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To assess the participation of cardiovascular eicosanoids (prostaglandins and thromboxanes) system in the initiation of genetic hypertension, we examined eicosanoids metabolism in the heart, aortic wall and kidney in prehypertensive and hypertensive rat models for spontaneous hypertension (SHR). Vasoconstrictor thromboxane A2 (TXA2) generation in the aortic wall was significantly enhanced by 49% in the prehypertensive and by 18% in the hypertensive SHR when compared to the respective normotensive Wistar-Kyoto rats. Cardiac TXA2 content was significantly increased as well by 14% in the prehypertensive and by 30% in the hypertensive SHR. Moreover, vascular vasodepressor eicosanoids generation was decreased by 10% for PGI2 and by 29% for PGD2 in the prehypertensive SHR although the alterations were eliminated in the hypertensive SHR. In contrast to the cardiovascular eicosanoids system, there was no difference in renocortical TXA2 content in either young or adult SHR while vasodepressor prostaglandins contents were decreased by 29% for PGE2 and by 33% for PGD2 in SHR when they were in the prehypertensive stage. Thus, in the prehypertensive stage of SHR, the cardiovascular eicosanoids system exhibited enhanced vasoconstrictor TXA2 and decreased vasodepressor prostaglandins, thereby producing a vasoconstrictor state. These data indicate that the alterations in the cardiovascular eicosanoids system partially contribute to the initiation of hypertension in SHR.

Alterations of the cardiovascular and renal prostaglandins and thromboxanes system in prehypertensive spontaneously hypertensive rats.