Canais iônicos como possíveis alvos farmacológicos para o tratamento da dismenorreia primária: uma revisão de literatura

Abstract

Primary dysmenorrhea (PD) is the most common gynecological disorder in women of fertile age, being characterized mainly by painful and intense uterine cramps, sweating, chills, headaches, and irritability. The main treatment for this dysfunction comprises three major classes of medications: non-steroidal anti inflammatory drugs (NSAIDs), antispasmodics and hormonal contraceptives, however, these alternatives may not be effective for the entire population, in addition to presenting significant side effects such as gastrointestinal and cardiovascular disorders and weight gain, reducing, or making it impossible to adhere to treatment. In view of clinical studies that demonstrated the potential of calcium channel blockers to reduce uterine cramps exacerbated by PD, the possible potential of ion channel modulation for the treatment of this disorder was hypothesized in this study. Through a literature review of a descriptive and observational nature, between the years 2000 2024, studies were selected from the SciELO, PubMed, SCOPUS and Google Scholar databases, in English or Portuguese, which guided the construction of a review on uterine physiology, pathophysiology, epidemiology and classic treatment of primary dysmenorrhea, as well as the modulation of sodium, potassium, calcium and chloride channels as tools to achieve uterine relaxation or inhibit its contraction. Despite the limitation of studies in relating the functionality of ion channels with DisP, it was possible to observe the potential that these transmembrane proteins have for the contractile and relaxing reactivity of this organ, allowing it to be theorized that the negative modulation of calcium channels (Cav 1 and Cav 3) and the calcium-activated chloride channel (CaCC), as well as the positive modulation of potassium channels (BKCa, KNa and Kv) and voltage-insensitive sodium channels (Navi) can be molecular alternatives to reduce exacerbated uterine contractility in PD.