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At least 73 records · Page 4Linked to original sources
PubMed1962

Relation in rat hind-limb blood vessels between nervous vasomotor tone and the response to vasoconstrictor drugs.

When the nervous component of the vasomotor tone of the blood vessels of the innervated rat hind limb perfused with blood was reduced by ganglion blockade, by section of the nerves to the hind limb, or by the indirect effect of drugs, the vasoconstrictor response of the blood vessels to noradrenaline was immediately increased. This increased peripheral response was observed only when the blood perfusing the hind limb was from the same animal or from a genetically similar animal. Reduction of the nervous component of the vasomotor tone also increased the constrictor response of the hind-limb blood vessels to adrenaline, ephedrine, tyramine and 5-hydroxytryptamine, but did not increase the response to angiotensin, vasopressin or S-methyl isothiourea. Pre-treatment with reserpine increased the hind-limb response to noradrenaline but reduced the response to ephedrine, tyramine and 5-hydroxytryptamine. The results suggest that, in rats, activity in the sympathetic nervous system directly influences the reactivity of peripheral blood vessels to noradrenaline and other sympathomimetic drugs.

Animals↗
PubMed1979

Interaction of a potential antimigraine drug (Org GC 94) with the vasomotor action of serotonin.

The interaction of a potential anti-migraine drug (Org GC 94) with the vasomotor action of 5-HT in vitro in feline, canine and human intra- and extracranial arteries, as well as in vivo in the canine nasal vascular bed as been investigated. In the two in vitro preparations, i.e. using superfusion or bath techniques, the intracranial vessels were more sensitive to 5-HT vasoconstriction than the extracranial ones. As both the maximum contraction and the slope of the dose-response curves were reduced by increasing concentrations of Org GC 94, the antagonism of 5-HT did not involve competitive blockade of 5-HT receptors. The dilator response was tested in arteries brought to a higher tone with prostaglandin F2 alpha. 5-HT produced a dose-dependent dilatation which, like the vasoconstriction, was antagonized in a non-competitive manner by Org GC 94. Intra-arterial injections of 5-HT provoked nasal vasoconstriction and this response was clearly potentiated by Org GC 94 in low doses while higher doses inhibited the vascular response to 5-HT. The specific effect of Org GC 94 in vivo may be the potentiation of 5-HT-induced vasoconstriction. The hypothesis is discussed that the so-called anti-5-HT agents act in migraine patients as partial agonists of 5-HT, mimicking rather than antagonizing 5-HT.

Animals↗
PubMed1976

Cryosurgery in vasomotor rhinopathy: experimental histopathology.

Experimental cryosurgery of the nasal mucosa in normal guinea pigss and in animals with drug-induced vasomotor rhinopathy showed complete closure of the initial ulceration by a temporary atypical epithelium within 2 week. 3-4 weeks after cryotreatment, normal ciliated epithelium covered the whole area. Within 4-5 weeks, the last signs of inflammatory reaction dinappeared. The treatment resulted in a definitive reduction of mucosal thickness, and in a numerically significant loss of vessels and glandular acini. The hintopathological results thus agreed with the clinical objective of the treatment in vasomotor rhinopathy (reduction of the nasal resistance and diminution of rhinorrhea).

Animals↗
PubMed1978

[Effect of neuroactive aminoacids on central mechanisms of vascular regulation].

In cats and rats, GABA and glycine depressed pressor vasomotor reactions and responses of sympathetic nerves to stimulation of the medial and vestibular nuclei of the bulbar reticular formation. These drugs depressed vasomotor responses to direct stimulation of the spinal lateral horns. GABA reduced the activated bulbo-spinal influences and inhibition of responses of the "spinal" vessels to stimulation of the solitary tract nucleus and paramedian reticular nuclei. GABA (100--200 mg/kg) depressed vasomotor responses to mechanoreceptor stimulation and increased the responses to chemoreceptor stimulation while glycine did not change them. GABA and glycine exerted no adrenolytic or myotropic effects. GABA did not affect identically the transmission in different sympathetic ganglions. Glycine did not alter the ganglionic transmission. The site and mode of the neuroactive aminoacids effect on the central mechanisms for vasomotor regulation are discussed.

Aminobutyrates↗
PubMed1991

Beneficial effects of intranasal applications of capsaicin in patients with vasomotor rhinitis.

Capsaicin, a nonenamide derived from Capsicum plants, has proven useful in patients with vasomotor rhinitis. In the present study, we studied the effects of 15 micrograms capsaicin suspended in 100 microliters solution in patients with known vasomotor rhinitis. Drug was given 3 times/day for 3 days to each patient by means of a spray delivered to the nasal mucosa. Acute effects induced by the drug included painful sensation and secretion of nasal fluid but were no longer observed at the last capsaicin application. Patients recorded their symptoms over a 1-month period. The mean symptom score involving nasal obstruction and nasal secretion was markedly reduced by capsaicin treatment. We advance the hypothesis that the beneficial effect of drug treatment may be due to its specific action on the peripheral endings of primary sensory neurons leading to their functional blockade. Further randomized, double-blind, placebo-controlled trial is now needed.

Administration, Intranasal↗
PubMed2000

Clinical pharmacokinetics of toremifene.

Toremifene is a chlorinated triphenylethylene derivative of tamoxifen approved for use in the treatment of patients with metastatic breast cancer. Toremifene is well tolerated in patients, and common adverse effects of this drug include vasomotor symptoms such as hot flashes and vaginal discharge. This compound is administered to patients orally at a dose of 60 mg/day, although alternative methods of administration have been investigated. Oral bioavailability is estimated to be approximately 100%. At steady state, toremifene and its metabolites are highly protein bound (>95%). Toremifene is metabolised in the liver by cytochrome P450 enzymes, and it is eliminated primarily in the faeces following enterohepatic circulation. The half-life of toremifene is approximately 5 days, and steady state is reached by 6 weeks depending on the dose given. The pharmacokinetics of toremifene have been shown to be altered by certain liver conditions, but age and kidney function do not appear to be as significant.

Animals↗