A review of vasomotor responses of arterioles on the surface of the mouse brain: the necessary prelude to studies using genetically manipulated mice.
OBJECTIVE
To review the published data concerning the vasomotor responses of arterioles on the surface of the mouse brain. This information is essential to the planning of studies using genetically manipulated mice to investigate the control of cerebral vascular resistance.


RESULTS
Cerebral vasomotor responses of mice have been reported using a wide variety of vasoactive agents. The responses are usually like those of other laboratory animals. Some agents are capable of eliciting opposing dilating and constricting responses. The initial tone of the arteriole is one of several factors that can determine the direction of the response elicited by such agents. Endothelium-dependent dilators and constrictors have been described. There are a variety of endothelium-derived relaxing factors (EDRFs). Only one of these is synthesized by nitric oxide synthase (NOS). Antisense data suggests that both the endothelial and the neuronal isoforms of NOS may exist in the endothelial cells of these vessels. Several diseases can be modeled in mice and cerebrovascular responses studied. Studies of genetically modified mice suggest that the endothelial form of NOS contributes to microvascular events, which limit ischemic damage to brain parenchyma. However, during and following ischemia there may be loss of this NOS or inability to mobilize a storage form of the EDRF, which it produces.


CONCLUSIONS
Data available from studies of mice provide a good basis for planning further studies, examining cerebrovascular control mechanisms in health and disease, by workers now using genetically modified mice. The latter represent a powerful and increasingly popular tool for this purpose.
Rosenblum
W I
WI
Department of Pathology, (Neuropathology), Medical College of Virginia of Virginia Commonwealth University, Richmond 23298-0017, USA.
D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D002545:Brain Ischemia / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000494:pharmacology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D051379:Mice; D008817:Mice, Mutant Strains; D009569:Nitric Oxide / Q000494:pharmacology / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000502:physiology; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D013045:Species Specificity; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
D002317:Cardiovascular Agents; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse