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DOCA-Salt Hypertension: an Update
Tyler Basting1,2, Eric Lazartigues3,4,5
1Department of Pharmacology and Experimental Therapeutics, School of Medicine, Louisiana State University Health Sciences Center, 1901 Perdido Street, Room 5218, New Orleans, LA, 70112, USA.
Hypertension, a complex disease causing 40% of cardiovascular deaths, involves genetic and environmental factors. The deoxycorticosterone acetate-salt (DOCA-salt) rodent model, primarily neurogenic, significantly impacts multiple organs beyond the nervous system.
Area of Science:
- Cardiovascular Research
- Nephrology
- Neuroscience
Background:
- Hypertension is a major contributor to cardiovascular mortality, stemming from complex genetic and environmental interactions.
- Current research utilizes diverse models to understand hypertension's multifaceted nature and target organ damage.
- Animal models, including genetic and surgically induced types, aim to elucidate primary hypertension mechanisms.
Purpose of the Study:
- To review the deoxycorticosterone acetate (DOCA), reduced renal mass, and high-salt diet (DOCA-salt) rodent model of hypertension.
- To highlight the neurogenic aspects of the DOCA-salt model and its impact on the central and peripheral nervous systems.
- To emphasize the involvement of multiple organ systems in this widely used experimental model.
Main Methods:
- Review of existing literature on hypertension models.
- Focus on the DOCA-salt rodent model.
- Analysis of neurogenic and multi-organ effects.
Main Results:
- The DOCA-salt model is a common experimental tool for studying hypertension.
- This model is primarily considered neurogenic, affecting both central and peripheral nervous systems.
- The DOCA-salt model demonstrates significant involvement of various other body organs.
Conclusions:
- The DOCA-salt model offers valuable insights into neurogenic hypertension.
- Understanding the multi-organ impact of the DOCA-salt model is crucial for comprehensive hypertension research.
- This model aids in investigating the complex interplay of factors contributing to hypertension and end-organ damage.
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