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J Physiol Volume 584, Number 1, 321-332, October 1, 2007 DOI: 10.1113/jphysiol.2007.138206
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INTEGRATIVE

Effects of the nitric oxide synthase inhibitor L-NMMA on cerebrovascular and cardiovascular responses to hypoxia and hypercapnia in humans

 Kojiro Ide1,4, Matthew Worthley3,4, Todd Anderson3,4 and Marc J. Poulin1,2,4,5

1 Departments of Physiology & Biophysics
2 Clinical Neurosciences
3 Cardiac Sciences and Libin Cardiovascular Institute, Faculties of
4 Medicine
5 Kinesiology, University of Calgary, Calgary Alberta, T2N 4 N1, Canada

Cerebral blood flow is highly sensitive to alterations in the partial pressures of O2 and CO2 (PO2 and PCO2, respectively) in the arterial blood. In humans, the extent to which nitric oxide (NO) is involved in this regulation is unclear. We hypothesized that the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA), attenuates the sensitivity of middle cerebral artery blood velocity (Formula ) to isocapnic hypoxia (end-tidal PO2 = 50 Torr) and euoxic hypercapnia (end-tidal PCO2 = +9 Torr above resting values) in 10 volunteers (age, 28.7 ± 1.3 years; height, 179.2 ± 2.4 cm; weight, 78.0 ± 3.7 kg; mean ± S.E.M.). The techniques of transcranial Doppler ultrasound and dynamic end-tidal forcing were used to measure Formula , and control end-tidal PO2 and end-tidal PCO2, respectively. At baseline (isocapnic euoxia), following intravenous administration of L-NMMA, mean arterial blood pressure (MAP) increased (76.3 ± 7.3 to 86.2 ± 9.4 mmHg) and heart rate (HR) decreased (59.5 ± 9.0 to 55.2 ± 9.5 beats min–1) but Formula was unchanged. Hypoxia-induced increases in MAP, HR and Formula were similar with and without L-NMMA (5.0 ± 0.7 versus 7.1 ± 1.0 mmHg, 11.5 ± 1.4 versus 12.4 ± 1.5 beats min–1, 6.5 ± 0.8 versus 6.6 ± 0.8 cm s–1 for {Delta}MAP, {Delta}HR and {Delta}Formula , respectively). Hypercapnia-induced increases in MAP, HR and Formula were similar with and without L-NMMA (7.4 ± 3.1 versus 8.1 ± 2.2 mmHg, 10.4 ± 4.6 versus 10.0 ± 4.2 beats min–1, 16.5 ± 1.5 versus 17.6 ± 1.5 cm s–1 for {Delta}MAP, {Delta}HR and {Delta}Formula , respectively) but the sensitivity of the Formula response at the removal of hypercapnia was attenuated with L-NMMA. In young healthy humans, pharmacological blockade of nitric oxide synthesis does not affect the increases in cerebral blood flow with hypoxia and hypercapnia, suggesting that nitric oxide is not required for the cerbrovascular responses to hypoxia and hypercapnia.

(Received 7 June 2007; accepted after revision 27 July 2007; first published online 2 August 2007)
Corresponding author M. J. Poulin: Department of Physiology & Biophysics, Faculty of Medicine, Heritage Medical Research Building, Room 212, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada. Email: poulin@ucalgary.ca






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