Related Experiment Videos
Effect of angiotensin-induced hypertension on rat coronary arteries and myocardium
Insights
Acute hypertension induced by angiotensin amide increases blood vessel permeability in rats. This leads to vascular damage and myocardial injury, particularly in smaller intramural arteries.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Renal Hypertension
Background:
- Angiotensin II is a potent vasoconstrictor that plays a key role in regulating blood pressure.
- Hypertension can lead to significant damage to blood vessels and organs.
Purpose of the Study:
- To investigate the effects of acute hypertension induced by angiotensin amide on the permeability and integrity of coronary arteries in rats.
- To examine the resulting vascular and myocardial lesions.
Main Methods:
- Acute hypertension was induced in rats via intravenous infusion of angiotensin amide.
- Horseradish peroxidase (HRP) or colloidal carbon was used as tracers to assess vascular permeability.
- Epicardial and intramural coronary arteries and myocardium were examined using electron microscopy.
Main Results:
- Angiotensin infusion accelerated vesicular transport in epicardial arteries and increased permeability of intramural arteries.
- Intramural arteries showed medial fragmentation and necrosis, unlike epicardial arteries.
- Myocardial damage resembling ischemic injury was observed.
Conclusions:
- Elevated pressure may increase epicardial artery permeability.
- Vasoconstriction by angiotensin likely causes altered permeability and lesions in intramural arteries.
- These vascular changes contribute to myocardial damage in angiotensin-induced hypertension.
Abstract:
Acute hypertension has been produced in rats by the intravenous infusion of angiotensin amide for 4 hours. Both control and hypertensive animals were injected intravenously prior to sacrifice with either horseradish peroxidase (HRP) or colloidal carbon. Epicardial arteries and blocks of ventricular myocardium containing intramyocardial arteries and arterioles have been processed for electron microscopy. HRP appears to penetrate the endoethelium of epicardial arteries from control animals within vesicles that bypass endothelial junctions and empty into interendoethelial clefts. Peroxidase does not traverse the endothelium of intramural arteries and arterioles of controls over the 10-minute period of observation. There is acceleration of lateral vesicular transport in the endothelium of epicardial arteries after angiotensin infusion and direct permeation of interendothelial clefts of intramural arterial vessels. Medial fragmentation and more extensive necrosis are observed in intramyocardial but not in epicardial arterial vessels. Foci of myocardial damage resembling irreversible ischemic or anoxic injury followed by reflow are described. It is suggested that the increased permeability of epicardial arteries may be due to elevated pressure, while the altered permeability and vascular lesions of intramural arteries and arterioles are more readily attributable to the vasoconstriction produced by angiotension. The vascular and myocardial lesions are also discussed in relation to the regional actions of angiotensin on the coronary circulation and known effects of this vasoactive peptide on myocardium.