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Role of Alpha‐adrenergic Inputs to PVN in the Cardiovascular Responses to Acute Hypoxia
Author(s) -
Beig Irfan,
Mifflin Steve
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.867.6
Subject(s) - prazosin , idazoxan , endocrinology , medicine , phentolamine , hypoxia (environmental) , adrenergic antagonist , heart rate , catecholaminergic , mean arterial pressure , antagonist , anesthesia , blood pressure , propranolol , catecholamine , chemistry , receptor , organic chemistry , oxygen
Previous studies indicate that catecholaminergic neurons in nucleus of solitary tract (NTS) contribute to intermittent hypoxia hypertension and that the hypothalamic paraventricular nucleus (PVN) plays a role in the cardiovascular response to hypoxia. The present study was designed to examine the role of alpha‐adrenergic receptors in PVN in the cardiovascular responses to acute hypoxia. Rats were anesthetized with chloralose and urethane and mean arterial pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA) and end tidal CO2 measured. The rat was placed in a stereotaxic frame for microinjections in PVN. After paralysis with gallamine, the rat was artificially ventilated with room air. Hypoxia was induced by ventilating the animal with 10% O2 for 30 seconds. When the parameters returned to the baseline, bilateral injections of vehicle or either α1 antagonist prazosin (500nmol) or α2 antagonist idazoxan (5nmol) were made in PVN and responses to hypoxia observed after 20 minutes. At the end of experiment brain was removed for localization of microinjection site. Hypoxia increased MAP with no change in HR or RSNA. The increase in MAP induced by systemic hypoxia was significantly blunted by bilateral administration of either prazosin (36 ± 3mmHg to 19 ± 4mmHg, n=11) or idazoxan (36 ± 2mmHg to 25 ± 5mmHg, n=10) in PVN. Changes in baseline blood pressure were not significant following prazosin (−2 ± 4mmHg) or idazoxan (0 ± 3mmHg). The results suggest that catecholaminergic inputs to PVN play a role in acute hypoxia induced increases in MAP. Support or Funding Information Supported by PO1 HL88052