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

Abstract

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.

Renal Denervation as a Therapeutic Approach for Hypertension

“…The investigation revealed that sodium retention was attributable in part to renal sympathetic efferent nerve activity, which was abolished by renal nerve ligation. On the basis of measurements of postprandial sodium excretion, similar conclusions were reached from work on renal denervated dogs with an arteriovenous fistula and the syndrome of compensated high-output heart failure 44 ; however, long-term ventricular pressure was not monitored in these models. The ligation of renal nerves protected against expression of postprandial natriuretic resistance and the development of congestion or rises in ventricular filling pressures.…”

Effects of long-term renal sympathetic denervation on heart failure after myocardial infarction in rats

“…We did not measure plasma levels of ANP or renin activity. Previous studies 8,11 have shown that RD did not significantly affect plasma ANP. In the present study, however, the plasma ANP level 4 weeks after the operation may be lower in MI rats with RD than in those with INN, since LV end-diastolic pressure was lower in MI rats with RD.…”

“…In the present study, however, the plasma ANP level 4 weeks after the operation may be lower in MI rats with RD than in those with INN, since LV end-diastolic pressure was lower in MI rats with RD. No significant changes in plasma renin activity induced by RD were observed, 11,13 whereas significant reduction in renin activity has been reported. 31 If the latter is true, RD may reduce the effects of angiotensin II and aldosterone on ventricular structure and function.…”

“…Acute and chronic renal sympathetic denervation (RD) increases sodium and water excretion [10][11][12] and improves the impaired response of ANP in heart failure, 7,8 although RD in rats with normal hearts did not affect hemodynamics or natriuresis 10,13 or increase natriuresis. 12 However, it remains unknown whether long-term renal sympathoinhibition could modify ventricular function after myocardial infarction (MI).…”

Renal sympathetic nerve ablation for treatment‐resistant hypertension

“…Percutaneous renal sympathetic denervation may be particularly beneficial in this setting and indeed complementary to β-adrenoceptor blockade given differing pathways of sympathetic abrogation.This is supported by animal studies which have demonstrated improved cardiac function and reduced pathological fibrosis following denervation [33,34]. Furthermore, denervation has improved renal blood flow in the (preclinical) heart failure setting and this may have significant implications for the cardiorenal syndrome [35]. A small pilot study of seven patients with chronic mild to moderate systolic heart failure (mean EF 43 ± 15%) did not raise any procedural or safety concerns [36], in particular no major drop in BP despite low baseline levels and no change in renal function, with a mild improvement in the 6 min walk test.…”