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|Title:||Afferent pathways in cardiovascular adjustments induced by volume expansion in anesthetized rats|
|Authors:||Colombari, Debora Simões de Almeida [UNIFESP]|
Colombari, Eduardo [UNIFESP]
Lopes, Oswaldo Ubriaco [UNIFESP]
Cravo, Sergio Luiz [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
|Publisher:||Amer Physiological Soc|
|Citation:||American Journal Of Physiology-regulatory Integrative And Comparative Physiology. Bethesda: Amer Physiological Soc, v. 279, n. 3, p. R884-R890, 2000.|
|Abstract:||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.|
|Appears in Collections:||Artigo|
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