Mechanism of cerebral arteriolar abnormalities after acute hypertension.

Abstract

Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. Scanning and transmission electron microscopy of such pial arterioles showed discrete destructive endothelial lesions the density of which correlated with the degree of vasodilation. Abnormalities of the vascular smooth muscle were seen in all dilated arterioles but affected only a small number of smooth muscle cells. The oxygen consumption of pial arterioles from cats subjected to hypertension was significantly reduced in comparison to that of vessels from normal animals. The arteriolar abnormalities induced by hypertension were inhibited by pretreatment with inhibitors of cyclooxygenase (indomethacin or AHR-5850) or by topical application on the brain surface of scavengers of free oxygen radicals (mannitol or superoxide dismutase). The results suggest that the mechanism of the arteriolar abnormalities from acute hypertension involves a sudden increase in prostaglandin synthesis that leads to generation of free oxygen radicals.

• Authors: H A Kontos, E P Wei, W D Dietrich, R M Navari, J T Povlishock, N R Ghatak, E F Ellis, J L Patterson Jr
• Journal: The American journal of physiology (Am J Physiol) Vol. 240 Issue 4 Pg. H511-27 (Apr 1981) ISSN: 0002-9513 [Print] United States
• PMID: 7223903 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Topics

• Animals
• Arteries (physiopathology)
• Arterioles (metabolism, physiopathology, ultrastructure)
• Brain (blood supply)
• Cats
• Hypertension (metabolism, physiopathology)
• Microscopy, Electron
• Microscopy, Electron, Scanning
• Muscle, Smooth, Vascular (physiopathology, ultrastructure)
• Oxygen Consumption