Introduction: Non-traumatic subarachnoid hemorrhage (SAH) is strongly linked to hypertension, a condition highly influenced by common genetic variants. For complex diseases influenced by genetic and environmental factors, genetic predisposition plays a key role in earlier onset. We tested the hypothesis that persons with a higher polygenic burden of hypertension-related alleles have SAH at younger ages. Methods: We analyzed data from the UK Biobank, a large cohort study that enrolled over 500,000 Britons aged 40-69. We included participants of European descent. We constructed two polygenic risk scores (PRS) using 807 independent genetic variants known to associate with higher systolic and diastolic blood pressure (BP). We fitted linear regression to assess the relationship between these PRS and the age-of-onset of SAH, using product terms to test for interaction with sex. We subsequently implemented Mendelian Randomization analyses using the inverse variance weighted and weighted median methods to evaluate causality. Results: We evaluated a total of 1,178 SAH cases (mean age, 58; female sex, 722 [61.3%]). When evaluating all participants jointly, there was no association between the systolic BP PRS and age-of-onset for SAH (p=0.130). There was a significant interaction between the PRS and sex (p=0.002): each additional standard deviation of the systolic BP PRS was associated with an earlier onset of SAH in females (beta, -1.45; 95% CI, -2.31 to -0.58; p=0.001), but not in males (adjusted beta, 0.83; 95% CI, -0.37 to 2.02; p=0.176). In MR analyses, a 10mmHg increase in genetically determined systolic BP was associated with a 5-year earlier onset of SAH in female participants using both the inverse variance weighted (beta, -4.72; 95% CI, -7.34 to -2.10; p<0.001) and weighted median approaches (beta, -5.05; 95% CI, -9.19 to -0.90; p=0.017). Analyses with the diastolic BP SNPs yielded comparable results (all p<0.05). Conclusions: Genetically determined hypertension is associated with earlier onset of non-traumatic SAH in women. These results indicate that genetic predisposition may play a more important causal role in younger patients and point to genetic information as possible tools for early identification of high-risk individuals.