Mento P F, Wang H H, Sawyer W H
Proc Soc Exp Biol Med. 1984 Jan;175(1):58-63. doi: 10.3181/00379727-175-41766.
The roles of arginine vasopressin (AVP), the sympathetic nervous system, and the renin-angiotensin system in maintaining elevated blood pressure in established DOC-salt hypertension in rats were studied by injection of specific antagonists of these systems. The specific AVP antagonist dPVDAVP decreased blood pressure by 19 +/- 3 mm Hg in hypertensive rats and 6 +/- 2 mm Hg in control rats. In a different group of rats ganglionic blockade with chlorisondamine also caused a greater decrease in blood pressure in DOC-salt rats compared to controls (99 +/- 6 vs 58 +/- 4 mm Hg, respectively). In rats with autonomic ganglia blocked subsequent vasopressin antagonism decreased blood pressure 29 +/- 4 mm Hg in DOC-salt rats and 14 +/- 2 mm Hg in control rats. Converting enzyme inhibition with captopril in rats with autonomic ganglia blocked caused a lesser decrease in blood pressure in DOC-salt rats than in controls (8 +/- 2 vs 14 +/- 2 mm Hg, respectively). These results indicate that both AVP and the sympathetic nervous system contribute to the maintenance of DOC-salt hypertension. The renin-angiotension system appears to be relatively less important.
通过注射这些系统的特异性拮抗剂,研究了精氨酸加压素(AVP)、交感神经系统和肾素-血管紧张素系统在维持大鼠已形成的去氧皮质酮-盐性高血压中血压升高方面的作用。特异性AVP拮抗剂dPVDAVP使高血压大鼠的血压降低19±3 mmHg,使对照大鼠的血压降低6±2 mmHg。在另一组大鼠中,与对照组相比,用氯异吲哚铵进行神经节阻断也使去氧皮质酮-盐性大鼠的血压下降幅度更大(分别为99±6 mmHg和58±4 mmHg)。在自主神经节被阻断的大鼠中,随后进行的加压素拮抗作用使去氧皮质酮-盐性大鼠的血压降低29±4 mmHg,使对照大鼠的血压降低14±2 mmHg。在自主神经节被阻断的大鼠中,用卡托普利抑制转化酶导致去氧皮质酮-盐性大鼠的血压下降幅度小于对照组(分别为8±2 mmHg和14±2 mmHg)。这些结果表明,AVP和交感神经系统都有助于维持去氧皮质酮-盐性高血压。肾素-血管紧张素系统似乎相对不太重要。