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Increasing renal pelvic pressure results in PGE2-mediated release of substance P, leading to increases in afferent renal nerve activity (ARNA) and natriuresis, that is, a renorenal reflex response. The renorenal reflexes are impaired in congestive heart failure (CHF). Impairment of the renorenal reflexes may contribute to the increased renal sympathetic nerve activity and sodium retention in CHF. Endothelin (ET)-l contributes to the pathological changes in cardiac and renal function in CHF. Therefore, we examined whether the ETa receptor antagonist BQ123 altered the responsiveness of renal mechanosensory nerves in CHF. The ARNA responses to increasing renal pelvic pressure were suppressed in CHF but not in sham-CHF rats. In CHF, increasing renal pelvic pressure by 7.5 mm Hg before and during renal pelvic perfusion with BQI23 increased ARNA 12% ± 3% and 21% ± 3% (p < 0.05 vs. vehicle). In isolated renal pelvises from CHF rats, [PGE.sub.2] increased substance P release from 5 ± 0 10 7 ± I pg/min without BQ123 and from 4 ± I to 9 ± 1 pg/min with BQ123 in the bath (p < 0.01 vs. vehicle). BQ123 had no effect on the ARNA responses or substance P release in sham-CHF. In conclusion, activation of [ET.sub.A] receptors contributes to the impaired responsiveness of renal mechanosensory nerves in CHF rats by a mechanism(s) at the renal sensory nerve endings. Key words: renal nerves, kidney, prostaglandins, substance P, renal pelvic pressure, sodium retention, sodium excretion. L'augmentation de la pression pelvienne renale provoque la liberation de substance P par l'intermediaire de la [PGE.sub.2], ce qui contribue a augmenter l'activite des nerfs renaux afferents (ANRA) et la natriurese, c.-a-d. une reponse du reflexe renorenal. Les reflexes renorenaux sont alteres durant l'insuffisance cardiaque congestive (ICC). L'alteration des reflexes renorenaux pourrait contribuer a augmenter l'activite des nerfs sympathiques renaux ainsi que la retention de sodium durant l'ICC. L'endoiheline-1 (ET-1) participe aux modifications pathologiques de la fonction cardiaque et renale durant l'ICC. Dans la presente etude, nous avons examine si l'aniagonisie du recepteur ETa, BQ123, modifie la reaclivite des nerfs mecano sensoriel s renaux durant l'ICC. Les reponses de l'ANRA a l'augmentation de pression pelvienne renale ont ete supprimees chez les rats ayant une ICC vs. une ICC-simulee. Durant l'ICC, l'augmentation de la pression pelvienne renale de 7.5 mmHg, avant et durant une perfusion renale avec BQ123. a augmente l'ANRA de 12 % ± 3 % et 21 % ± 3 % (p < 0,05 vs. vehicule). Dans les pelvis renaux des rats ICC, la [PGE.sub.2] a augmente la liberation de la substance Pde5 ± 0a7 ± l pg/min en l'absence de BQ123, et de 4 ± 1 a 9 ± 1 pg/min en presence de BQ123 (p < 0,01 vs. vehicule). BQI23 n'a pas influe sur les reponses de l'ANRA ou la liberation de substance P chez les rats ICC-S. Ainsi, l'activation des recepteurs [ET.sub.A] contribue a alterer la reactivite des nerfs mecanosensoriels chez les rats ICC, par un ou des mecanismes se deroulant au niveau des terminaisons nerveuses sensorielles renales. Mots-cles : nerfs renaux, rein, prostaglandines. substance P, pression pelvienne renale. [Traduit par la Redaction], Introduction The majority of the afferent renal sensory nerves are located in the renal pelvic wall (Liu and Barajas 1993; Kopp et al. 2000a, 2004, 20076). These nerves are activated [...]

Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which decreases ERSNA to prevent sodium retention. High-sodium diet enhances ARNA, suggesting an important role for ARNA in suppressing ERSNA during excess sodium intake. Mean arterial pressure (MAP) is elevated in afferent renal denervated by dorsal rhizotomy (DRX) rats ted high-sodium diet. We examined whether the increased MAP in DRX is due to impaired arterial baroreflex function. In DRX and sham DRX rats fed high-sodium diet, arterial baroreflex function was determined in conscious rats by intravenous nitroprusside and phenylephrine or calculation of transfer function gain from arterial pressure to ERSNA (spontaneous baroreflex sensitivity). Increasing MAP did not suppress ERSNA to the same extent in DRX as in sham DRX, -60 [+ or -] 4 vs. -77 [+ or -] 6%. Maximum gain, -4.22 [+ or -] 0.45 vs. -6.04 [+ or -] 0.90% [DELTA]ERSNA/mmHg, and the maximum value of instantaneous gain, -4.19 [+ or -] 0.45 vs. -6.04 [+ or -] 0.81% AERSNA/mmHg, were less in DRX than in sham DRX. Likewise, transfer function gain was lower in DRX than in sham DRX, 3.9 [+ or -] 0.2 vs. 6.1 [+ or -] 0.5 NU/mmHg. Air jet stress produced greater increases in ERSNA in DRX than in sham DRX, 35,000 [+ or -] 4,900 vs. 20,900 [+ or -] 3,410%'s (area under the curve). Likewise, the ERSNA responses to thermal cutaneous stimulation were greater in DRX than in sham DRX. These studies suggest impaired arterial baroreflex suppression of ERSNA in DRX ted high-sodium diet. There were no differences in arterial baroreflex function in DRX and sham DRX ted normal-sodium diet. Impaired arterial baroreflex function contributes to increased ERSNA, which would eventually lead to sodium retention and increased MAP in DRX rats fed high-sodium diet. dorsal rhizotomy; high-sodium diet; renorenal reflexes: spontaneous baroreflex sensitivity; reflex renal nerve stimulation

Experiments were performed on cirrhotic rats to investigate the effect of type 1 angiotensin II (ANG II)-receptor antagonist treatment on cardiac baroreflex regulation of renal sympathetic nerve activity (RSNA) and renal sodium handling in these rats. Results suggested that central nervous system effects of ANG II may contribute to the increased basal level of RSNA and the abnormal arterial and cardiac baroreflex regulation of RSNA in common bile duct ligation.

