McCarron D A, Ellison D H, Anderson S
Am J Physiol. 1984 Jan;246(1 Pt 2):F96-100. doi: 10.1152/ajprenal.1984.246.1.F96.
Parathyroid hormone's cardiovascular effects were assessed in a model of experimental hypertension with known abnormalities of calcium metabolism. Mean arterial pressure (MAP) changes and serum ionized calcium responses were measured in the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto (WKY), following injections of synthetic human PTH 1-34. Six 22-wk-old SHR and six WKY were given intra-arterial serial injections (0.1-100 micrograms/kg) of hPTH 1-34. Both the SHR (P less than 0.001) and WKY (P less than 0.001) demonstrated log dose-dependent hypotensive responses that were maximal at 1 min, with recovery occurring between 15 and 30 min. The slopes, however, of the dose-response curves differed (P less than 0.01). The SHR experienced a greater maximal delta MAP [-93.7 +/- 2.4 (SHR) vs. -71.2 +/- 1.6 mmHg (WKY), P less than 0.01]. Furthermore, the duration of the hypotensive action of hPTH 1-34 was significantly longer (P less than 0.001) in the SHR. Even when corrected for base-line MAP the SHR demonstrated a significant (P = 0.025) enhancement of this vasodilator response at doses of 5 micrograms/kg and greater at time intervals between 3 and 9 min after injection. A transient decrease [2.25 +/- 0.10 (pre) vs. 2.17 +/- 0.11 meq/liter (1 min post), P less than 0.01] in serum ionized calcium occurred at 1 min. We conclude that hPTH 1-34 is a potent vasoactive peptide in both the normotensive WKY and the SHR. The greater maximal hypotensive response to hPTH 1-34 and the prolongation of this cardiovascular effect in the SHR may be an additional manifestation of this experimental animal's acknowledged abnormalities of cellular membrane calcium and phospholipid metabolism.
在一个已知钙代谢异常的实验性高血压模型中评估了甲状旁腺激素的心血管效应。在自发性高血压大鼠（SHR）及其血压正常的对照Wistar-Kyoto（WKY）中，注射合成人甲状旁腺激素1-34后，测量平均动脉压（MAP）变化和血清离子钙反应。给6只22周龄的SHR和6只WKY进行动脉内连续注射（0.1 - 100微克/千克）的hPTH 1-34。SHR（P < 0.001）和WKY（P < 0.001）均表现出对数剂量依赖性降压反应，在1分钟时最大，在15至30分钟之间恢复。然而，剂量 - 反应曲线的斜率不同（P < 0.01）。SHR经历了更大的最大MAP变化[-93.7 ± 2.4（SHR）对 -71.2 ± 1.6 mmHg（WKY），P < 0.01]。此外，hPTH 1-34在SHR中的降压作用持续时间明显更长（P < 0.001）。即使校正基线MAP后，SHR在注射后3至9分钟的时间间隔内，在5微克/千克及更高剂量时仍表现出这种血管舒张反应的显著增强（P = 0.025）。血清离子钙在1分钟时出现短暂下降[2.25 ± 0.10（注射前）对2.17 ± 0.11毫当量/升（注射后1分钟），P < 0.01]。我们得出结论，hPTH 1-34在血压正常的WKY和SHR中都是一种有效的血管活性肽。SHR对hPTH 1-34更大的最大降压反应以及这种心血管效应的延长可能是这种实验动物公认的细胞膜钙和磷脂代谢异常的另一种表现。
