Abstract
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.
Original language | English |
---|---|
Pages (from-to) | 148-156 |
Number of pages | 9 |
Journal | Brain Research |
Volume | 883 |
Issue number | 1 |
DOIs | |
Publication status | Published - 10 Nov 2000 |
Keywords
- Angiotensin
- Receptor autoradiography
- Restraint
- SHR
- Vasopressin
- WKY
Cite this
}
Characterisation of vasopressin V(1A), angiotensin AT1 and AT2 receptor distribution and density in normotensive and hypertensive rat brain stem and kidney : Effects of restraint stress. / McDougall, Stuart J.; Roulston, Carlie A.; Widdop, Robert E.; Lawrence, Andrew J.
In: Brain Research, Vol. 883, No. 1, 10.11.2000, p. 148-156.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Characterisation of vasopressin V(1A), angiotensin AT1 and AT2 receptor distribution and density in normotensive and hypertensive rat brain stem and kidney
T2 - Effects of restraint stress
AU - McDougall, Stuart J.
AU - Roulston, Carlie A.
AU - Widdop, Robert E.
AU - Lawrence, Andrew J.
PY - 2000/11/10
Y1 - 2000/11/10
N2 - 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.
AB - 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.
KW - Angiotensin
KW - Receptor autoradiography
KW - Restraint
KW - SHR
KW - Vasopressin
KW - WKY
UR - http://www.scopus.com/inward/record.url?scp=0034634362&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(00)02917-6
DO - 10.1016/S0006-8993(00)02917-6
M3 - Article
VL - 883
SP - 148
EP - 156
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1
ER -