Reduced hypotensive action of arachidonic acid in the spontaneously hypertensive rat.

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Abstract
Prostaglandins (PG) E2 and I2 are potent vasodepressor agents and their endogenous release may contribute to the regulation of blood pressure (BP). A decreased response to or a decreased capacity of the vasculature to synthesize vasopressor PG was studied to determine if they could contribute to the increased vascular resistance characteristic of hypertension. The change in mean arterial blood pressure (MAP) to intraaortic (i.a.) injection of PGE2 and PGI2 at 0.01, 0.1, 1.0 and 10.0 and of sodium nitroprusside (NaNP) at 0.1, 1.0 and 10.0 nmol/100 g body weight (gbw) was measured in anesthetized, 30 wk old male rats of the spontaneously hypertensive (SHR), normotensive Wistar-Kyoto (WKY) and Wistar (W) strains. The percent decrease in MAP to equivalent doses of NaNP did not differ among the 3 strains of rats except at 1.0 nmol/100 gbw, a dose to which W rats showed a greater depressor response than either SHR or WKY rats. No major differences were found among the strains in their response to the administration of PGI2 except to a dose of 0.1 nmol/100 gbw to which SHR and W rats responded with a greater percent decrease in MAP than WKY rats. The percent decrease in MAP to PGE2 was generally greater in SHR than WKY rats but did not differ between SHR and W rats at any dose. The i.a. injection of arachidonic acid (AA) caused dose-dependent percent decreases in MAP in all strains and produced significantly smaller hypotensive responses at doses of 10 and 100 nmol/100 gbw in SHR compared to WKY or W rats. At doses of 300 nmol AA or greater, hypotensive responses did not differ significantly between SHR or WKY rats whereas the W rat exhibited percent reductions in MAP that were significantly larger than those obtained in the other 2 strains of rats. SHR do not have a reduced ability to respond to exogenous PGE2, PGI2 of NaNP; SHR appear to have a decreased capacity to utilize AA for the synthesis of vasodepressor PG.