Abstract
The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 263 |
| Issue number | 1 32-1 |
| State | Published - 1992 |
| Externally published | Yes |
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Keywords
- differential regional vascular response
- hypoxia-induced vasoconstriction
- intact animal
ASJC Scopus subject areas
- Physiology
Cite this
Endothelium-derived relaxing factor in pulmonary and renal circulations during hypoxia. / Perrella, M. A.; Edell, E. S.; Krowka, M. J.; Cortese, Denis; Burnett, J. C.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 263, No. 1 32-1, 1992.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endothelium-derived relaxing factor in pulmonary and renal circulations during hypoxia
AU - Perrella, M. A.
AU - Edell, E. S.
AU - Krowka, M. J.
AU - Cortese, Denis
AU - Burnett, J. C.
PY - 1992
Y1 - 1992
N2 - The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.
AB - The pulmonary and renal vasculatures, in contrast to the systemic vasculature, constrict during hypoxia. The endothelium has been implicated in mediating these vascular responses to acute hypoxia via the production of endothelium-derived vasoactive factors. The present study, performed in anesthetized dogs, was designed to investigate the role of endothelium- derived relaxing factor (EDRF) to attenuate the vasoconstrictor response of the pulmonary and renal circulations during acute hypoxia. In response to hypoxia, pulmonary (2.2 ± 0.3 to 4.5 ± 0.6 mmHg · l-1 · min) and renal (0.60 ± 0.07 to 0.90 ± 0.14 mmHg · ml-1 · min) vascular resistances increased. Inhibition of endogenous EDRF with N(G)-monomethyl-L-arginine resulted in similar increases in pulmonary (3.0 ± 0.1 to 4.8 ± 0.4 mmHg · l-1 · min) and renal (0.67 ± 0.07 to 0.90 ± 0.09 mmHg · ml-1 · min) vascular resistances as in hypoxia. However, in the presence of both hypoxia and EDRF inhibition, an exaggerated pulmonary vascular response was observed (2.2 ± 0.2 to 7.4 ± 0.9 mmHg · l-1 · min), in contrast to the renal vascular response to EDRF inhibition during hypoxia (0.61 ± 0.05 to 0.95 ± 0.10 mmHg · ml-1 · min), which was not different from hypoxia or EDRF inhibition individually. The endothelium-derived contracting factor endothelin, which modestly increased during hypoxia (11.7 ± 1.9 to 15.6 ± 2.4 pg/ml), may also contribute to this vasoconstrictive response to hypoxia. This study suggests in the intact animal that EDRF serves to oppose the pulmonary vasoconstrictor response to hypoxia and further characterizes the role of endothelium-derived factors in the regulation of vascular function during hypoxia.
KW - differential regional vascular response
KW - hypoxia-induced vasoconstriction
KW - intact animal
UR - http://www.scopus.com/inward/record.url?scp=0026740607&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026740607&partnerID=8YFLogxK
M3 - Article
C2 - 1636793
AN - SCOPUS:0026740607
VL - 263
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
SN - 0193-1849
IS - 1 32-1
ER -