Journal of Applied Physiology
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J Appl Physiol 97: 1032-1039, 2004. First published May 14, 2004; doi:10.1152/japplphysiol.00255.2004
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Effects of long-term captopril and L-arginine treatment on ventilation and blood pressure in obese male SHHF rats

E. H. Schlenker, C. K. Kost, Jr., and M. M. Likness

Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, Vermillion, South Dakota 57069

Submitted 10 March 2004 ; accepted in final form 12 May 2004

We investigated the effects of captopril (Cap) and L-arginine (Arg) on hypertension and cardiopulmonary function. Our hypothesis was that Cap therapy or Arg will improve cardiopulmonary risk factors for hypertension and hypoventilation in the obese spontaneously hypertensive heart failure rat, which is characterized by hypertension, obesity, and disorders of lipid and carbohydrate metabolism. For the first study, one group of rats received Cap in drinking water, and a second group received deionized water (DI). For the second study, rats were further subdivided. Some Cap-treated rats continued on this treatment, and the other half were now given DI to determine whether there would be residual effects of Cap treatment. A subgroup of rats who had received DI was then given Arg, whereas the rest remained on DI. In the first study, Cap-treated rats exhibited decreases in systolic and diastolic blood pressures, frequency of breathing, and minute ventilation, but ventilatory control was maintained. In contrast, blood pressures and relative ventilation to metabolism were higher in the DI-treated group. Removal of Cap increased blood pressure and decreased tidal volume while these rats maintained frequency. Although Arg-treated rats did not exhibit a decrease of blood pressure, ventilation was maintained in this group by preserving tidal volume. Thus Cap and Arg affected ventilation through different mechanisms independent of blood pressure.

spontaneously hypertensive heart failure rat; hypertension; metabolic syndrome X; ventilatory equivalent; frequency


Address for reprint requests and other correspondence: E. H. Schlenker, 414 E. Clark St., Div. of Basic Biomedical Sciences, Univ. of South Dakota School of Medicine, Vermillion, SD 57069 (E-mail: eschlenk{at}usd.edu).






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