Role of the Kidney in the Pathogenesis of Congestive Heart Failure

Barger, A. C.; Muldowney, Francis P.; Liebowitz, Martin R.

doi:10.1161/01.cir.20.2.273

Cited by 101 publications

(38 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, it would avoid the offsetting antinatriuretic influence of the decrease in arterial pressure that occurs with blockade of systemic ␣ 1 -adrenoceptors. This recapitulates the important experiment of Barger, 37,38 in which unilateral renal denervation in CHF dogs resulted in an ipsilateral diuresis and natriuresis without changes in RBF, GFR, or arterial pressure. It also focuses on increased RSNA as one of the contributing factors to the defect in renal sodium excretory capacity so fundamental to a prevailing concept of the development of hypertension.…”

Section: The Futuresupporting

confidence: 81%

Neural Control of the Kidney

DiBona

2003

Hypertension

159

View full text Add to dashboard Cite

Abstract-This article provides a chronological perspective on the development of knowledge concerning the neural control of renal function and is divided into three parts: the past, the present, and the future. The PastResearch in the area of the neural control of renal function was not very active for the first half of the 20th century. This can be attributed to 2 factors. First, the renowned renal physiologist, Homer Smith, rendered an opinion that the renal nerves were of little functional consequence. [1][2][3] This was based on his interpretation of experiments involving renal denervation in anesthetized and surgically operated animals. He criticized this approach, as he believed that the starting level of renal sympathetic nerve activity (RSNA) would be quite elevated, owing to the associated stress, so that "denervation hyperemia and diuresis appear to be a release from enhanced vasoconstriction engendered by anesthesia and traumatic operative procedures." 3 Second, there was a lack of convincing evidence that the renal innervation extended beyond the renal vasculature to either the tubules or the juxtaglomerular apparatus. The demonstration by Luciano Barajas 4 that all segments of the renal tubule (as well as the juxtaglomerular apparatus) were innervated by norepinephrine-containing renal sympathetic nerve terminals that make contact with the renal tubular epithelial cell basement membrane paved the way for increased research activity in this area. This critical observation reconfirmed once again the important relationship between structure and function.Given the powerful influence of changes in renal hemodynamics (ie, arterial pressure, glomerular filtration rate [GFR] and renal blood flow [RBF]) on urinary sodium excretion (U Na V), it was evident that the influence of changes in RSNA on U Na V must be examined in experimental protocols in which these variables remained constant. By using electrical stimulation of the efferent renal sympathetic nerves at frequencies just subthreshold for decreases in RBF, it was shown that a reversible decrease in U Na V occurred in the absence of changes in GFR (ie, filtered sodium load), RBF, and arterial pressure. 5 These results indicated that lowfrequency renal sympathetic nerve stimulation increased overall renal tubular sodium reabsorption via a direct action on the renal tubule, independent of changes in renal hemodynamics. Additional experiments demonstrated that this effect occurred in the proximal convoluted tubule, the thick ascending limb of Henle's loop, the distal convoluted tubule, and the collecting duct. 6,7 Subsequent work (reviewed in DiBona and Kopp 8 ) showed that this was owing to the release of norepinephrine from renal sympathetic nerve terminals with stimulation of postsynaptic ␣ 1 -adrenoceptors located on the basolateral membrane of renal tubular epithelial cells throughout the nephron. Subsequent intracellular signaling events resulted in an increase in activity of the sodium pump (Na ϩ ,K ϩ -ATPase), with increased transepithelial sod...

show abstract

Section: The Futuresupporting

confidence: 81%

Neural Control of the Kidney

DiBona

2003

Hypertension

159

View full text Add to dashboard Cite

show abstract

“…The enhanced sympathetic tone under these circumstances is believed to contribute to improved cardiac performance by increasing the heart rate and myocardial contractility, thereby sustaining perfusion to vital organs (39). It has been experimentally demonstrated that the antidiuresis and antinatriuresis induced by constriction of the thoracic vena cava or tricuspid insufficiency in dogs was abolished by pretreatment with systemic or intrarenally administered adrenergic blockers (40)(41)(42)(43) or, as in the present study, surgical denervation (43)(44)(45). In some of these studies, whole kidney plasma flow rate, estimated by renal clearance of para-aminohippuric acid, was found to change to a relatively small and variable degree after the adrenergic inhibition (40,41).…”

Section: Discussionmentioning

confidence: 99%

Role of renal sympathetic nerves in mediating hypoperfusion of renal cortical microcirculation in experimental congestive heart failure and acute extracellular fluid volume depletion.

Kon¹,

Yared²,

Ichikawa³

1985

J. Clin. Invest.

View full text Add to dashboard Cite

To evaluate the pathophysiologic importance of renal nerves in regulating the renal vasomotor tone, we measured several parameters of renal cortical microcirculation before and after acute renal denervation (DNx) in the following three groups of anesthetized Munich-Wistar rats: (group 1) congestive heart failure after surgically induced myocardial infarction (n = 10), (group 2) acute extracellular fluid volume depletion after deprivation of drinking water for 48 h (n = 8), and (group 3) sham or nontreated controls (n = 6). In the myocardial-infarcted rats, DNx led to a uniform increase in glomerular plasma flow rate of, on average, 36%. Single nephron glomerular filtration rate of myocardialinfarcted rats also increased despite a reduction in glomerular capillary hydraulic pressure. These changes were associated with a fall in arteriolar resistances, particularly in the efferent arteriole. The glomerular capillary ultrafiltration coefficient rose in all but one myocardial-infarcted animal. A similar hemodynamic pattern was seen after DNx in water-deprived animals. In every water-deprived animal, glomerular plasma flow rate and single nephron GFR increased on average by 28 and 14%, respectively. Again, afferent and efferent arteriolar resistances decreased significantly. Furthermore, the ultrafiltration coefficient increased uniformly and substantially with DNx.To ascertain the potential importance of the interaction between the renal nerves and angiotensin II in these circumstances, we compared the renal cortical hemodynamics in additional groups of water-deprived rats (group 4) after DNx (n = 15), (group 5) during inhibition of angiotensin II with saralasin (n = 15), and (group 6) during treatment with both saralasin and DNx (n = 15). No appreciable difference was detected between group 4 vs. 6. In contrast, substantial differences were noted between group 5 vs. 6: on average, the glomerular plasma flow rate was 26% higher and the afferent and efferent arteriolar resistances 25% and 27% lower, respectively, in group 6.Portions of these studies were presented at the annual meeting of the American Society of Nephrology, Washington, DC, 1984, and at the Annual Meeting of the Federations of American Societies for Experimental Biology, Washington, DC, 1985, and were published in abstract form (1984. Am. Soc. Nephrol. 17:134; and 1985. Clin. Res. 33:489A).Address correspondence to Dr. Kon, Laboratory of Renal Physiology.Receivedfor publication 8 January 1985 and in revisedform 12 July 1985.These observations provide direct evidence to indicate pathophysiologic importance of renal nerves in the profound intrarenal circulatory adjustments in prerenal circulatory impairment. The vasoconstrictive effects of renal nerves appear to be mediated in part by their stimulatory influence on angiotensin II release and their direct constrictor actions on pre-and postglomerular vessels as well.

show abstract

“…Since all of the cases who responded to the aldosterone antagonist did not excrete increased amounts of aldosterone metabolites in urine, the authors suggested that a reduced rate of removal from plasma may have increased the circulating level of hormone. Further work will be necessary to evaluate other factors that sensitize the animal with congestive failure to the sodium-retaining effect of adrenal steroids (31,32).…”

Section: Methodsmentioning

confidence: 99%