Role of vasoconstrictors in the systemic hypertension of rats
acclimatized to hypoxia.
Moue, Yoshihiro, Peter G. Smith, Richard L. Clancy, and Norberto C.
Gonzalez.
Department of Physiology, University of Kansas Medical Center,
Kansas City, Kansas 66160-7401
APStracts 2:0295A, 1995.
Exposure to hypoxia (2-5 weeks) results in systemic hypertension in
rats and in humans. The possible mechanism(s) were investigated in
rats acclimatized (A) for 3 wks to barometric pressure 370 Torr, and
in non-acclimatized littermates (NA), by administering [alpha]
adrenergic (phentolamine, PHLM), angiotensin II (AII ANTAG), and
arginine-vasopressin (V1 ANTAG) receptor antagonists. Both A and NA
were studied in hypoxia (FIO2 0.10). Baseline mean arterial blood
pressure (MABP) was higher in A than in NA: 126 +/- 4 vs 101 +/- 2
mmHg (p<0.05). Neither AII nor V1 ANTAG influenced baseline
MABP; however, both contributed to MABP recovery after PHLM. After
simultaneous blockade of AII and V1, PHLM lowered MABP by 65 +/- 2
and 45 +/- 3 mmHg in A vs NA, respectively (p<0.05). After
combined blockade of the three systems, the smooth muscle relaxant
sodium nitroprusside (SNP) did not further modify MABP, which
remained higher in A. It is concluded that: 1. the hypertension in A
is partly due to a higher [alpha] adrenergic tone; 2. neither AII nor
AVP contribute to the hypertension, but participate in MABP control
after PHLM; 3. no other vasoconstrictor agents operate in either
group; 4. the higher MABP in A after SNP may reflect additional
hypertensive mechanisms.
Received 14 December 1994; accepted in final form 28 June 1995.
APS Manuscript Number A1274-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.