Biomedical subjects

C Forster

Publications and source records attributed to C Forster.

108 records · Page 6Linked to original sources

PubMed1983

Dopamine receptors in human basilar arteries.

After phenoxybenzamine (10(-5) M), pretreatment, and in the presence of propranolol (10(-6) M) and indomethacin (2.8 X 10(-6) M), dopamine caused a marked concentration-dependent relaxation of isolated strips of human basilar artery contracted with PGF2 alpha. This effect was mimicked by apomorphine, 6,7-ADTN and SK&F 38393, but N,N-diethyl dopamine, N,N-di-n-propyl-dopamine and 5,6-ADTN caused only slight relaxation. (+)-Butaclamol, cis-alpha-flupenthixol, fluphenazine and haloperidol competitively antagonised the relaxant effects of dopamine, but sulpiride was ineffective in concentrations as high as 1.3 X 10(-4) M. These findings show that the dopamine receptors in the human basilar artery closely resemble those in the smooth muscle of the rabbit isolated mesenteric and splenic arteries, and the dog renal and mesenteric arteries in vivo, but differ from those located presynaptically on sympathetic nerve terminals.

Basilar Artery↗

PubMed1982

Analysis of the 5-hydroxytryptamine induced contraction of the human basilar arterial strip compared with the rat aortic strip in vitro.

1) Experiments were performed to investigate the nature of the contraction produced by 5-hydroxytryptamine in the human basilar arterial strip in vitro and to compare it with that produced in the rat aortic strip in vitro. 2) The human basilar arterial strip was found to be significantly more sensitive to 5-HT compared to the rat aortic strip. 3) Methysergide, cyproheptadine and methergoline were competitive, selective antagonists against 5-HT on the rat aorta with pA2 values of 7.97, 8.76 and 9.49 respectively. In contrast 5-HT was antagonised by these agents in a manner which was not competitive on the human basilar artery. Both 5-HT and NA were antagonised by BW 501 C67 (alpha-anilino-N-2-m-chlorphenoxy propylacetamide hydrochloride) in a manner which was not competitive on both rat aortic and human basilar arterial strips. 4) Phentolamine (10(-7) to 10(-5) M) was found to be a competitive antagonist against noradrenaline on both the rat aortic strip (pA2 6.9) and the human basilar arterial strip (pA2 7.3). Phentolamine at 10(-5) M shifted the 5-HT curve on the human basilar artery to the right with a reduction in maximum response. 5) Methysergide (10(-9) to 10(-4) M) was found to possess contractile activity on some human basilar arterial strips, the maximum response being approximately 60% of that produced by 5-HT. Phentolamine at 10(-5) M shifted the dose-response curve to methysergide to the right with a slight reduction in the maximum response obtained. 6) The results from this study suggest that the receptor(s) mediating 5-HT-induced contraction of the human basilar artery may be different from the classical "D-receptor" which mediates contraction to 5-HT on the rat aorta.

Animals↗

PubMed1982

Prostacyclin and cerebral vessel relaxation.

The authors have studied the ability of prostacyclin to reverse contractions of human basilar arteries in vitro that were induced by a wide range of substances implicated in the etiology of cerebral arterial spasm. Prostacyclin (10(-10) to 10(-6)M) caused a dose-related reversal of contractions induced by 5-hydroxytryptamine, noradrenaline, angiotensin II, prostaglandin (PG)F2 alpha, and U-46619 (a thromboxane-A2 mimetic). These agents were tested at concentrations or volumes that produced almost maximum or maximum responses and those that produced approximately 50% of the maximum response. Contractions induced by maximum concentrations of angiotensin II and U-46619 were least affected by prostacyclin. In addition, contractions induced by thromboxane-A2 generated from guinea-pig lung were reversed in a dose-dependent fashion by prostacyclin. This ability of prostacyclin to physiologically antagonize contractions of the human basilar artery in vitro induced by high concentrations of various spasmogenic agents suggests that such a potent vasodilator agent or more stable analogue may be of value in the treatment of such disorders as cerebral arterial spasm following subarachnoid hemorrhage.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1981

Comparison of the contraction produced by various tryptamine analogues on human basilar arterial and rat aortic strips in vitro.

The effect of various closely related analogues of 5-hydroxytryptamine were studied on the human basilar arterial and rat aortic strips in vitro. All analogues (except 5-methoxytryptamine) contracted both preparations producing maximal responses equivalent to that obtained with 5-hydroxytryptamine. Maximum responses to 5-methoxytryptamine were equivalent to and only 60% of the maximum obtained with 5-hydroxytryptamine on human basilar artery and rat aorta, respectively. The order of potency of the analogues on the human basilar artery was different from that obtained on the rat aorta. 5-methyltryptamine, N-methyltryptamine and tryptamine were equipotent on both tissues, whereas 5-hydroxytryptamine and 5-methoxytryptamine were 229 and 296 times more potent, respectively, on the human basilar artery compared to the rat aorta. Both tissues appear to be deficient in monoamine oxidase, since nialamide or iproniazid did not potentiate responses to tryptamine. It is concluded that the receptor type mediating contraction of the human basilar artery to 5-hydroxytryptamine is different from the classical smooth muscle D-receptor.

5-Methoxytryptamine↗

PubMed1980

Vascular smooth muscle response to fibrinogen degradation products and 5-hydroxytryptamine: possible role in cerebral vasospasm in man.

1 Experiments were performed to determine the effects of fibrin(ogen) degradation products on the following in vitro vascular preparations: rabbit aortic strip, rat aortic strip and human basilar arterial strip. 2 Citrated plasma and streptokinase were incubated at 37 degrees C to produce a crude preparation of fibrinogen degradation products and 0.1 ml aliquots were removed at various time intervals. These samples were tested for intrinsic activity and possible interactions with EC50 and threshold concentrations of 5-hydroxytryptamine on the vascular preparations. 3 Enhancement of the responses obtained by both concentrations of 5-hydroxytryptamine was produced by samples taken throughout the streptokinase incubation period, the maximum effect being seen at 90 min. 4 The 90 min incubate produced volume-dependent (25-400 microliters) potentiations of the responses developed in the three vascular preparations to the EC50 and threshold concentrations of 5-hydroxytryptamine. 5 It is suggested that fibrin(ogen) degradation products may be involved in the intense vasoconstriction of the cerebral arteries following subarachnoid haemorrhage.

Animals↗

PubMed1980