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Testosterone acts as a coronary vasodilator by a calcium antagonistic action
K M English1, R D Jones, T H Jones
1Department of Cardiology, Royal Hallamshire Hospital, Sheffield, UK.
Insights
Testosterone (T) acts as a vasodilator, primarily inhibiting calcium-dependent vascular contraction. This finding explains T
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Vascular Pharmacology
Background:
- Testosterone (T) exhibits vasodilatory properties in vitro and in vivo.
- Supplemental T therapy improves angina symptoms and reduces ischemia in humans.
Purpose of the Study:
- To investigate the mechanism by which testosterone affects vascular contraction.
- To determine if testosterone primarily inhibits calcium-dependent pathways in vascular smooth muscle.
Main Methods:
- Isolated left anterior descending coronary arteries from adult male Wistar rats were used.
- Vascular contractions were induced by potassium chloride and phorbol-12,13-dibutyrate (PDBu).
- The effect of testosterone on these contractions was measured in the presence and absence of extracellular calcium.
Main Results:
- Testosterone abolished 100% of calcium-dependent contraction induced by potassium chloride.
- Testosterone reduced contractions induced by prostaglandin-F-2-alpha by 82.3%.
- Testosterone inhibited PDBu-induced contractions by approximately 50%, regardless of extracellular calcium presence.
Conclusions:
- Testosterone's vasodilatory effect is primarily mediated by inhibiting calcium-dependent mechanisms in vascular smooth muscle.
- These findings provide mechanistic insight into testosterone's beneficial effects on cardiovascular health, particularly in conditions like angina.
Abstract:
T acts as a vasodilator in vitro and in vivo. Supplemental T therapy in humans with angina improves symptoms and reduces objective measures of ischemia. In left anterior descending coronary arteries taken from adult male Wistar rats, T abolishes 100+/-4.2% of calcium-dependent contraction induced by potassium chloride, 82.3+/-6.1% of the mostly calcium-dependent contraction induced by prostaglandin-F-2-alpha, but only 45.3+/-3.4% of the contraction induced by phorbol-12,13-dibutyrate (PDBu) in the presence of extracellular calcium, and 54.5+/-4.5% of the contraction induced by PDBu in the absence of extracellular calcium. These findings suggest that T is primarily inhibiting the calcium-dependent elements of vascular contraction.