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Effect of nitric oxide synthase inhibition on cardiorespiratory responses in the conscious rat.
J Appl Physiol (1985). 1996 Nov; 81(5):2068-77.JA

Abstract

Nitric oxide synthase (NOS) blockade was used to test the cardioventilatory responses to hypercapnia and hypoxia in freely behaving animals. Chronically instrumented adult Sprague-Dawley rats were studied before and after intravenous administration of either 100 mg/kg of NG-nitro-L-arginine methyl ester (L-NAME), a nonspecific NOS blocker, or 10 mg/kg of S-methyl-L-thiocitrulline (SMTC), a selective neural NOS inhibitor. L-NAME injection induced sustained blood pressure (BP) elevation with transient tachycardia and increased minute ventilation (VE), which returned to baseline within minutes. SMTC elicited similar, although transient, BP increases; however, heart rate and VE decreased. L-NAME and SMTC did not modify overall steady-state hypercapnic responses. In control conditions, hypoxia induced early VE increases with further VE enhancements at 30 min. L-NAME increased the early VE response to 10% O2 but induced late VE reductions in hypoxia. SMTC did not change early VE responses but induced marked reductions in the later VE hypoxic responses. In control animals, hypoxia induced a significant heart rate increase. This increase was absent during the early response after SMTC and was followed in both L-NAME- and SMTC-treated animals by significant heart rate reductions to values below room air. Similarly, the sustained BP response to hypoxia in control animals was absent after administration of NOS inhibitors. These findings suggest that NOS activity exerts excitatory influences on respiration and cardiac chronotropy and sustained vasomotor tone during hypoxia. We speculate that NOS-mediated mechanisms may play an important role in hypoxia-induced ventilatory roll-off during wakefulness.

Authors+Show Affiliations

Constance S. Kaufman Pediatric Pulmonary Research Laboratory, Department of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8941531

Citation

Gozal, D, et al. "Effect of Nitric Oxide Synthase Inhibition On Cardiorespiratory Responses in the Conscious Rat." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 81, no. 5, 1996, pp. 2068-77.
Gozal D, Torres JE, Gozal YM, et al. Effect of nitric oxide synthase inhibition on cardiorespiratory responses in the conscious rat. J Appl Physiol (1985). 1996;81(5):2068-77.
Gozal, D., Torres, J. E., Gozal, Y. M., & Littwin, S. M. (1996). Effect of nitric oxide synthase inhibition on cardiorespiratory responses in the conscious rat. Journal of Applied Physiology (Bethesda, Md. : 1985), 81(5), 2068-77.
Gozal D, et al. Effect of Nitric Oxide Synthase Inhibition On Cardiorespiratory Responses in the Conscious Rat. J Appl Physiol (1985). 1996;81(5):2068-77. PubMed PMID: 8941531.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of nitric oxide synthase inhibition on cardiorespiratory responses in the conscious rat. AU - Gozal,D, AU - Torres,J E, AU - Gozal,Y M, AU - Littwin,S M, PY - 1996/11/1/pubmed PY - 1996/11/1/medline PY - 1996/11/1/entrez SP - 2068 EP - 77 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J Appl Physiol (1985) VL - 81 IS - 5 N2 - Nitric oxide synthase (NOS) blockade was used to test the cardioventilatory responses to hypercapnia and hypoxia in freely behaving animals. Chronically instrumented adult Sprague-Dawley rats were studied before and after intravenous administration of either 100 mg/kg of NG-nitro-L-arginine methyl ester (L-NAME), a nonspecific NOS blocker, or 10 mg/kg of S-methyl-L-thiocitrulline (SMTC), a selective neural NOS inhibitor. L-NAME injection induced sustained blood pressure (BP) elevation with transient tachycardia and increased minute ventilation (VE), which returned to baseline within minutes. SMTC elicited similar, although transient, BP increases; however, heart rate and VE decreased. L-NAME and SMTC did not modify overall steady-state hypercapnic responses. In control conditions, hypoxia induced early VE increases with further VE enhancements at 30 min. L-NAME increased the early VE response to 10% O2 but induced late VE reductions in hypoxia. SMTC did not change early VE responses but induced marked reductions in the later VE hypoxic responses. In control animals, hypoxia induced a significant heart rate increase. This increase was absent during the early response after SMTC and was followed in both L-NAME- and SMTC-treated animals by significant heart rate reductions to values below room air. Similarly, the sustained BP response to hypoxia in control animals was absent after administration of NOS inhibitors. These findings suggest that NOS activity exerts excitatory influences on respiration and cardiac chronotropy and sustained vasomotor tone during hypoxia. We speculate that NOS-mediated mechanisms may play an important role in hypoxia-induced ventilatory roll-off during wakefulness. SN - 8750-7587 UR - https://www.unboundmedicine.com/medline/citation/8941531/Effect_of_nitric_oxide_synthase_inhibition_on_cardiorespiratory_responses_in_the_conscious_rat_ L2 - https://journals.physiology.org/doi/10.1152/jappl.1996.81.5.2068?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -