CHEMICAL LESION OF THE CIRCUMVENTRICULAR ORGANS WITH MONOSODIUM GLUTAMATE REDUCES THE BLOOD-PRESSURE OF SPONTANEOUSLY HYPERTENSIVE BUT NOT OF ONE-KIDNEY ONE-CLIP HYPERTENSIVE RATS

Subcutaneous injection of monosodium glutamate (MSG) on days 1, 5 and 9 of the experiment (5 g/kg per day) significantly reduced the blood pressure of a group of 10 spontaneously hypertensive rats (SHR) measured 7 and 14 days after treatment (200 +/- 7 mmHg vs 172 +/- 8 mmHg or 185 +/- 3 mmHg, respectively), without affecting that of 11 age-matched Wistar Kyoto (WKY) rats (127 +/- 7 mmHg vs 123 +/- 5 mmHg and 119 +/- 5 mmHg, respectively). Using autoradiographic methods and I-125-Sar1-angiotensin II, receptor binding was shown to be higher in the subfornical organ (SFO) of SHR (332 +/- 31 fmol/mg protein) when compared to WKY rats (240 +/- 30 fmol/mg protein) and similar (222 +/- 21 vs 170 +/- 14 fmol/mg protein) in the paraventricular nucleus (PVN). Binding to angiotensin-converting enzyme (ACE) was evaluated using the ACE inhibitor I-125-35 IA as ligand. Binding to ACE was lower in SHR in the PVN and the globus pallidus (GP) of SHR when compared to WKY rats (PVN: 111 +/- 9 vs 172 +/- 13 and GP: 163 +/- 2 vs 213 +/- 7 fmol/mg protein) and similar in the SFO, choroid plexus (ChP) and caudate nucleus (CD) of both strains (SFO: 779 +/- 107 vs 805 +/- 169; ChP: 2,780 +/- 2 10 vs 3,140 +/- 360 and CD: 461 +/- 42 vs 424 +/- 18 fmol/mg protein). No changes in angiotensin II (Ang II) receptor number or binding to ACE were detected in these brain areas after MSG treatment of SHR or WKY rats. Similar MSG treatment did not affect the development of one kidney-one clip(1K-1C) experimental hypertension in a group of 10 Wistar rats when compared to a group of 8 saline-treated animals. 1K-1C surgery was performed 7 days after MSG treatment and blood pressure measured before (saline 123 +/- 1 mmHg vs MSG 126 +/- 1 mmHg) and both 7 (151 +/- 4 mmHg vs 158 +/- 3 mmHg) and 15 days (163 +/- 4 mmHg vs 172 +/- 6 mmHg) after surgery. The results support the hypothesis of a differential role of central MSG-sensitive mechanisms in genetic and experimental renal forms of hypertension.