Why the study?
Does chronic NTS-X increase the sensitivity to circulating ANG II for drinking and vasopressin release in rats?
Does chronic NTS-X increase the sensitivity to circulating ANG II for drinking and vasopressin release in rats?
Chronic NTS lesions enhance the dipsogenic response to systemic ANG II but do not affect ANG II-induced vasopressin release in rats.
Answers are grounded in this paper and cite their sources.
NTS lesions selectively enhance ANG II thirst responses in rats; leaves open NTS contributions to human fluid homeostasis and requires translational studies.
Rats with chronic nucleus of the solitary tract lesions (NTS-X) drink water and release vasopressin (VP) in response to reduced blood volume despite an absence of neural signals from cardiac and arterial baroreceptors. The present study determined whether rats with NTS-X have a greater sensitivity to circulating ANG II, which may contribute to the drinking and VP responses to hypovolemia. In conscious control rats and rats with NTS-X, ANG II was infused intravenously for 1 h at 10, 100, or 250 ng. kg(-1). min(-1). At the two higher doses, ANG II stimulated more water intake with a shorter latency to drink in rats with NTS-X than in control rats. In contrast, infusion of ANG II produced comparable increases in plasma VP in the two groups. At the two higher doses, ANG II produced an enhanced increase in arterial pressure (AP) in rats with NTS-X, and the bradycardia seen in control rats was reversed to a tachycardia. Infusion of hypertonic saline, which did not alter AP or heart rate, produced comparable drinking and VP release in the two groups. These results demonstrate that chronic NTS-X increases the dipsogenic response of rats to systemic ANG II but has no effect on ANG II-induced VP release or the osmotic stimulation of these responses.
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Schreihofer et al. (2000) studied this question.
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