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Nephrosis augments contractile response to adrenoceptor agonists by the decrease in release of endothelium-derived
1Department of Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan.
Summary
Nephrotic rat aortas show increased contractions due to altered endothelium-derived relaxing factor release. This study investigates the role of adrenoceptors and cyclic GMP in these vascular changes.
Area of Science:
- Vascular biology
- Pharmacology
- Nephrology
Background:
- Nephrotic syndrome can alter vascular function.
- Endothelium-derived relaxing factor (EDRF) plays a crucial role in regulating vascular tone.
Purpose of the Study:
- To investigate the contractile responses of thoracic aorta in nephrotic rats.
- To explore the role of adrenoceptors and cyclic GMP in altered vascular function in nephrotic aorta.
Main Methods:
- Thoracic aortas from nephrotic and normal rats were used.
- Contractile responses to norepinephrine, B-HT 933, KCl, and U46619 were measured.
- Effects of endothelium removal, zaprinast (a cyclic GMP phosphodiesterase inhibitor), and methylene blue (a guanylate cyclase inhibitor) were assessed.
Main Results:
- Nephrotic rat aortas exhibited enhanced contractions to norepinephrine and B-HT 933 compared to normal rats.
- These enhanced responses were abolished by endothelium removal or methylene blue treatment.
- Cyclic GMP levels were lower in nephrotic aortas, and norepinephrine increased cyclic GMP via alpha-1 adrenoceptors.
Conclusions:
- Augmented contractile response to norepinephrine in nephrotic aorta is linked to decreased EDRF release via alpha-1 adrenoceptors.
- Enhanced response to B-HT 933 may involve reduced spontaneously released EDRF.
- EDRF signaling pathways are implicated in vascular dysfunction in nephrotic syndrome.