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At least 343 records · Page 19Linked to original sources
PubMed1975

Histamine receptors in the vasculature of the rabbit ear.

Histamine has a dual action on the isolated perfused ear preparation of the rabbit. The amine induced a dose-dependent rise in perfusion pressure when the preparation was perfused with Krebs' solution. This pressor response was reversed to a depressor effect when meypramine was added to the perfusion fluid. This depressor effect of the amine was also dose-related. Metiamide competitively inhibited the depressor effect of histamine. Prior treatment of the ear vessels with metiamide alone caused an increase in histamine-induced perfusion pressure. From these results it was concluded that the predominant pressor effect of histamine on the vascular bed of the rabbit ear is mediated through the H1-receptors and the depressor effect of the amine through histamine H2-receptors.

Acetylcholine↗
PubMed1996

Production of pulmonary vasodilation by tolazoline, independent of nitric oxide production in neonatal lambs.

OBJECTIVE: To determine whether tolazoline reduces pulmonary vascular resistance (PVR) by means of endogenous nitric oxide production. DESIGN: Thirty newborn lambs (2 to 7 days of age) were anesthetized with pentobarbital, and their lungs were ventilated through an endotracheal tube. Intravascular catheters were placed in the left ventricle, descending aorta, right atrium, and pulmonary artery for continuous monitoring of intravascular pressures. Cardiac output was measured with radiolabeled microspheres. Arterial carbon dioxide pressure and pH were maintained in a normal range throughout the experiments. Animals were randomly assigned to the following groups: group 1, lungs ventilated with a hypoxic gas mixture and administered tolazoline; group 2, given N omega-nitro-L-arginine (L-NA) (5 mg/min intravenously for 60 minutes) and tolazoline; group 3, given L-NA with hypoxia and tolazoline. Acetylcholine (0.5 microgram/kg) was injected into the right atrium to assess pulmonary nitric oxide synthase activity before and after the L-NA infusion. Data were analyzed by analysis of variance. RESULTS: L-NA inhibited the acetylcholine-induced reduction in mean pulmonary artery pressure (MPAP) by more than 75%. Hypoxia and L-NA increased both MPAP and PVR. Tolazoline produced immediate reductions in both MPAP and PVR in all three groups (group 1, 27% +/- 3% and 50% +/- 5%; group 2, 34% +/- 5% and 50% +/- 6%; and group 3, 31% +/- 4% and 46% +/- 5%, respectively). CONCLUSIONS: These results suggest that tolazoline produces vasodilation independent of nitric oxide production. Understanding the mechanism by which tolazoline produces pulmonary vasodilation may provide insight into the clinical use of this drug and information regarding other potential endogenous mediators of pulmonary vasomotor tone in the neonate.

Animals↗
PubMedDate not supplied

Pretreatment with the dopamine agonist quinpirole inhibits central antihypertensive mechanisms in rats.

1. Intravenous or central treatment of spontaneously hypertensive rats (SHR) with the dopamine D2 receptor agonist quinpirole caused a short-lasting pressor response with little effect on heart rate. 2. At 30 min after intravenous administration of quinpirole, the antihypertensive effect of rilmenidine was significantly inhibited. This interaction of quinpirole and rilmenidine was similarly observed when quinpirole was administered either intravenously (0.3 or 0.1 mg/kg), in the lateral cerebral ventricles (0.1 mg/kg) or intracisternally (0.1 mg/kg) or when rilmenidine was administered intravenously (1 mg/kg) or intracisternally (0.1 mg/kg). 3. The apparent desensitization to the antihypertensive effect of rilmenidine 30 min after pretreatment with quinpirole was not observed after a 4 or 24 h interval. 4. These data suggest that quinpirole has prolonged effects on central sympathetic vasomotor mechanisms that are the target of centrally acting antihypertensive drugs. These and previous results show a functional interaction between central dopamine D2 receptor activation and sympathetic responses mediated by a wide range of different receptors, including imidazoline and 5-hydroxytryptamine 5-HT1A-receptors and alpha 2-adrenoceptors.

Animals↗
PubMed1975

Magnesium-neurohypophyseal hormone interactions in contraction of vascular smooth muscle.

The contractile responses of helically cut rat aortic strips to neurohypophyseal hormones and synthetic analogues in the presence and absence of 1.2 mM external magnesium ions [Mg++]o was studied. These experiments demonstrate that 1) [Mg++]o potentiates the contractile actions of a variety of neurohypophyseal peptides on vascular smooth muscle. 2) [Mg++]o can alter both the ED50s (i.e., hormone-receptor affinities) and intrinsic activities (or maximum contractile responses) of these molecules on vascular muscle. 3) The amino acid moieties in positions 1, 2, 3, and 8 of the vasopressin molecule interact, differentially, with [Mg++] to produce contraction of vascular muscle. 4) The length of the side chain, and basicity, in position 8 of the vasopressin molecule are probably important in Mg potentiation in mammalian vascular muscle. 5) Interaction of Mg with an aromatic group in position 3 might be critical for potency of vasopressin hormones of mammalian vascular muscle; the ED50 for oxytocin is not shifted to lower concentrations in the presence of [Mg++]o. Collectively, these data suggest that Mg probably acts at more than one site in vascular smooth muscle in the production of neurohypophyseal peptide-activated contractions. In addition, the present findings indicate that the Mg dependence of these peptides on at least one vascular muscle, rat aorta, is a direct function of the rat pressor potency of the molecules.

Animals↗
PubMed2000

Stroke associated with marijuana abuse.

We present the case of a 15-year-old with a cerebellar infarct that involved multiple arterial territories. It was temporally related to, and probably caused by, heavy marijuana use. While the mechanism of marijuana-associated stroke is unclear, the drug is known to cause hypotension and to impair peripheral vasomotor reflexes. We suspect that the child had diminished cerebral autoregulatory capacity and developed the stroke during a period of hypotension.

Adolescent↗
PubMed1990

Vasomotor flushes.

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Adrenergic alpha-Agonists↗