Enhanced Depressor Response to Nitric Oxide in the Rostral Ventrolateral Medulla of Spontaneously Hypertensive Rats

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Abstract

Possible impairment of the L-arginine[horizontal bar]nitric oxide (NO) pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) was investigated by microinjecting NG-nitro-L-arginine methyl ester (L-NAME), NOC 18 (an NO donor), or L-arginine. Unilateral injection of L-NAME (10 nmol/50 nL) into the rostral ventrolateral medulla significantly increased mean arterial pressure (MAP) in both SHR and Wistar-Kyoto rats (WKY). The increases in MAP did not differ significantly between the two strains (15 +/- 3 versus 10 +/- 2 mm Hg, respectively; n=8). In contrast, microinjection of L-arginine elicited significant (P<.05) dose-dependent decreases in MAP in both strains, and these depressor responses were significantly greater in SHR than in WKY (in 10 nmol of L-arginine: [horizontal bar]29 +/- 2 versus [horizontal bar]15 +/- 2 mm Hg, respectively; n=8, P<.01). Similarly, microinjection of NOC 18 (10 nmol/50 nL) reduced MAP in both strains, and the depressor response was also significantly greater in SHR than in WKY ([horizontal bar]38 +/- 7 versus [horizontal bar]22 +/- 3 mm Hg, respectively; n=8, P<.05). These results suggest that the L-arginine[horizontal bar]NO pathway in the rostral ventrolateral medulla is impaired in SHR and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension. (Hypertension. 1998;31:1030-1034.)

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