Pressor responses produced by peripheral osmoreceptor activation in commissural nucleus of the solitary tract‐lesioned rats.

Abstract

Previous studies demonstrated that intragastric (ig) 2 M NaCl load (that activates peripheral and central osmoreceptors) produced increases in mean arterial pressure (MAP) and enhanced dipsogenic responses in commissural nucleus of the solitary tract (commNTS) lesioned rats. Lesions of commNTS also increased water intake produced by ig 0.6 M NaCl load (that activates peripheral, not central, osmoreceptors ‐ Am. J. Physiol., 269: R 1085, 1995), which suggests that commNTS mechanisms inhibit peripheral osmoreceptor‐induced thirst. In the present study we investigated the effects of ig 0.6 M NaCl load on MAP and heart rate (HR) in commNTS lesioned rats. Male Holtzman rats (300–330 g, n = 5–8/group) with chronic (15 days) sham or electrolytic lesions (1 mA, 10 s) of the commNTS were used. MAP and HR were measured 60 min before and 60 min after ig 0.6 M NaCl load (2 ml). Plasma Na+ concentration was analyzed after ig 0.15 M or 0.6 M NaCl in the same animals, 3 days after MAP and HR recordings. Ig 0.6 M NaCl induced pressor responses in commNTS lesioned rats (11 ± 3 mmHg), but did not affect MAP in sham rats (−3 ± 2 mmHg) or HR in both groups. Ig 0.6 M NaCl produced no change on plasma Na+ concentration in sham (142 ± 3 vs. 0.15 M NaCl: 140 ± 1.2 mEq/l) or in commNTS lesioned rats (144 ± 0.4 vs. 0.15 M NaCl: 141 ± 1 mEq/l). The results suggest that similar to water intake, commNTS mechanisms also inhibit peripheral osmoreceptor‐induced pressor responses.Supported by: FAPESP, CNPq.