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Systolic blood pressure (SBP) represents the maximum pressure exerted by the blood against the arterial walls during the contraction of the heart's left ventricle [1]. It is a critical physiological parameter used to assess cardiovascular health and serves as the primary metric for diagnosing and managing hypertension, which is defined by major guidelines as a reading of 130 mmHg or higher [2]. While SBP is a fundamental clinical endpoint in drug development and cardiology, it is a physiological measurement rather than a specific molecular target like a protein or receptor [3]. Pharmacological agents lower SBP by targeting systems such as the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system, and ion channels to promote vasodilation or reduce extracellular fluid volume [4]. Effective management of SBP is essential for reducing the risk of life-threatening events, including stroke, myocardial infarction, and chronic kidney failure [5]. Sources: [1] StatPearls: https://www.ncbi.nlm.nih.gov/books/NBK482465/ [2] AHA/ACC Hypertension Guidelines: https://www.ahajournals.org/doi/10.1161/HYP.0000000000000065 [3] NIH/NHLBI: https://www.nhlbi.nih.gov/health-topics/high-blood-pressure [4] Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/diagnosis-treatment/drc-20373417 [5] PubMed/Lancet: https://pubmed.ncbi.nlm.nih.gov/26607730/
Systolic blood pressure is not a molecular target; however, it is modulated by drugs that act on biological targets (such as ACE, ARBs, calcium channels, and adrenergic receptors) to induce vasodilation, reduce cardiac output, or decrease blood volume [1][4].
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