Characteristics of Histamine Receptors in Human Cerebral Arteries

Abstract

Histamine and 2,2-pyridylethylamine, an H1-receptor agonist, (both 10(-8)-10(-3) M) caused contraction of human cerebral artery preparations in the absence of active tension, while dimaprit, an H2-receptor agonist, caused vasorelaxation. The histamine-induced vasoconstriction was blocked non-competitively by tripelennamine, an H1-receptor antagonist. In the presence of cimetidine, an H2-receptor antagonist, histamine-induced contraction was enhanced. The histamine-induced contraction was not affected by phentolamine or propranolol, but abolished by nifedipine. In prostaglandin F2 alpha-precontracted arteries, histamine and dimaprit caused relaxation, while 2,2-pyridylethylamine had no apparent effect. Histamine-induced relaxation was much greater in the presence than in the absence of an H1-antagonist. The vasorelaxation induced by histamine in the presence of an H1-antagonist was also inhibited by an H2-antagonist. Histamine caused no apparent relaxation in precontracted preparations without endothelium. The present results provide further evidence that histamine causes either vasocontraction or vasodilation in human cerebral arteries, and suggest that vasocontraction and vasorelaxation are due to the activation of H1- and H2-receptors, respectively. The relaxation induced by histamine may also be related to the endothelium-derived relaxing factors released from endothelial cells.

Functional Analysis Of Histamine Receptor Subtypes Involved In Endothelium‐Mediated Relaxation Of The Human Uterine Artery

“…Because the selective H 3 receptor agonist imetit failed to initiate any relaxation, our data suggest that the H 3 receptor is not expressed functionally in these types of vessels. These results are in line with previous findings in human cerebral arteries 23 …”

“…These results are in line with previous findings in human cerebral arteries. 23 For our future plans to work on this model using human uterine arteries, it was essential to determine whether these vessels can be stored in the incubator for up to 5 days to allow molecular modulation using, for example, antisense/sense vectors introduced into the arterial wall. Our data that endothelium-dependent relaxation to histamine and acetylcholine, as well as the contractile response to phenylephrine, was not modulated during the storage in the incubator suggest that, under these conditions, blood vessel reactivity remained constant over 5 days.…”

Effects of pH on Vascular Tone in Rabbit Basilar Arteries

“…Gokina and Bevan (8, 9) reported that Ca 2+ influx through VDCC might be responsible for over the 80% of histamine-induced sustained contraction (26). The same result was also reported in human cerebral arteries (33) and observed in this study (Fig. 3C, 4, 5B).…”

Role of endothelium and nitric oxide in histamine‐induced responses in human cranial arteries and detection of mRNA encoding H1‐ and H2‐receptors by RT‐PCR

“…In many of the previous studies, in contrast to the present, the locations of the different receptors were not determined. The presence of both H 1 ‐ and H 2 ‐receptors in the cranial arteries seems well established, and the only conflicting result is that of a relaxant H 2 receptor coupled to the endothelium in cerebral arteries (Takagi et al , 1993). However, this study concerned large cerebral arteries and most of the vasculature demonstrated arteriosclerotic changes, which is in contrast to the small calibre arteries used in the present study which were macroscopically free from any arteriosclerosis.…”