Stallone J N
Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272.
Am J Physiol. 1995 Jan;268(1 Pt 2):R40-9. doi: 10.1152/ajpregu.1995.268.1.R40.
Deoxycorticosterone acetate (DOCA)-salt hypertension develops to a greater extent in male (M) than in female (F) rats. To determine the role of the vasculature, reactivity to arginine vasopressin (AVP) and prostanoid output were examined in the isolated perfused mesenteric vasculature of hypertensive (HT) and normotensive-control (NTC) M and F rats after acute (1-wk) and chronic (4-wk) DOCA-salt treatment. Systolic blood pressure was significantly higher in M than in F HT rats (187 +/- 3 vs. 151 +/- 3 mmHg after 4 wk; P < 0.02). After acute treatment, vascular reactivity to AVP (maximal perfusion pressure) in HT was elevated in M (181 +/- 18 mmHg; P < 0.02) but not in F (135 +/- 6 mmHg) compared with NTC (90 +/- 6 mmHg, M vs. 119 +/- 5 mmHg, F). After chronic treatment, vascular reactivity to AVP in HT was elevated in both sexes (P < 0.02), although more in F (175 +/- 13 mmHg) than in M (141 +/- 11 mmHg). In contrast, vascular responsiveness to phenylephrine did not differ significantly between M and F NTC or HT preparations after either acute or chronic treatment. Sex differences in basal and AVP-induced 6-ketoprostaglandin (6-keto-PG) F1 alpha and PGE2 output by HT and NTC vasculature were reciprocal to sex differences in the vasoconstriction responses to AVP. After acute treatment, AVP-stimulated 6-keto-PGF1 alpha output by HT was elevated slightly in F (33.6 +/- 1.7 ng/3 min; P < or = 0.02) but not in M (49.9 +/- 4.3 ng/3 min) compared with NTC (23.5 +/- 2.6 ng/3 min, F vs. 34.7 +/- 4.9 ng/3 min, M). After chronic treatment, output by HT was enhanced in both sexes (P < or = to 0.02), although more in M (109 +/- 15.4 ng/3 min) than in F (68 +/- 6.6 ng/3 min)> These findings suggest that sex differences in the relative balance between AVP-induced vasoconstriction and vasodilatory prostanoid release may contribute to male-female differences in mesenteric vascular reactivity to AVP in NT and that disturbances in this balance may be responsible, at least in part, for the sex- and time-dependent changes in reactivity to AVP observed during the development of DOCA-salt hypertension.
醋酸脱氧皮质酮（DOCA）-盐性高血压在雄性（M）大鼠中比在雌性（F）大鼠中发展得更为严重。为了确定血管系统的作用，在急性（1周）和慢性（4周）DOCA-盐处理后，对高血压（HT）和正常血压对照（NTC）的雄性和雌性大鼠的离体灌注肠系膜血管系统中对精氨酸加压素（AVP）的反应性和前列腺素输出进行了检测。雄性HT大鼠的收缩压显著高于雌性HT大鼠（4周后分别为187±3 mmHg和151±3 mmHg；P<0.02）。急性处理后，与NTC相比，HT大鼠中雄性对AVP的血管反应性（最大灌注压）升高（181±18 mmHg；P<0.02），而雌性未升高（135±6 mmHg）（雄性NTC为90±6 mmHg，雌性NTC为119±5 mmHg）。慢性处理后，HT大鼠中两性对AVP的血管反应性均升高（P<0.02），尽管雌性升高幅度更大（175±13 mmHg），高于雄性（141±11 mmHg）。相反，无论是急性还是慢性处理后，雄性和雌性NTC或HT制剂对去氧肾上腺素的血管反应性均无显著差异。HT和NTC血管系统中基础和AVP诱导的6-酮前列腺素（6-酮-PG）F1α和PGE2输出的性别差异与对AVP的血管收缩反应的性别差异相反。急性处理后，与NTC相比，HT大鼠中AVP刺激的6-酮-PGF1α输出在雌性中略有升高（33.6±1.7 ng/3 min；P≤0.02），而在雄性中未升高（49.9±4.3 ng/3 min）（雌性NTC为23.5±2.6 ng/3 min，雄性NTC为34.7±4.9 ng/3 min）。慢性处理后，HT大鼠中两性的输出均增强（P≤0.02），尽管雄性增强幅度更大（109±15.4 ng/3 min），高于雌性（68±6.6 ng/3 min）。这些发现表明，AVP诱导的血管收缩和血管舒张性前列腺素释放之间相对平衡的性别差异可能导致正常血压状态下肠系膜血管对AVP反应性的雌雄差异，并且这种平衡的紊乱可能至少部分地导致了DOCA-盐性高血压发展过程中观察到的对AVP反应性的性别和时间依赖性变化。
