Heterogeneous vasomotor responses of anatomically distinct feline cerebral arteries

Abstract

1 The vasomotor reactivity to a number of neurotransmitters and blood-borne substances was evaluated in several anatomically distinct arteries of the cat cerebral circulation. Few regional differences were observed in their vasoconstrictor responses to noradrenaline, dopamine, 5-hydroxytryptamine and prostaglandin F2a. Only the anterior cerebral artery reacted strongly to all vasoconstrictor agents. 2 Adenosine, acetylcholine and histamine induced pronounced relaxation in the vast majority of the major cerebral arteries. The relaxation elicited by adenosine showed a slight degree of heterogeneity between the arteries and the overall response accounted for 81 + 6% of the pharmacologically-induced tone. On the other hand, the dilatation induced by acetylcholine and histamine varied as a function of the anatomical localization of the cerebral arteries. The acetylcholine-induced vasodilatation was significantly more pronounced in the middle cerebral, anterior communicating and anterior cerebellar arteries, with respective responses of 72, 66 and 83% of the induced tone as compared to 43% in the other vessels. However, all arteries were equally sensitive to acetylcholine with an overall mean pD2 value of 7.47 + 0.06. The most heterogeneous results were obtained with histamine and applied both to the magnitude of the maximal response and the sensitivity of the various arteries to this amine. The intensity of the relaxation varied from 20% (anterior communicating artery) to 118% (posterior cerebellar artery). 3 Among the neuropeptides studied, substance P and bradykinin were considerably less potent than vasoactive intestinal peptide on all the cerebral arteries. The least responsive vessel to bradykinin was the anterior cerebral artery with a maximal response of 22 + 5% of the induced-tone and a pD2 value of 7.56 + 0.24. All vessels responded weakly to substance P and those from the vertebrobasilar circulation were significantly less sensitive to this neuropeptide with pD2 values around 8.07 as compared to 9.82 in the more rostral arteries. Although all vessels were equally sensitive to vasoactive intestinal peptide, the dilator responses were significantly less pronounced in the middle cerebral and basilar arteries (maximal response of 86 + 5% and 69 + 6% of the induced-tone, respectively, as compared to 110 + 9% in the other vessels). 4 The vertebrobasilar arteries were as reactive, if not more reactive, to vasoconstrictors than the vessels originating from the carotid circulation. In contrast, the dilator responses were less marked in most caudal arteries. Such dichotomies may be important in the regulation of local cerebral blood flow. 5 The results emphasize the considerable heterogeneity in the vasomotor responses to a given substance among the various cerebral arteries. Further, they suggest the presence of multiple receptor populations which mediate opposite effects and which are distributed in different proportions among the cephalic arteries.

The effect of phenylephrine on arterial and venous cerebral blood flow in healthy subjects

“…However, the vertebral arteries together with the ICAs form the circle of Willis, with contribution of ICA and vertebral artery blood flow to total CBF estimated to be 75% and 25%, respectively, at rest (Schoning et al, 1994). noradrenaline) (Hamel et al, 1988) or cerebral CO 2 reactivity (Ito et al, 2000). There are differences in the cerebrovascular responses to sympathoexcitation between different arteries (Delp et al, 2001;Sato & Sadamoto, 2010); thus, different response of the ICA and vertebral arteries to PE infusion remains possible.…”

Cognitive and cerebrovascular improvements following kinin B1 receptor blockade in Alzheimer’s disease mice

“…Bradykinin (BK) and kallidin (Lys-BK) are the endogenous ligands for the constitutive B 2 R whereas the C-terminal metabolites desArg 9 -BK and Lys-desArg 9 -BK are the preferential agonists of the inducible B 1 R [4]. In the brain vasculature, BK dilates most cerebral arteries [5] through activation of B 2 R and release of endothelial-derived nitric oxide (NO). BK also regulates blood–brain barrier (BBB) permeability [6].…”

Pharmacological FMRI: Measuring Opioid Effects on the BOLD Response to Hypercapnia

“…Another study in rats suggests that endogenous opioids may be important in the regulation of cerebral blood flow during hypercapnia (Dora et al, 1992). Hamel et al (1988) demonstrated differing reactivity to various vasoactive substances in a selection of isolated feline cerebral arteries. There appears to be marked variation between species and whether investigating endogenous or exogenous opioids.…”