Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 537, Issue 2, Pages 613-621Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1111/j.1469-7793.2001.00613.x
Keywords
-
Categories
Funding
- NCRR NIH HHS [RR-00585, M01 RR000585] Funding Source: Medline
- NHLBI NIH HHS [R01 HL046493, HL-46493] Funding Source: Medline
- NIA NIH HHS [R01 AG007004, AG07004] Funding Source: Medline
- NIDDK NIH HHS [DK-09826, F32 DK009826] Funding Source: Medline
- NINDS NIH HHS [NS-32352, N01NS32352] Funding Source: Medline
Ask authors/readers for more resources
1. Limb vascular beds exhibit a graded dilatation in response to hypoxia despite increased sympathetic vasoconstrictor nerve activity. We investigated the extent to which sympathetic vasoconstriction can mask hypoxic vasodilatation and assessed the relative contributions of beta -adrenergic and nitric oxide (NO) pathways to hypoxic vasodilatation. 2. We measured forearm blood flow responses (plethysmography) to isocapnic hypoxia (arterial saturation similar to 85%) in eight healthy men and women (18-26 years) after selective alpha -adrenergic blockade (phentolamine) of one forearm. Subsequently, we measured hypoxic responses after combined alpha- and beta -adrenergic blockade (phentolamine and propranolol) and after combined alpha- and beta -adrenergic blockade coupled with NO synthase inhibition (N-G-monomethyl-L-arginine, L-NMMA). 3. Hypoxia increased forearm vascular conductance by 49.0 +/- 13.5% after phentolamine (compared to +16.8 +/- 7.0% in the control arm without phentolamine, P < 0.05). After addition of propranolol, the forearm vascular conductance response to hypoxia was reduced by -50%, but dilatation was still present (+24.7 +/- 7.0 %, P < 0.05 vs. normoxia). NT hen L-NMMA was added, there was no further reduction in the forearm vascular conductance response to hypoxia (+28.2 +/- 4.0 %, P < 0.05 vs. normoxia). 4. Thus, selective regional -adrenergic blockade unmasked a greater hypoxic vasodilatation than occurs in the presence of functional Sympathetic nervous system responses to hypoxia. Furthermore, approximately half of the hypoxic vasodilatation in the forearm appears to be mediated by beta -adrenergic receptor-mediated pathways. Finally, since considerable dilatation persists in the presence of both beta -adrenergic blockade and NO synthase inhibition, it is likely that an additional vasodilator mechanism is activated by hypoxia in humans.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available