Nitroglycerin-induced headache.
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Arteriovenous Anastomosis↗
Biomedical subjects
E M Van Gelderen
Publications and source records attributed to E M Van Gelderen.
Carotid blood flow distribution, haemodynamics and inotropic responses following calcitonin gene-related peptide in the pig.
The sensory neuropeptide, calcitonin gene-related peptide (alpha-CGRP), has been implicated in the pathogenesis of migraine headache. The present study aimed to evaluate the effects of intracarotid infusions of human alpha-CGRP (10, 30 and 100 pmol/kg.min; n = 8), as compared to that of saline (4 times; n = 8) on haemodynamics and blood flow distribution within the carotid circulation of the anaesthetized pig, using the radioactive microsphere method. Furthermore, the effects of antimigraine drugs, dihydroergotamine (100 micrograms/kg i.v.; n = 4) or sumatriptan (300 micrograms/kg i.v.; n = 4), on these parameters were studied in the presence of the infusion of the highest concentration of human alpha-CGRP. Additionally, putative positive inotropic responses to human alpha-CGRP (10(-9)-10(-7) M) were investigated in porcine isolated atrial and ventricular trabeculae. Human alpha-CGRP increased carotid artery blood flow and conductance dose-dependently, together with an enhancement in vascular pulsations. These effects were associated with a fall in systemic blood pressure with concomitant increases in heart rate and cardiac output. The increase in carotid blood flow was reflected by an increase in total capillary blood flow, predominantly to extracerebral tissues including the dura, whereas blood flow through arteriovenous anastomoses remained stable. Both dihydroergotamine and sumatriptan reduced carotid blood flow and its capillary fraction without affecting systemic vascular conductance. In tissues, these drugs reversed blood flow increases due to human alpha-CGRP in most extracerebral tissues, but failed to reduce dural blood flow. In porcine isolated atrial and ventricular trabeculae, noradrenaline (10(-8)-10(-5) M) increased force of contraction in a concentration-dependent manner. In contrast, human alpha-CGRP (10(-9)-10(-7) M) failed to increase force of contraction in atrial trabeculae (n = 6) and exerted only a moderate concentration-dependent positive inotropic effect in ventricular trabeculae (approximately 25% of the response to 10(-5) M noradrenaline, n = 10). These data indicate that human alpha-CGRP caused arteriolar dilatation together with a fall in blood pressure in the pig. The tachycardia may be reflex-mediated, but the peptide also exerts a moderate positive inotropic action on ventricular trabeculae. The fall in systemic arterial blood pressure and the marked increase in capillary blood flow most likely prevented the opening of arteriovenous anastomoses. Furthermore, the antimigraine drugs, dihydroergotamine and sumatriptan, were able to reverse blood flow changes induced by human alpha-CGRP in the porcine carotid circulation.
Animals↗
Effect of N(G)-nitro-L-arginine methyl ester on the hypotensive and hypertensive responses to 5-hydroxytryptamine in pithed rats.
The potential ability of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 1 to 10 mg/kg), to modulate blood pressure responses to 5-hydroxytryptamine (5-HT), 5-carboxamidotryptamine (5-CT) and (1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane) (DOI) was studied in pithed rats. The hypotensive responses to 5-HT in the presence of ketanserin were augmented by L-NAME as well as by phenylephrine infusion, both of which themselves increased blood pressure. L-NAME also tended to prolong the duration of the response of 5-HT. Likewise, the hypotensive responses to 5-CT were potentiated. The magnitude of the hypertensive responses to 5-HT was unaffected by L-NAME or phenylephrine. However, in contrast to phenylephrine, L-NAME prolonged the duration of these responses. The magnitude and duration (middle dose only) of the hypertensive responses to DOI were augmented by L-NAME, but phenylephrine was ineffective. These results suggest that L-NAME increases blood pressure, probably by inhibiting the basal release of NO in animals with a low vascular tone. However, the hypotensive responses to 5-HT and 5-CT seem to be largely independent of NO release by the endothelium, but the hypertensive responses to 5-HT and DOI appear to be limited by the release of NO in the pithed rat.
Animals↗
Involvement of alpha 1- and alpha 2-adrenoceptors in the vasoconstriction caused by ergometrine.
In pithed normotensive rats, the pressor effects evoked by i.v. serotonin (5-HT) and ergometrine were analysed using the relatively selective alpha 1-, alpha 2- and serotonin antagonists prazosin, yohimbine methysergide, respectively. The pressor response to ergometrine was reduced by both prazosin and yohimbine but only moderately affected by methysergide. On the other hand, the rise in diastolic pressure brought about by serotonin was strongly depressed by methysergide but not influenced by the blockade of either alpha 1- or alpha 2-adrenoceptors. The calcium antagonist nifedipine shifted the dose-pressor response curve of ergometrine to the right in a dose-related, non-parallel manner. The maximum pressor response was diminished by nifedipine. In contrast, the rise in pressure provoked by serotonin was not affected by nifedipine. The results thus show that in the pithed rat the vasoconstrictor response to ergometrine is mediated by alpha-adrenoceptors (both alpha 1 and alpha 2) rather than by serotonin receptors. These findings question the role of serotonin receptors in the vasoconstriction induced by ergometrine.
Animals↗