Circulating neuropeptide Y does not produce pulmonary hypertension during massive sympathetic activation.
Adrenal Glands/drug effects/physiology; Adrenalectomy; Animals; Dogs; Hypertension; In Vitro Techniques; Neuropeptide Y/*physiology; Norepinephrine/pharmacology; Pulmonary Circulation/drug effects; Pulmonary/chemically induced/*physiopathology; Sympathetic Nervous System/*physiology; Veratrine/pharmacology
We tested the possibility that neuropeptide Y (NPY) may contribute to the pulmonary hypertension that occurs after massive sympathetic activation produced by intracisternal veratrine administration in the chloralose-anesthetized dog. In six dogs, veratrine caused arterial NPY-like immunoreactivity (NPY-LI) to rise from 873 +/- 150 (SE) pg/ml to peak values of 3,780 +/- 666 pg/ml by 60-120 min. (In 3 animals, adrenalectomy significantly reduced the increases in NPY-LI.) In five additional dogs, we infused porcine NPY for 30 min in doses that increased arterial NPY-LI to 8,354 +/- 1,514 pg/ml and observed only minor changes in pulmonary hemodynamics. In three isolated perfused canine left lower lung lobe (LLL) preparations, increasing doses of NPY were administered, producing levels of plasma NPY-LI, at the highest dose, that exceeded those observed after veratrine administration by three orders of magnitude. No changes in LLL arterial or double-occlusion capillary pressures were observed at any dose. Similarly, no changes in LLL hemodynamics were observed in three additional lobes when NPY was administered while norepinephrine was being infused. We conclude that it is unlikely that NPY plays a role as a circulating vasoactive agent in producing the pulmonary hypertension and edema that occur in this model.
Lang S A; Maron M B; Maender K C; Pilati C F
Journal of applied physiology (Bethesda, Md. : 1985)
1992
1992-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1992.73.1.117" target="_blank" rel="noreferrer noopener">10.1152/jappl.1992.73.1.117</a>
Effect of neuropeptide Y on hemodynamics of the rabbit lung.
Animals; Cisterna Magna; Hemodynamics/*physiology; In Vitro Techniques; Injections; Neuropeptide Y/blood/pharmacology/*physiology; Norepinephrine/pharmacology; Perfusion; Pulmonary Circulation/drug effects/*physiology; Rabbits; Sympathetic Nervous System/drug effects/physiology; Vascular Resistance/drug effects/physiology; Vasoconstriction/drug effects/physiology; Vasoconstrictor Agents/pharmacology; Veratrine/administration & dosage/pharmacology
We evaluated the effect of neuropeptide Y (NPY) on the hemodynamics of the isolated rabbit lung perfused at constant flow and outflow pressure. Doses of 10(-8) and 10(-7) M NPY increased pulmonary arterial pressure (Ppa) from 11.5 +/- 1.0 (SE) mmHg to, respectively, 16.4 +/- 1.5 and 26.0 +/- 3.8 mmHg (P \textless 0.05, n = 5 mmHg lungs), with 78 +/- 4% of the increase at 10(-7) M resulting from an increased arterial resistance. At the latter dose, pulmonary capillary pressure increased from 5.8 +/- 0.9 to 9.4 +/- 1.0 mmHg (P \textless 0.05). When administered in the presence of norepinephrine, 10(-8) and 10(-7) M NPY (n = 6) produced extreme increases in Ppa to 66.1 +/- 20.5 and 114.7 +/- 25.5 mmHg, respectively, that were due primarily to an increased arterial resistance. To determine the significance of circulating NPY as a pulmonary vasoactive agent, we measured plasma NPY-like immunoreactivity in anesthetized rabbits after massively activating the sympathetic nervous system with veratrine. NPY-like immunoreactivity increased from 74 +/- 10 to 111 +/- 10 (SE) pM (P \textless 0.05). Thus, although NPY is a potent vasoconstrictor in the rabbit lung, it is not likely that plasma NPY concentrations rise sufficiently, even after massive sympathetic nervous system activation, to produce pulmonary vasoconstriction in the intact rabbit.
Lang S A; Maron M B
Journal of applied physiology (Bethesda, Md. : 1985)
1998
1998-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1998.84.2.618" target="_blank" rel="noreferrer noopener">10.1152/jappl.1998.84.2.618</a>
Oxytocin induces preservation of social recognition in male rats by activating alpha-adrenoceptors of the olfactory bulb.
Male; Animals; *Social Behavior; Rats; Adrenergic beta-Antagonists/pharmacology; Adrenergic beta-Agonists/pharmacology; Microdialysis; Adrenergic alpha-Antagonists/pharmacology; Phentolamine/pharmacology; Isoproterenol/pharmacology; Clonidine/pharmacology; Norepinephrine/pharmacology; Social Dominance; Adrenergic alpha-Agonists/pharmacology; Memory/*drug effects/physiology; Olfactory Bulb/*drug effects/physiology; Oxytocin/*pharmacology; Timolol/pharmacology; Receptors; Adrenergic; Wistar; alpha/*drug effects/physiology; Oxytocin/drug effects/*physiology
In this report, a series of four experiments was performed to evaluate the relationship between the olfactory bulb norepinephrine system and intra-olfactory bulb infusion of oxytocin in the preservation of social memory responses. The present data indicate that oxytocin exerts this preservation of social recognition through a specific, receptor-mediated mechanism within the olfactory bulb (experiment 1). The involvement of the olfactory bulb norepinephrine system is revealed by the demonstration that retrodialysis of oxytocin into the olfactory bulb increases norepinephrine release (experiment 4). Our data suggest that the increased output of olfactory bulb norepinephrine resulting from oxytocin appears to activate alpha-adrenoceptors to produce this preservation in recognition because infusions of clonidine into the olfactory bulb preserve recognition responses in a manner similar to that observed with oxytocin (experiment 2). In addition, a co-infusion of oxytocin with phentolamine abolishes recognition responses (experiment 3). Accordingly, this model affords the opportunity to study neuropeptide-catecholamine interactions, link these interactions with a specific behavioural outcome and identify a novel function/site of action for oxytocin in the male.
Dluzen D E; Muraoka S; Engelmann M; Ebner K; Landgraf R
The European journal of neuroscience
2000
2000-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).