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Articles in PresS, published online ahead of print November 1, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00309.2001
Submitted on April 17, 2001
Accepted on October 30, 2001
1 Psychiatry, University of Southern California (USC), Los Angeles, CA, USA; Neurology, University of Southern California (USC), Los Angeles, CA, USA; Research, Greater Los Angeles VA Healthcare System, Los Angeles, CA, USA
2 Research, Greater Los Angeles VA Healthcare System, Los Angeles, CA, USA; Physiology, University of California at Los Angeles (UCLA), Los Angeles, CA, USA
3 Physiology, University of California at Los Angeles (UCLA), Los Angeles, CA, USA; Cardiovascular Research Laboratory, University of California at Los Angeles (UCLA), Los Angeles, CA, USA
4 Center for Studies in Physics and Biology, Rockefeller University, New York, NY, USA
5 Molecular Pharmacology and Toxicology, University of Southern California (USC), Los Angeles, CA, USA
6 Cell and Neurobiology, University of Southern California (USC), Los Angeles, CA, USA; Molecular Pharmacology and Toxicology, University of Southern California (USC), Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: holschne{at}hsc.usc.edu.
The recent development of mice doubly deficient for monoamine-oxidase A and B has raised questions about the impact of these mutations on cardiovascular function, in so far as these animals demonstrate increased tissue levels of the vasoactive amines serotonin, norepinephrine, dopamine and phenylethylamine. We recorded femoral arterial pressures and electrocardiograms in adult MAO-A/B deficient mice during halothane/nitrous oxide anesthesia, as well as 30 minutes postoperatively. Both during anesthesia and recovery, systolic, diastolic and mean arterial pressures were 10-15 mm Hg lower in MAO-A/B deficient mice compared to normal controls (P<0.01). Mutants also showed a greater baroreceptor-mediated reduction in heart rate in response to hypertension following intravenous pulses of phenylephrine or angiotensin-II. Tachycardia elicited in response to hypotension following nitroprusside was greater in mutants than in controls. Heart rate responsiveness to changes in arterial pressure was abolished following administration of glycopyrrolate, with no differences in this phenomenon noted between genotypes. These data suggest that prevention of hypertension may occur in chronic states of catecholaminergic/indoleaminergic excess by increased gain of the baroreflex.
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