Chronic experimental myocardial infarction produces antinatriuresis by a renal nerve-dependent mechanism

Abstract

The present study focused on the role of sympathetic renal nerve activity, in mediating congestive heart failure-induced sodium retention following experimental chronic myocardial infarction. Groups of male Wistar rats (240-260 g) were studied: sham-operated coronary ligation (CON3W, N = 11), coronary ligation and sham-operated renal denervation (INF3W, N = 19), 3 weeks of coronary ligation and sympathetic renal nerve denervation (INF3WDX, N = 6), shamoperated coronary ligation (N = 7), and 16 weeks of coronary ligation (INF16W, N = 7). An acute experimental protocol was used in which the volume overload (VO; 5% of body weight) was applied for 30 min after the equilibration period of continuous iv infusion of saline. Compared to control levels, VO produced an increase (P < 0.01, ANOVA) in urine flow rate (UFR; 570%) and urinary sodium excretion (USE; 1117%) in CON3W. VO induced a smaller increase (P < 0.01) in USE (684%) in INF3W. A similar response was also observed in INF16W. In INF3WDX, VO produced an immediate and large increase (P < 0.01) in UFR (547%) and USE (1211%). Similarly, in INF3W VO increased (P < 0.01) UFR (394%) and USE (894%). Compared with INF3W, VO induced a higher (P < 0.01) USE in INF3WDX, whose values were similar to those for CON3W. These results suggest that renal sympathetic activity may be involved in sodium retention induced by congestive heart failure. This premise is supported by the observation that in bilaterally renal denervated INF3WDX rats myocardial infarction was unable to reduce volume expansion-induced natriuresis. However, the mechanism involved in urinary volume regulation seems to be insensitive to the factors that alter natriuresis.

Effects of Renal Sympathetic Denervation on Post-Myocardial Infarction Cardiac Remodeling in Rats

“…[16] Retention of fluid and sodium is one of the most important characteristics of heart failure, caused by the joint action of a variety of capacity-control mechanisms including the renin-angiotensin-aldosterone system, prostaglandins, natriuretic peptides, vasopressin and sympathetic nervous system. [17] Among all these mechanisms, activation of the sympathetic nervous system is the most important one. As renal sympathetic output increases, renal blood flow is reduced and sodium and water reabsorption is enhanced; in addition, sympathetic activation can increase renin secretion and the resistance of the renal efferent artery.…”

Noninvasive and invasive evaluation of cardiac dysfunction in experimental diabetes in rodents

“…The following indices were obtained: heart rate (HR), LV systolic pressure (LVSP), LV end-diastolic pressure (LVEDP), and maximum rate of LV pressure rise and fall (+dP/dt max and -dP/dt max). After LV pressure basal records, the LV function was recorded during a volume overload protocol performed by an injection of saline (0.27 mL/min/kg) during 3 minutes adapted from Souza's study [13]. According to the volume overload protocol, the restoration of LV parameters was measured there for 3 minutes.…”

Influence of renal denervation on blood pressure, sodium and water excretion in acute total obstructive apnea in rats

“…After renal denervation the flank incision was sutured and the procedure was repeated on the opposite side to denervate the right kidney. This surgical procedure was performed 15 days before the experimental protocol because it is known that it prevents the renal vasoconstrictor response to suprarenal lumbar sympathetic nerve stimulation and the antinatriuretic response to environmental stress and reduces renal tissue norepinephrine concentration to <5% of control for up to 15 days post-denervation (22,23).…”

“…For urinary measurements, a suprapubic incision was made and a polyethylene catheter was inserted and sutured into the bladder. This catheter was then exteriorized and secured by suturing it to the adjacent muscle and skin (23). Rats also underwent tracheal catheterization to induce severe OA episodes via total occlusion of the tracheal polyethylene catheter.…”

“…Initially, the animals received iv infusions of isotonic saline (55 μL/min) to enhance renal excretion of water and sodium (23). After an equilibration period for the stabilization of renal excretory responses the experimental protocol was performed and divided into 3 periods: control (C), apnea (A) and recovery (R).…”