Afferent pathways in cardiovascular adjustments induced by volume expansion in anesthetized rats

Department of Physiology, Universidade Federal de São Paulo-Escola Paulista de Medicina, São Paulo, Brazil 04023-900 The role of baroreceptors, cardiopulmonary receptors, and renal nerves in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (Pharmacia; 1% body wt, 0.4 ml/min) we...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2000-09, Vol.279 (3), p.884-R890
Hauptverfasser: Colombari, Debora S. A, Colombari, Eduardo, Lopes, Oswaldo U, Cravo, Sergio L
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Sprache:eng
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Zusammenfassung:Department of Physiology, Universidade Federal de São Paulo-Escola Paulista de Medicina, São Paulo, Brazil 04023-900 The role of baroreceptors, cardiopulmonary receptors, and renal nerves in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (Pharmacia; 1% body wt, 0.4 ml/min) were studied in urethan-anesthetized rats. In control animals, VE produced a transitory increase in mean arterial pressure (MAP), which peaked at 10 min (17 ± 4 mmHg) and increases in renal (128 ± 6 and 169   ± 19% of baseline at 10 and 40 min, respectively) and hindlimb vascular conductance (143 ± 6 and 150 ± 10%). These cardiovascular adjustments to VE were unaffected by bilateral vagotomy. After sinoaortic denervation, the increase in MAP induced by VE was greater than in control rats (30 ± 4 mmHg). However, renal vasodilation in response to VE was blocked, whereas hindlimb vasodilation was similar to that observed in control rats. After unilateral renal denervation (ipsilateral to flow recording), the initial renal vasodilation was blocked. However, 40 min after VE, a significant renal vasodilation (125 ± 4%) appeared. The hindlimb vasodilation and MAP responses were unaffected by renal denervation. These results demonstrate that the baroreceptor afferents are an essential component of cardiovascular adjustments to VE, especially in the control of renal vascular conductance. They also suggest that renal vasodilation induced by VE is mediated by neural and hormonal mechanisms. blood flow; cardiovascular afferents; baroreceptor afferents; renal nerves
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.2000.279.3.R884