Research shows that the type one angiotensin II receptor antagonist losartan decreases renal sympathetic nerve activity (RSNA) in rats with nephrotic syndrome that have intact arterial baroreceptors and denervated arterial baroreceptors. Thus, losartan has an augmenting effect on the renal sympathoinhibitory response, stimulates sodium load excretion and the cardiac baroreflex regulation of RSNA.

The effects of Loasartan, an antagonist of the type I receptor of angiotensin, on the cardiac reflex control of renal sodium handling in rats with congestive heart failure are investigated. Losartan decreased the pressure at the atria and increased the baroreceptor activity of the heart. Further, it improved the ability of the kidneys to handle acute and chronic sodium loads.

Chronic changes in dietary sodium intake cause physiological changes in endogenous angiotensin II activity, which affect basal efferent renal sympathetic nerve activity (ERSNA) and its control of arterial baroreflexes. This effect of angiotensin II is maximal during increased activity and minimal or absent during decreased activity of the renin-angiotensin system. Losartan administration influences the basal mean arterial pressure, heart rate and ERSNA, and its arterial baroreflex modulation only during normal and increased activity of the renin-angiotensin system.

The properties of efferent renal sympathetic nerve activity (ERSNA) in chronic renal sodium handling in the rat were characterized using three methods: mean integrated voltage over time, power spectrum analysis, and sympathetic peak detection analysis. These disease models assumed that ERSNA increases sodium excretion and water retention.

The specific groups of renal sympathetic nerve fibers involved in the regulation of kidney function were investigated by measuring the diameters and conduction velocities of the renal nerve fibers, and by identifying renal postganglionic units stimulated by the splanchnic nerve. Fibers were identified based on their involvement in specific function such as renal blood blood and urinary blood flow.

The efferent renal sympathetic nerve activity that occurs during heart failure may be mediated by the renin-angiotensin system. Rats suffering from congestive heart failure did not exhibit the same levels of renal nerve activity when the angiotensin receptors of the baroreflex mechanism were blocked losartan. Their ability to regain baroreflex control of renal nerve activity was lower even when losartan treatment was withdrawn, pointing to a disruption in the baroreflex regulation of the kidney.

A study conducted on rats with nephrotic syndrome (NS) to test whether hypoalbuminemia reflects the decrease in cardiac output and cardiopulmonary baroreflex controls renal sympathetic nerve activity (RSNA) indicates that the arterial pressure of NS rats with hypralbuminemia is similar to that of control rats and it lowers the cardiac indexes. The findings also show that NS rats and control rats have similar arterial baroreflex functions but a decrease in the control of RSNA leads to an increase in RSNA.

Chaotic behavior of renal sympathetic nerve activity: effect of baroreceptor denervation and cardiac failure. Am J Physiol Renal Physiol 279: F491-F501, 2000.--Nonlinear dynamic analysis was used to examine the chaotic behavior of renal sympathetic nerve activity in conscious rats subjected to either complete baroreceptor denervation (sinoaortic and cardiac baroreceptor denervation) or induction of congestive heart failure (CHF). The peak interval sequence of synchronized renal sympathetic nerve discharge was extracted and used for analysis. In control rats, this yielded a system whose correlation dimension converged to a low value over the embedding dimension range of 10-15 and whose greatest Lyapunov exponent was positive. Complete baroreceptor denervation was associated with a decrease in the correlation dimension of the system (before 2.65 [+ or -] 0.27, after 1.64 [+ or -] 0.17; P [is less than] 0.01) and a reduction in chaotic behavior (greatest Lyapunov exponent: 0.201 [+ or -] 0.008 bits/data point before, 0.177 [+ or -] 0.004 bits/data point after, P [is less than] 0.02). CHF, a state characterized by impaired sinoaortic and cardiac baroreceptor regulation of renal sympathetic nerve activity, was associated with a similar decrease in the correlation dimension (control 3.41 [+ or -] 0.23, CHF 2.62 [+ or -] 0.26; P [is less than] 0.01) and a reduction in chaotic behavior (greatest Lyapunov exponent: 0.205 [+ or -] 0.048 bits/data point control, 0.136 [+ or -] 0.033 bits/data point CHF, P [is less than] 0.02). These results indicate that removal of sinoaortic and cardiac baroreceptor regulation of renal sympathetic nerve activity, occurring either physiologically or pathophysiologically, is associated with a decrease in the correlation dimensions of the system and a reduction in chaotic behavior. nonlinear dynamics; chaos; congestive heart failure; aortic baroreceptor denervation; renal sympathetic nerve activity

Studies the effects of reflex on the components of synchronized renal sympathetic nerve activity. Methodology of the study; Overview of the results of peripheral thermal receptor stimulation; Discussion of the results.