To investigate whether plasma sodium pump inhibitory activity is controlled by cardiopulmonary and aortic baroreceptors, mean arterial pressure, right atrial pressure, sodium and water balances, plasma renin activity, plasma aldosterone concentration and plasma antinatriferic activity (PAA; plasma sodium pump inhibitory activity) were determined before, during and after Ringer volume expansion (10% of body wt) in anaesthetized dogs. Animals were studied with intact reflexes (CTR, n = 7) and after acute cervical bilateral vagosympathetic denervation (VGT, n = 8). With the exception of PAA, none of the parameters were different between groups before, during or after Ringer volume expansion. The PAA (microA cm-2) was similar for both groups before expansion and before either sham (CTR) or vagosympathectomy (VGT) was performed (CTR = 3.6 +/- 0.4 vs. VGT = 4.3 +/- 0.3). Compared to baseline, PAA at the end of the volume expansion phase increased in both groups (CTR = 6.1 +/- 0.8, P < 0.05; VGT = 9.1 +/- 0.7, P < 0.0005); however, this PAA value was significantly greater in the VGT group than in the CTR group (P < 0.01). At the end of the post-expansion phase, PAA levels returned toward baseline in both groups (CTR = 4.4 +/- 0.5 vs. VGT = 4.8 +/- 0.2; n.s. vs. baseline); however, this PAA value in the CTR group was not significantly different from its pak value. The present data confirm that PAA is increased in response to saline volume expansion, and suggest that PAA synthesis and/or release is under inhibitory vagosympathetic control during saline volume expansion.

1. To investigate the participation of both vagal cardiopulmonary baroreceptor activity and efferent renal sympathetic nerve activity (ERSNA) in the natriuretic response to saline volume expansion (SVE), three series of experiments were undertaken in anaesthetized rats. 2. In the first two series of experiments, the natriuretic (series A) and ERSNA (series B) responses to SVE were evaluated in both sham operated and cervical bilateral vagotomized rats. The acute experiment consisted of two baseline (BL) periods, treatment (sham control (CTR) or real cervical bilateral vagotomy), a volume expansion phase (Ringer's solution, 10% bodyweight) and a postexpansion phase. The results of these two series indicate that vagotomy significantly enhances basal ERSNA (37 +/- 8%; P < 0.05 vs BL) and significantly attenuates the renal sympathoinhibitory response (by approximately 50%; P < 0.05 vs CTR) but not the natriuretic response to SVE, suggesting the potential expression of a vagotomy induced compensatory natriuretic mechanism. 3. To assess this, the natriuretic response to SVE was evaluated in chronic sham operated or renal denervated groups of rats in which vagotomy was or was not performed (series C). There were no differences among groups in either systemic haemodynamics or plasma protein concentration. Vagotomy plus chronic renal denervation induced a supranormal natriuretic and diuretic response (approximately 30%; P < 0.01) to SVE when compared with similar natriuretic and diuretic responses of the remaining groups. 4. These data support the idea that, in intact rats on a normal sodium diet, neither cardiopulmonary baroreceptors nor renal nerves are necessary for the elimination of an acute intravenous isotonic sodium load and indicate that during SVE the activation of vagal cardiopulmonary baroreceptors exerts an inhibitory effect on both ERSNA and the expression of a natriuretic mechanism. Such a natriuretic mechanism is expressed only when SVE is induced in vagotomized rats (compensating for the vagotomy mediated antinatriuretic effects of an enhanced ERSNA), but is unmasked only when, in addition, renal nerves are chronically transected. All of this offers an efficient element of safety in eliminating an acute isotonic sodium load when cardiopulmonary baroreceptors are severed.

To assess whether progressive arterial baroreceptor denervation results in salt‐sensitive changes in blood pressure, mean arterial pressure (MAP) was measured in six groups of conscious male Wistar rats before and ∼30 days after bilateral: a) sham denervation (SH), b) sino‐aortic denervation (SD) and c) aortic denervation (AD). During the last 21 days of post‐denervation period three groups received high sodium diet (HNa = 8%) and the other three groups low sodium diet (LNa = 0.04%). The remaining baroreflex control of ERSNA was examined in the anesthetized state as %Δ ERSNA vs MAP. The modelling indicated that there were no effects of denervation nor diet on MAP ∼ 30 days after denervation. However, the modelling of Δ MAP (MAP after – MAP before) indicated effect of both denervation and diet but not interaction, the highest and more lasting Δ MAP being observed in AD + HNa group (21± 3 mmHg). The modelling of remaining baroreflex control of ERSNA indicated effect of denervation but not of diet.Conclusion:AD + HNa is a novel experimental model of salt‐sensitive normotension, though AD does not impair the remaining baroreflex control of ERSNA.Supported by: SMRF06‐UASLP Range % Slope %/mmHg X to ½ range mmHg Lower Plateau % Gmax SH 119± 7 −.085±.007 130±5 −85±6 −2.5±0.1 AD 125± 9 −.065±.005* 128±4 −82±5 −2.0±0.2 SD 61± 6* −.059±.005* 153±7* −66±6* −.9±.1* p<0.05 vs SH. Conclusion:AD + HNa is a novel experimental model of salt‐sensitive normotension, though AD does not impair the remaining baroreflex control of ERSNA.Supported by: SMRF06‐UASLP

To ascertain determinants of the change of RIHP during saline volume expansion, plasma protein concentration ([Pr]p),hematocrit (Ht) and time courses of left renal medullary blood flow (RMBF),left renal cortical blood flow (RCBF), left RIHP and left renal excretory response were evaluated simultaneously in anesthetized,acutely left renal denervated, hormonally clampped and renal perfusion pressure (RPP) controlled rats before (C) and during volume expansion (E) with either saline (SVE: 1.1 ml/min i.v., 5% body wt) or 5% BSA saline solution (AVE: 0.30 ml/min, i.v., 1.4% body wt).At post‐expansion, RPP vs %RMBF, RPP vs %RCBF and RPP vs RIHP relationships were obtained. Blood flows were measured by laser‐Doppler flowmetry and RIHP by sub‐capsular catheter. There were no statistical significant differences between groups in delta(Δ = E‐C) of urinary flow (V), Uosm, UosmV, UNaV and Ht. Δ[Pr]p was −0.89 ± 0.09 g/dl in SVE group vs −0.02 ± 0.08 g/dl in AVE group (p = 0.0001). ΔRIHP was 2.9 ± 0.8 mmHg in SVE group,vs 0.5 ± 0.3 mmHg in AVE group(p = 0.006).ΔRIHP showed interaction group × time and %RMBF showed effect of group and time, AVE group showing greater increase in %RMBF than SVE group. A linear relationship between RPP vs ΔRIHP was observed in both groups. Conclusion: Data modeling indicated that Δ[Pr]p and ΔHt are primary determinants of ΔRIHP in SVE. Supported by: SMRF05‐UASLP