Gestational effects on volume-sensitive cardiopulmonary receptor reflexes in the rat

We tested the hypothesis that augmented reflex sympathoinhibition mediated by volume-sensitive cardiopulmonary (CP) receptors contributes to the vasodilation of pregnancy by comparing responses to acute volume expansion in 21-day-pregnant and age-matched virgin rats (n = 7) that were anesthetized (pentobarbital sodium, 50 mg/kg ip), paralyzed (gallamine triethiodide, 25 mg/kg iv), ventilated, and had undergone bilateral sinoaortic denervation. CP receptors were stimulated with intra-atrial injections of saline (50, 100, 200, and 300 μl), and the following variables were recorded: 1) mean right atrial pressure (MRAP) to index the afferent stimulus intensity; 2) cell discharge in the nucleus tractus solitarii (NTS), the primary central terminus for CP afferents; and 3) mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) to assess efferent reflex effects. Basal MAP was significantly lower in pregnant (71.5 ± 3.8 mmHg) than in virgin rats (86.6 ± 3.1 mmHg), and plasma volume was expanded in the pregnant group (17.6 ± 1.1 vs. 10.0 ± 0.7 ml, P < 0.05). Baseline MRAP was similar between groups. Saline injections evoked graded increases in MRAP, which were larger in gravid animals (P < 0.05). Volume injections evoked similar changes in NTS cell discharge between groups, but the responses were nongraded. Despite larger changes in MRAP in gravid rats, reflex effects on RSNA and HR were similar to those in control animals, and effects on MAP were attenuated in the pregnant group. We conclude that larger changes in MRAP in pregnant rats during stimulation of CP receptors are not associated with larger changes in central or efferent components of this reflex. These data suggest blunting, not augmentation, of CP receptor-mediated control of blood pressure during pregnancy, possibly involving mechanisms at the level of the CP receptor.