PST 2238: A New Antihypertensive Compound that Modulates Na+,K+-ATPase and Antagonizes the Pressor Effect of OLF

Over recent years, pharmacological treatment of essential hypertension (EH) has been evolving from an empirical approach based on “group therapy” to a more individual approach that addresses specific pressor mechanisms affecting certain patients (39). This evolution is also due to the huge individual variation of blood pressure response to the available antihypertensive drugs, none of which is effective throughout the whole population of hypertensive patients. One of the major problems with the treatment of hypertension is poor patient compliance, which results from the side effects and the lack of obvious immediate benefits of treatment, reducing the acceptability of drugs. The final result is that only ∼30% of patients are adequately treated. These problems arise mainly from the lack of a complete understanding of the mechanisms underlying the development of primary hypertension and the secondary involvement of major organs (mainly heart and brain). Although the antihypertensive efficacy of different classes of drugs is similar when populations are compared, there is a great deal of individual variability in the response to a given therapeutic regime. This is because hypertension develops as a consequence of the interaction between polygenic and environmental backgrounds, which differ among patients. Therefore, the future success of a new therapy for hypertension will depend upon the ability to understand the molecular and genetic mechanisms operating in a subset of patients and the ability to develop new drugs able to correct such mechanisms (23). Prassis-Sigma Tau has developed a new class of antihypertensive compounds in accordance with this line of thought and their research is aimed at correcting a genetic molecular mechanism previously demonstrated to be involved in the pathogenesis of hypertension in rats and humans.