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Sympathetic and platelet adrenergic activity and salt sensitivity: an experimental study
L Somova1, L Mackraj, S Chetty
1Department of Human Physiology and Physiological Chemistry, University of Durban-Westville, South Africa.
Methods and Findings in Experimental and Clinical Pharmacology
|January 29, 1999
Summary
Genetically predisposed salt-sensitivity in Dahl rats is linked to increased sympathetic nervous system activity and platelet aggregation, contributing to hypertension. Dietary sodium significantly impacts these factors and disease development.
Area of Science:
- Cardiovascular Research
- Renal Physiology
- Pharmacology
Background:
- Salt-sensitivity is a key factor in hypertension pathogenesis.
- The role of adrenergic susceptibility and platelet activity in salt-dependent hypertension requires further elucidation.
Purpose of the Study:
- To investigate the hypothesis that genetically predisposed salt-sensitivity increases adrenergic susceptibility and platelet activity, contributing to hypertension in Dahl rats.
Main Methods:
- Utilized Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rat models.
- Administered low- and high-sodium diets.
- Assessed hypertension development, sodium/water retention, plasma volume, sympathetic nervous system (SNS) activity (catecholamines, heart rate), and platelet aggregation.
Main Results:
- DS rats developed hypertension irrespective of diet; high sodium exacerbated it.
- Na-loading increased sodium/water retention and plasma volume in DS rats.
- SNS activity and platelet aggregation were elevated in DS rats, further stimulated by Na-loading.
- Platelet alpha 2-adrenoceptors showed low binding capacity and affinity in both rat strains.
Conclusions:
- Genetically determined salt-sensitivity in DS rats is associated with increased SNS activity and platelet hyper-reactivity, playing a role in salt-dependent hypertension.
- While platelet alpha 2-adrenoceptors may not directly mediate increased activity, genetic defects in these receptors could still contribute to hypertension pathogenesis.