Enhanced Na⁺, K⁺-ATPase activity and endothelial modulation decrease phenylephrine-induced contraction in aorta from...

Area of Science:

• Cardiovascular Physiology
• Pharmacology

Background:

• Ouabain is a cardiac glycoside that inhibits Na+, K+-ATPase.
• Long-term ouabain administration can affect vascular function and blood pressure.

Purpose of the Study:

• To investigate the long-term effects of ouabain on vascular reactivity and Na+, K+-ATPase activity in normotensive and hypertensive rat aortas.

Main Methods:

• Wistar and spontaneously hypertensive rats (SHRs) received ouabain or vehicle for 5-20 weeks.
• Vascular responses to phenylephrine and KCl were measured in thoracic aortas.
• Endothelial, nitric oxide (NO), and cyclooxygenase (COX) pathways were analyzed, along with protein expression of NOS and COX-2.

Main Results:

• Ouabain treatment reduced phenylephrine-induced contraction and enhanced KCl-induced relaxation in both rat strains.
• Endothelial modulation of adrenergic response increased, with enhanced NO and reduced COX-derived vasoconstrictor factors.
• Long-term ouabain increased eNOS and decreased COX-2 expression in Wistar rats, while decreasing COX-2 and increasing nNOS in SHRs.

Conclusions:

• Long-term ouabain treatment modulates aortic vascular response in normotensive and hypertensive rats.
• These adaptations involve increased NO synthesis and reduced COX-2 activity, potentially counteracting ouabain-induced hypertension.