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Circulating digitalis-like substance is increased in DOCA-salt hypertension
Biochemical and Biophysical Research Communications
|July 18, 1984
Summary
Elevated blood pressure in DOCA-salt rats correlates with increased circulating digitalis-like substances. This study quantifies this substance in hypertension models, revealing its link to elevated blood pressure.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pharmacology
Background:
- Hypertension is a significant global health concern.
- The role of endogenous digitalis-like substances in blood pressure regulation is under investigation.
- Deoxycorticosterone acetate (DOCA)-salt treatment is a common model for studying salt-sensitive hypertension.
Purpose of the Study:
- To investigate the presence and levels of digitalis-like substances in the plasma of rats with DOCA-salt induced hypertension.
- To compare digitalis-like activity in different hypertension models and control groups.
- To characterize the nature of the identified digitalis-like substance.
Main Methods:
- Measurement of blood pressure in control, salt-treated, and DOCA-salt treated rats.
- Quantification of digitalis-like activity using radioimmunoassay for digoxin and a rat brain synaptosomal membrane receptor binding assay.
- Partial purification of plasma substances using Sephadex G-25 gel filtration.
- Assessment of Na+-K+ ATPase inhibitory activity.
Main Results:
- DOCA-salt treated rats exhibited significantly higher blood pressure compared to control and salt-treated rats.
- Digoxin-like immunoreactivity was detected in DOCA-salt treated rats but not in controls.
- Receptor binding activity and Na+-K+ ATPase inhibitory activity were significantly elevated in DOCA-salt hypertensive rats, primarily in the second purified peak.
Conclusions:
- A circulating digitalis-like substance is increased in DOCA-salt hypertension.
- This substance may play a role in the pathogenesis of salt-sensitive hypertension.
- Further research is needed to identify the exact chemical structure and precise mechanism of action of this endogenous compound.