Abstract
Female rats treated with deoxycorticosterone acetate (DOCA) and salt do not get as hypertensive as male DOCA-salt treated rats. The adrenal gland contributes to the development and maintenance of DOCA-salt hypertension in male rats. However, little is known about adrenal medullary function in DOCA-salt hypertensive female rats. This study tested the hypothesis that bilateral removal of the adrenal medullae would result in a greater fall in blood pressure in male DOCA-salt compared to female DOCA-salt rats. Five weeks after initiating DOCA-salt treatment, average 24 hour mean arterial pressure (MAP) in female rats was significantly attenuated compared to male rats (142 +/- 4 versus 1686 +/- 4 versus 168 +/- 6 mm Hg, respectively). Female DOCA-salt rats consumed significantly more saline per day than male DOCA-salt rats (22.3 +/- 1.8 versus 33.4 +/- 1.8 mL/100 grams body weight, respectively). Following adrenal medullectomy, DOCA-salt males experienced a significant decrease in MAP during the dark period after surgery (182 +/- 4 to 154 +/- 4 mm Hg) that was not observed in female DOCA-salt rats (150 +/- 6 to 135 +/- 3 mm Hg). In the following light period, MAP remained significantly decreased when compared to the light period before surgery in DOCA-salt male (171 +/- 4 to 156 +/- 4 mm Hg), while no effect was observed in DOCA-salt female rats. Adrenal medullectomy significantly increased heart rate (HR) in all groups for 12 days. Male sham and DOCA-salt rats had significantly higher catecholamine content in the adrenal medulla than female sham and DOCA-salt rats, respectively. These data suggest that the adrenal medullae contribute more to the maintenance of blood pressure in DOCA-salt hypertension in male rats than female rats. (Hypertension. 1998;31[part 2]:403-408.). © 1998 Lippincott Williams & Wilkins, Inc.
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CITATION STYLE
Lange, D. L., Haywood, J. R., & Hinojosa-Laborde, C. (1998). Role of the Adrenal Medullae in Male and Female DOCA-Salt Hypertensive Rats. Hypertension, 31(1), 403–408. https://doi.org/10.1161/01.HYP.31.1.403
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