In the present study, we have examined neurochemical correlates that may be involved in the differential cardiovascular responses observed in normotensive and hypertensive rats during stress. Using a restraint stress paradigm, both normotensive Wistar Kyoto (WKY) and Spontaneously Hypertensive rats (SHR) underwent acute (1 h restraint in a perspex tube), chronic (1 h restraint for ten consecutive days) or no restraint (control) stress. Following cessation of restraint, rats were processed by incubating sections of brain stem and kidney with [125I]-HO-LVA (0.03 nM) or [125I]Sar1Ile8-AngiotensinII (0.5 nM), in the presence of PD123319 (10 μM) or losartan (10 μM), to determine the distribution and density of vasopressin V(1A), angiotensin AT1 and AT2 receptors, respectively. Analysis of autoradiograms indicated changes in the density of radioligand binding in acutely and chronically-stressed rats, as compared to controls. For example, V(1A) binding in the medial nucleus tractus solitarius (SolM) decreased in the WKY but increased in the SHR. AT1 binding in SolM did not significantly change in the WKY but decreased in the SHR with repeated restraint. In kidney slices, AT1 binding decreased with stress in the WKY (-17%) but increased in SHR (+10-15%). AT2 binding in the kidney showed a pattern similar to that of AT1 binding in SHR, but not WKY. Graded increases in V(1A) binding were measured in kidney medulla and cortex of both strains (+50-60% with chronic restraint). These results suggest that physiological adaptation to restraint is associated with specific changes in V(1A), AT1 and AT2 receptor density within brain nuclei and kidney. (C) 2000 Elsevier Science B.V.
- Receptor autoradiography