Takahashi H, Matsusawa M, Ikegaki I, Nishimura M, Yoshimura M, Yamada H, Sano Y
2nd Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Clin Exp Hypertens A. 1988;10(6):1285-7. doi: 10.1080/07300077.1988.11878920.
Since angiotensin (ang) II blockers attenuate the centrally-induced pressor responses to a Na+, K+-ATPase inhibitor, ouabain, a brain renin-ang system is assumed to be involved in this pressor mechanism. Centrally-induced pressor responses to hypertonic saline were also blocked with ang II blockers. Thereby, the increase in the plasma level of digoxin-like immunoreactivity was abolished with simultaneous infusions of an ang II analogue or atrial natriuretic polypeptide (ANP). These results indicate that the pressor responses to sodium salts are mediated via inhibition of the brain Na+, K+-ATPase, and that the brain renin-ang system is involved in this mechanism. We noted the existence of a digoxin-like immunoreactive substance (DLI) containing neurons in the hypothalamus (PVN, SON) with the fibers densely distributed in the AV3V area including OVLT, SFO and the median eminence, an area where receptors for ang II are also distributed (1,2). Since pressor responses to intracerebroventricular (ICV) infusions of hypertonic NaCl are abolished with ICV pretreatment with ang II blockers, a brain renin-ang system may be involved in this mechanism. We then searched for a possible relationship between the central effects of NaCl, a brain renin-ang system and an endogenous Na+, K+-ATPase inhibitor in the hypothalamus.
