Endothelial dependent relaxation demonstrated in vivo in cerebral arterioles.

Abstract

Wei EP, Kontos HA, Said SI: Mechanism of action of vasoactive intestinal polypeptide on cerebral arteries. Amer J Physiol 239: H765-768, 1980 Wilson DA, O'Neill JT, Said SUMMARY The endothelium of mouse pial arterioles was injured in situ with a light/dye technique. The response of the arterioles to acetylcholine or to bradykinin was compared before and after the injury. All vessels failed to dilate after injury. In fact the predominant response now became constriction. The injured vessels were still capable of dilating to papaverine. Uninjured vessels continued to dilate to acetylcholine or bradykinin. The data show that relaxation of pial arterioles to acetylcholine or bradykinin is dependent on a normal endothelium. This is in keeping with demonstrations by others that an endothelial dependent relaxing factor or factors is(are) the mediator of the dilation to either acetylcholine or bradykinin. The present demonstration of such endothelial dependence is important because in contrast with the bulk of the literature it deals with in vivo, rather than in vitro data, and with microcirculation rather than large vessels. It is also important because it concerns brain circulation. The data suggests that endothelial injury, known to occur in a wide variety of pathologic states, could enhance vasospastic potential by eliminating dilating influences and/or converting them to constricting forces.

The Role of Endothelium and Nitric Oxide in Rat Pial Arteriolar Dilatory Responses to CO2in vivo

“…Nevertheless, the capacity for "pinpoint" illumination to impair endothelium-dependent va sodilation also appears to be a function of the extent of upstream exposure to the vasodilating agent. Thus, the response to locally applied Ach was blocked after such limited endothelial injury, and is consistent with previous findings from others (Rosenblum, 1986;Haberl et aI., 1990). …”

“…In controls (n = 8), only light or dye alone was given. Mercury light exposure or intravenous fluo rescein dye alone do not alter cerebral microvascu lar reactivity (Rosenblum, 1986).…”

Cerebral blood flow and cerebrovascular reactivity after inhibition of nitric oxide synthesis in conscious goats

“…With regard to the site(s) of the cerebral circulation where synthesis of nitric oxide takes place, experimental data show the cerebral microvessels do not release (Kontos et al, 1988) or release a minimal amount (Rosenblum, 1986) of nitric oxide, and that basal production of this substance seems to be dependent on cerebral vessels size, being greater in large than in small arteries (Faraci, 1991). Also, although the endothelium appears to be a main source of nitric oxide, other sources of this vasodilator such as cerebral arterial nerves (Bredt et al, 1990) and cerebrovascular musculature (Katusic, 1991) seem also to exist.…”

Functional Increases in Cerebral Blood Volume over Somatosensory Cortex

“…While trends remain intact, such effects prevent the numerical interpretation of fluorescence intensity as plasma (dye) volume when comparing pre-and poststimu Ius states. Furthermore, cortical trauma during preparation might introduce additional errors since mechanical trauma, photochemical procedures, and fluorescent compounds all abnormally influence en dothelial vasoreactivity (Rosenblum, 1986;Haberl et ai., 1990;Marshall and Kontos, 1990).…”