We investigated the effect of intracerebroventricular (icv) ANF (alpha-rat atriopeptin III) on renal sodium excretion in unilaterally nephrectomized, conscious unrestrained rats fitted with a chronic ureteral catheter. Isotonic NaCl (1 ml/h) was infused intravenously. ANF injected at doses (icv) of 1 ng (n = 6), 100 ng (n = 7), and 1 microgram (n = 7) reduced urinary sodium excretion (all values mumol/45 min, means +/- SE) from 111.6 +/- 24.4 to 83 +/- 20 (P less than 0.05), from 96.9 +/- 25.2 to 55 +/- 14 (P less than 0.01), and from 90.8 +/- 14.2 to 51 +/- 9 (P less than 0.01), respectively, whereas urinary flow rate did not change. The antinatriuretic effect was immediate in onset and lasted for greater than or equal to 60 min. Blood pressure remained unaltered. ANF (100 ng icv) increased efferent sympathetic renal nerve activity (+36%; n = 6, P less than 0.05), plasma renin activity (4.6 +/- 0.6 to 7.5 +/- 0.5 pmol angiotensin I.ml-1.h-1; n = 9, P less than 0.01), plasma angiotensin II (68.7 +/- 2.5 to 84.7 +/- 3.4 fmol/ml; n = 8, P less than 0.01), and aldosterone (22.3 +/- 3.6 to 37.2 +/- 4.0 ng/ml; n = 9, P less than 0.02). Renal denervation reduced the antinatriuretic effect of ANF by 37%. We conclude that brain ANF has antinatriuretic actions, which may be partly explained by activation of renal nerves.

Renal and systemic effects of urodilatin in rats with high-output heart failure

1992 ◽  
Vol 262 (4) ◽  
pp. F615-F621
Author(s):  
Z. A. Abassi ◽  
J. R. Powell ◽  
E. Golomb ◽  
H. R. Keiser
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Neutral Endopeptidase ◽  
Urine Flow ◽  
Systemic Effects ◽  
Arterial Blood ◽  
Before And After ◽  
High Output Heart Failure ◽  
Diuretic Response ◽  
The Absolute

Urodilatin is a recently discovered natriuretic peptide [ANP-(95-126)] of renal origin, with a primary structure similar to ANP-(99-126). However, urodilatin is not biologically inactivated by renal endopeptidase, and it is a more potent natriuretic agent than ANP-(99-126). The present study was carried out to investigate the renal and systemic effects of urodilatin in rats before and after the induction of congestive heart failure (CHF) by creation of an aortocaval fistula (ACF). Administration of urodilatin in incremental doses (0.75-12 micrograms.kg-1.h-1) to Inactin-anesthetized sham-operated control rats resulted in dose-dependent increases in urine flow, glomerular filtration rate (GFR), excretion of guanosine 3',5'-cyclic monophosphate (cGMP), sodium, and potassium, and a significant decrease in mean arterial blood pressure. In rats with ACF the baseline values for GFR and sodium excretion were significantly lower than in control rats. Urodilatin infusion in rats with ACF led to significant increases in urine flow and sodium excretion, but the absolute levels of diuresis and natriuresis were significantly lower in rats with CHF than in normal rats. When urodilatin was infused into rats with ACF pretreated with neutral endopeptidase inhibitor (NEP-I; SQ-28,063 at a dose of 40 mg/kg iv), the absolute urine flow and sodium excretion were not different from that obtained in control rats. Thus the attenuated natriuretic and diuretic response to ANP-(99-126) in heart failure was not observed with urodilatin.(ABSTRACT TRUNCATED AT 250 WORDS)

Failure of renal denervation to attenuate hypertension in Dahl NaCl-sensitive rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2428-2432 ◽  
Author(s):  
J. Michael Wyss ◽  
Wanida Sripairojthikoon ◽  
Suzanne Oparil
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renal Nerves ◽  
Urinary Volume ◽  
Volume Output

In previous experiments we have demonstrated that the renal nerves play a significant role in all genetic and (or) induced models of hypertension that we have studied. The current experiments extended this research by investigating the contribution of the renal nerves to hypertension in the Dahl NaCl-sensitive rat. This was investigated by assessing the effect of bilateral phenol renal denervation carried out prior to initiation of a high NaCl (8% NaCl) diet. In two separate studies, renal denervation did not affect systolic blood pressure in either Dahl NaCl-sensitive rats or their normotensive counterparts, Dahl NaCl-resistant rats. Further, denervation did not increase absolute urinary sodium excretion, percent urinary sodium excretion, urinary volume output, or food or water intake; nor did it differentially alter creatinine clearance or body weight. Denervation was verified at the termination of each study by a greater than 80% depletion of renal noradrenaline stores. These results indicate that the renal nerves do not provide a major contribution to hypertension in the Dahl NaCl-sensitive rat.

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