EFFECT OF CHRONIC HYPOXIA ON RAT PULMONARY RESISTANCE VESSELS - VASODILATATION BY ATRIAL-NATRIURETIC-PEPTIDE

被引:35
作者
ROGERS, TK [1 ]
STEWART, AG [1 ]
MORICE, AH [1 ]
机构
[1] UNIV SHEFFIELD,DEPT MED,SHEFFIELD S10 2TN,S YORKSHIRE,ENGLAND
关键词
ANOXIA; ATRIAL NATRIURETIC PEPTIDE; CHRONIC HYPOXIA; MICROCIRCULATION; PROSTAGLANDIN-F2-ALPHA; PULMONARY ARTERY; PULMONARY CIRCULATION; SMALL-VESSEL MYOGRAPHY; VASOCONSTRICTOR; VASODILATOR;
D O I
10.1042/cs0830723
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
1. We have investigated the vasoreactivity of isolated pulmonary resistance vessels of rats after acclimatization to chronic hypoxia in a normobaric, hypoxic chamber. Vasoconstriction, in response to KCl and prostaglandin F2alpha, and vasodilatation, in response to atrial natriuretic peptide, were studied isometrically in a small-vessel myograph. Resting tensions were set to simulate transmural pressures of 17.5 mmHg or 35 mmHg. 2. There were no significant differences between intergroup internal vessel diameters or maximal contractile responses to either agonist. Both control and chronically hypoxic vessels generated significantly greater active contractions at 35 mmHg than at 17.5 mmHg. There were significant positive correlations between vessel diameter and maximum contractility for both control and chronically hypoxic vessels, but when contraction was expressed as equivalent transmural pressure no correlation existed. 3. There was a significant increase in potency (as measured by the concentration necessary to produce 50% of the maximum response) of KCl in chronically hypoxic vessels compared with control vessels at 35 mmHg, but not at 17.5 mmHg. In contrast, the potency of prostaglandin F2alpha was significantly increased in chronically hypoxic vessels at 17.5 mmHg, but not at 35 mmHg. Thus the change in contractile responses of vessels from chronically hypoxic animals, in terms of maximal response and potency, is dependent on both resting pressure and agonist used. 4. After exposure to chronic hypoxia, atrial natriuretic peptide induced significantly greater maximal relaxation of pulmonary resistance vessels at both resting pressures, but its potency was unaffected.
引用
收藏
页码:723 / 729
页数:7
相关论文
共 23 条
  • [1] ADAMS SP, 1987, ENDOCRIN METAB CLIN, V16, P1
  • [2] ARAI H, 1988, BIOCHEM BIOPH RES CO, V148, P239
  • [3] BEVAN J A, 1988, P55
  • [4] MICROPUNCTURE MEASUREMENT OF LUNG MICRO-VASCULAR PRESSURE DURING 5-HT INFUSION
    BHATTACHARYA, J
    NANJO, S
    STAUB, NC
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1982, 52 (03) : 634 - 637
  • [5] DIETZ JR, 1984, AM J PHYSIOL, V247, P1093
  • [6] ATRIAL STRETCH, NOT PRESSURE, IS THE PRINCIPAL DETERMINANT CONTROLLING THE ACUTE RELEASE OF ATRIAL NATRIURETIC FACTOR
    EDWARDS, BS
    ZIMMERMAN, RS
    SCHWAB, TR
    HEUBLEIN, DM
    BURNETT, JC
    [J]. CIRCULATION RESEARCH, 1988, 62 (02) : 191 - 195
  • [7] RESOLUTION OF PULMONARY-HYPERTENSION AND OTHER FEATURES INDUCED BY CHRONIC HYPOXIA IN RATS DURING COMPLETE AND INTERMITTENT NORMOXIA
    HERGET, J
    SUGGETT, AJ
    LEACH, E
    BARER, GR
    [J]. THORAX, 1978, 33 (04) : 468 - 473
  • [8] GROWTH OF HEART AND LUNGS IN HYPOXIC RODENTS - MODEL OF HUMAN HYPOXIC DISEASE
    HUNTER, C
    BARER, GR
    SHAW, JW
    CLEGG, EJ
    [J]. CLINICAL SCIENCE AND MOLECULAR MEDICINE, 1974, 46 (03): : 375 - &
  • [9] A COMPARISON OF THE VASODILATOR RESPONSES TO ATRIAL PEPTIDES IN THE PULMONARY AND RENAL-ARTERIES OF THE PIG INVITRO
    JANSEN, TLTA
    MORICE, AH
    BROWN, MJ
    [J]. BRITISH JOURNAL OF PHARMACOLOGY, 1987, 91 (03) : 687 - 691
  • [10] ATRIAL NATRIURETIC PEPTIDE LOWERS PULMONARY ARTERIAL-PRESSURE IN HYPOXIA-ADAPTED RATS
    JIN, H
    YANG, RH
    THORNTON, RM
    CHEN, YF
    JACKSON, R
    OPARIL, S
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1988, 65 (04) : 1729 - 1735