Brain stem mechanisms and the inhibition of angiotensin-induced drinking.

The present studies examine the effect of lesions of the ventrolateral region of the lateral parabrachial nucleus (VLLPBN) and of the area postrema and medial region of the nucleus of the solitary tract (AP/mNTS) on water intake induced by intracerebroventricular administration of angiotensin II (ANG II) and of the cholinergic receptor agonist, carbachol. Water intake was measured in rats with bilateral electrolytic lesions of the VLLPBN or thermocautery ablation of the AP/mNTS after intracerebroventricular delivery of ANG II (50 and 100 ng/2 microliter), carbachol (100 and 250 ng/2 microliter), and isotonic saline (2 microliter). Rats with lesions of the VLLPBN drank significantly more water during a 30-min test period to both doses of ANG II, but not to carbachol, than did sham lesion rats. Similarly, AP/mNTS lesion rats drank significantly more than sham lesion animals in response to the high dose of ANG II but not to carbachol. These results suggest that the previously reported exaggerated drinking responses to systemically administered ANG II demonstrated by rats with either VLLPBN or AP/mNTS lesions is not the result of a direct peripheral action of the octapeptide. Furthermore, the similarity of the induced drinking responses produced by these two lesions suggests that the AP/mNTS and the VLLPBN may be linked in a common thirst-mediating pathway.