Role of renal nerves in control of sodium excretion in chronic congestive heart failure

The aim of this study was to examine the contribution of the renal nerves to the sodium retention in chronic congestive heart failure produced by rapid ventricular pacing. In 10 female dogs the left kidney was denervated and the urinary bladder was split to allow separate 24-h urine collection from an innervated and a denervated kidney in the same dog. The dogs were placed on an 80-meq/day sodium intake and permitted to recover for at least 2 wk. Control measurements were made for 5 days followed by ventricular pacing at 270-300 beats/min for 6 days. Cardiac output (CO), measured with an electromagnetic flow probe around the ascending aorta, fell from a control of 2.4 +/- 0.3 to 1.4 +/- 0.2 l/min (6 day average) during pacing while mean arterial pressure (MAP) fell from 91 +/- 4 to 71 +/- 3 mmHg. In six dogs, sodium excretion fell to an average of less than 2 meq/day (80 meq/day intake) during the 6-day pacing period in both the innervated and denervated kidneys. In four dogs, sodium excretion returned back toward control on days 3-6 of pacing despite sustained reductions in CO and MAP. However, there were no differences in renal hemodynamics or electrolyte excretion between innervated and denervated kidneys in either the compensated or decompensated dogs. These results suggest that other control mechanisms, besides the renal nerves, are primarily responsible for the sodium retention in this model of chronic congestive heart failure.

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ANF-mediated renal cGMP generation in congestive heart failure

AJP Renal Physiology ◽

10.1152/ajprenal.1991.260.4.f562 ◽

1991 ◽

Vol 260 (4) ◽

pp. F562-F568 ◽

Cited By ~ 6

Author(s):

K. B. Margulies ◽

D. M. Heublein ◽

M. A. Perrella ◽

J. C. Burnett

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sodium Excretion ◽

Biological Marker ◽

Target Cells ◽

Chronic Congestive Heart Failure ◽

Sodium Retention ◽

Cgmp Production ◽

Rapid Ventricular Pacing

Previous studies have demonstrated that the biological actions of atrial natriuretic factor (ANF) are mediated via increases in its intracellular second messenger guanosine 3',5'-cyclic monophosphate (cGMP). Because cGMP egresses rapidly from target cells after ANF binding to particulate guanylate cyclase-linked receptors, extracellular cGMP may be a useful biological marker for the action of ANF in vivo under pathophysiological conditions. The present studies tested the hypothesis that the avid sodium retention and renal ANF resistance characteristic of chronic congestive heart failure (CHF) are associated with attenuated renal cGMP responses to ANF. We assessed the natriuretic and cGMP responses to endogenous and exogenous ANF during the evolution of CHF produced by 6 days of rapid ventricular pacing in conscious dogs (n = 6). Simultaneous measurement of plasma and urinary cGMP concentrations allowed determination of the net renal generation of cGMP, an indicator of the renal contribution to total urinary cGMP excretion. In early CHF, increased sodium excretion and renal cGMP production were observed in association with increases in plasma ANF. Exogenous ANF administration (10 micrograms/kg iv) before CHF also produced parallel increases in sodium excretion and renal cGMP production. In more advanced CHF produced by 6 days of pacing, we observed avid sodium retention in association with reversal of earlier increases in renal cGMP production despite progressive increases in circulating ANF. Natriuretic and renal cGMP responses to exogenous ANF were similarly attenuated in chronic CHF. These studies suggest that 1) renal cGMP production is a useful biological marker for the renal natriuretic action of ANF; 2) endogenous ANF contributes to the maintenance of sodium excretion in early CHF via increases in renal cGMP production; and 3) the avid sodium retention and renal ANF resistance in advanced CHF are, in part, linked to attenuated renal cGMP responses to endogenous and exogenous ANF.

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Baro- and ventricular reflexes in conscious dogs subjected to chronic tachycardia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.4.h1084 ◽

1992 ◽

Vol 263 (4) ◽

pp. H1084-H1089 ◽

Cited By ~ 9

Author(s):

J. S. Chen ◽

W. Wang ◽

K. G. Cornish ◽

I. H. Zucker

Keyword(s):

Heart Failure ◽

Heart Rate ◽

Congestive Heart Failure ◽

Clinical Signs ◽

Chronic Congestive Heart Failure ◽

Ventricular Pacing ◽

Arterial Baroreflex ◽

Failure State ◽

Before And After ◽

Blood Pressure Responses

It has been well documented that the arterial baroreflex is depressed in chronic congestive heart failure. Furthermore, cardiopulmonary reflexes have also been shown to be depressed in heart failure. Because cardiac reflexes can be mediated by both mechanical and chemical stimuli, we undertook the current study to determine whether chemically activated cardiac reflexes (Bezold-Jarisch) are abnormally depressed in dogs with chronic heart failure at a point in time when arterial baroreflexes were clearly depressed. We studied heart rate and arterial pressure responses in 13 conscious instrumented dogs before and after chronic ventricular pacing at 250 beats/min for 4-5 wk. At the time the study was done each dog showed both hemodynamic and clinical signs of congestive heart failure. The arterial baroreflex was evaluated by analyzing the heart rate response to acute injections of phenylephrine and nitroglycerin. The Bezold-Jarisch reflex was assessed in nine dogs by determining the heart rate and blood pressure responses to intracoronary injections of various doses of veratridine. Arterial baroreflex responses were uniformly depressed following ventricular pacing. The phenylephrine slope was reduced by 55.8 +/- 6.9% (P < 0.001), and the nitroglycerin slope was reduced by 67.9 +/- 5.0% (P < 0.0001) in the heart failure state. Significant bradycardia and hypotension were seen at each dose of veratridine given (0.01, 0.1, and 0.4 microgram/kg). When compared with the prepaced control state, the magnitude of the hypotension was no different in the heart failure state in response to any dose of veratridine.(ABSTRACT TRUNCATED AT 250 WORDS)

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A perspective on diuretic resistance in chronic congestive heart failure

Therapeutic Advances in Cardiovascular Disease ◽

10.1177/1753944717718717 ◽

2017 ◽

Vol 11 (10) ◽

pp. 271-278 ◽

Cited By ~ 10

Author(s):

Niel Shah ◽

Raef Madanieh ◽

Mehmet Alkan ◽

Muhammad U. Dogar ◽

Constantine E. Kosmas ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sodium Intake ◽

Diuretic Therapy ◽

Management Strategies ◽

Chronic Congestive Heart Failure ◽

Diuretic Resistance ◽

Pump Failure ◽

Complex Disorder ◽

Development And Management

Chronic congestive heart failure (CHF) is a complex disorder characterized by inability of the heart to keep up the demands on it, followed by the progressive pump failure and fluid accumulation. Although the loop diuretics are widely used in heart failure (HF) patients, both pharmacodynamic and pharmacokinetic alterations are thought to be responsible for diuretic resistance in these patients. Strategies to overcome diuretic resistance include sodium intake restriction, changes in diuretic dose and route of administration and sequential nephron diuretic therapy. In this review, we discuss the definition, prevalence, mechanism of development and management strategies of diuretic resistance in HF patients.

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