Key result
Angiotensin II drives ~85% greater MAP increase and worse renal damage in female versus male hamsters.
Why the study?
Little is known about the effects of angiotensin II infusion on hypertension and renal injury in the Syrian hamster, including sex-specific differences.
Does Angiotensin II infusion induce sex-specific differences in blood pressure and renal pathology in Syrian hamsters?
Does Angiotensin II infusion induce sex-specific differences in blood pressure and renal pathology in Syrian hamsters?
Female Syrian hamsters show heightened vulnerability to Ang II-induced hypertension and renal damage compared to males, providing a novel model for studying sex-specific mechanisms of hypertension.
Answers are grounded in this paper and cite their sources.
Sex differences in this hamster model should not guide clinical care; leaves open translational validation of sex-specific Ang II hypertension mechanisms.
Background Biological sex is a critical determinant in cardiovascular and renal disease outcomes. Although angiotensin II (Ang II) infusion is widely used to model hypertension in mice and rats, little is known about its effects in the Syrian hamster, a small rodent increasingly used for translational research. This study aimed to develop a model of chronic Ang II-induced hypertension in Syrian hamsters and investigate sex-specific differences in blood pressure, renal pathology, and components of the renin-angiotensin system (RAS). Methods Male and female Syrian hamsters (8–9 weeks old) were infused subcutaneously with Ang II (200 ng/kg/min) or saline via osmotic minipumps for four weeks. Mean arterial pressure (MAP) and kidney wet weight were determined on the euthanasia day. The kidneys were analyzed for renal pathology; renal RAS enzymes (ACE and ACE2) were measured by colorimetric assay and qPCR; cytokines (IL-6 and IL-1β) were measured by qPCR; and the angiotensin receptor type 1 (AT1R) was measured by radioligand binding and qPCR. Results Ang II infusion increased MAP in both sexes but elicited a significantly greater response in females (+ 50 mmHg) than males (+ 27 mmHg, p < 0.005). Female hamsters exhibited pronounced kidney injury, including acute tubular necrosis, glomerular sclerosis, and vascular fibrinoid necrosis, along with a 2-fold increase in kidney weight normalized to body weight. Ang II significantly downregulated renal ACE, ACE2, and AT 1 R expression and activity in females but not in males. Renal IL-6 and IL-1β mRNA levels were elevated 20-fold and 3.9-fold, respectively, in females, compared to modest increases in males. Conclusions Female Syrian hamsters exhibit heightened vulnerability to Ang II-induced hypertension and renal damage compared to males, marked by exaggerated blood pressure elevation, enhanced renal inflammation, and suppression of classical RAS components. This novel hamster model provides a unique platform for studying sex-specific mechanisms of hypertension and renal pathology, with translational relevance for subpopulations of women who are at increased risk of Ang II-dependent hypertension-associated renal disease.
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Ji et al. (2025) studied Angiotensin II-induced hypertension (n=57). Angiotensin II vs. Saline (vehicle) was evaluated on Mean arterial pressure (MAP) increase (p=<0.005). Angiotensin II infusion increased mean arterial pressure significantly more in female Syrian hamsters (+50 mmHg) than in males (+27 mmHg, p<0.005), alongside more severe renal damage.
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