Endothelium-derived relaxing factor modulates noradrenergic constriction of cerebral arterioles in rabbits.

Abstract

Background and Purpose: Cerebral arterioles are relatively unresponsive to norepinephrine. We tested the hypothesis that release of endothelium-derived relaxing factor is stimulated by norepinephrine and attenuates adrenergic constriction of pial arterioles.Methods: In seven anesthetized New Zealand White rabbits, diameter of pial arterioles was measured through a cranial window. Responses to topical application of norepinephrine and arginine vasopressin were examined before and during application of N

Adrenoreactivity of Rat Pial Arteries under Conditions of Stabilized Systemic Blood Pressure

“…Address for correspondence: vshuv@kolt.infran.ru. V. N. ShuvaevaNumerous experiments demonstrated the existence of differentia ted adrenoreactivity in various segments of the same blood vessel or described the development of opposite reactions within the vascular network to norepinephrine [6,[8][9][10]. Our previous detailed analysis of the reaction of consecutive arteries in the precapillary subdivision of the meningeal microcirculatory bed in rats to intravenous norepinephrine also showed that this agent provokes both constrictor and dilator vascular responses [5].…”

The Role of Adrenoceptors in the Retina

“…Endothelium-dependent attenuation of retinal α 1 -AR-mediated vasoconstriction appears physiologically plausible, since it would confer a safety net by protecting the retina against inappropriate reductions in blood flow induced by elevated levels of catecholamines during exercise, hemorrhage, or stress. Based on studies in various vascular beds, including cerebral vessels, it is well documented that vascular responses to α 1 -adrenergic stimuli are modulated by the vascular endothelium and are altered when endothelial function is impaired [96][97][98][99][100][101][102][103][104][105][106]. Apparently, the endothelium mitigates the vasoconstrictive impact of elevated circulating catecholamine levels particularly in organs whose uncompromised blood supply and functioning are of vital importance during fight and flight responses [34,39,107].…”

Comparison of Dopamine and Norepinephrine after Traumatic Brain Injury and Hypoxic-Hypotensive Insult

“…The absence of response to norepineprine of the smaller cerebral arteries (Sercombes et al, 1990) may be explained by their lowest sympathetic innervation (Faraci and Heistad, 1990;Paulson et al, 1990;Ursino, 1991) and by the release of nitric oxyde (Bauknight et al, 1992). Intravenous infusions of aadrenergic (Olesen, 1972;Rogers et al, 1988;Sokrab and Johansson, 1989;Tuor et al, 1986) and b-adrenergic agonists (Bandres et al, 1992;Olesen, 1972) are without significant effects on cerebral blood flow in normal brains unless variations in MAP are slow (Barzo et al, 1993) and within autoregulatory range.…”