PubMed · 6162264
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D Regoli, J Barabé, F Marceau, R Couture, P Gaudreau. 1980. [Vasoactive polypeptide receptors].. https://pubmed.ncbi.nlm.nih.gov/6162264/
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Pentobarbital and chlordiazepoxide administered intracerebroventricularly (i.c.v.) attenuated dose dependently the pressor action of i.c.v. angiotensin II and angiotensin III in the conscious spontaneously hypertensive rat (SHR) and the normotensive control Wistar Kyoto rat (WKY). Attenuation of the pressor action by the two drugs was more marked in the WKY than in the SHR. Based on the fact that both drugs act via the gamma-aminobutyric acid (GABA) receptors, the data support the suggestions (i) that a central GABAergic system regulates blood pressure, (ii) that there is probable dysfunction of the GABA receptors in SHR.
The transgenic (TG) rat carrying the mouse renin gene (mRen-2d) has provided a unique opportunity to explore central interactions between the brain renin-angiotensin (RAS) and vasopressin (AVP) systems. To evaluate the hypothalamic vasopressin axis in the TG rat, we measured the central nervous system concentrations of AVP and determined the effect of angiotensin II (ANG II) and its NH2-terminal heptapeptide [angiotensin-(1-7)] on blood pressure, heart rate, and AVP release using brain microdialysis. Intracerebroventricular infusion of ANG II or ANG-(1-7) in control rats increased local AVP release from the paraventricular and supraoptic nuclei. The ANG II infusion was associated with a significant increase in blood pressure not observed with ANG-(1-7). In contrast, the angiotensin peptide-induced central AVP responses and the ANG II-induced blood pressure increase were absent in the TG animal. The plasma AVP responses to ANG II and ANG-(1-7) were comparable in the control and TG rats. The TG rats exhibited a 22-fold higher level of AVP in the dorsal lower brain stem but had lower AVP levels in the posterior pituitary and the median eminence compared with control rats. These results suggest that insertion of the mouse renin gene into the rat genome leads to alterations in the AVP axis in terms of AVP peptide content and angiotensin-induced cardiovascular and AVP responses.