Hinojosa-Laborde C, Guerra P, Haywood J R
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764.
Hypertension. 1992 Jul;20(1):96-102. doi: 10.1161/01.hyp.20.1.96.
The contribution of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure was investigated in high sodium-fed rats 4 weeks after the induction of one-kidney, figure-8 renal wrap hypertension. Arterial pressure was significantly greater in renal-wrapped rats than in sham-operated animals. The contribution of the sympathetic nervous system was assessed functionally by measuring the arterial pressure response to ganglionic blockade and estimating the apparent rate of release of norepinephrine. The contribution of vasopressin was assessed by administration of the vascular antagonist d(CH2)5Tyr(Me)-AVP. Whole-animal vascular responsiveness and cardiac baroreceptor reflex sensitivity were determined by graded intravenous bolus injections of angiotensin II, vasopressin, and phenylephrine. Hypertensive rats demonstrated an exaggerated reduction in arterial pressure to autonomic blockade before and after blockade of vascular vasopressin receptors. There was a significant 27% increase in the apparent rate of release of norepinephrine into the plasma. Administration of d(CH2)5Tyr(Me)-AVP did not affect arterial pressure when given alone. However, after ganglionic blockade, inhibition of the vasopressin system elicited similar falls in blood pressure in both normotensive and hypertensive rats. Arterial pressure dose-response effects of phenylephrine, angiotensin II, and vasopressin were similar between renal-wrapped and sham-operated animals; however, cardiac baroreceptor reflex sensitivity was suppressed in the hypertensive rats. These studies indicate that the maintenance of arterial pressure in chronic, high sodium renal-wrap hypertension is associated with an augmented sympathetic nervous system function.
在诱导一侧肾脏、8字形肾包裹性高血压4周后的高钠喂养大鼠中，研究了交感神经系统和血管加压素对维持动脉血压的作用。肾包裹大鼠的动脉血压显著高于假手术动物。通过测量对神经节阻断的动脉血压反应并估计去甲肾上腺素的表观释放率，从功能上评估交感神经系统的作用。通过给予血管拮抗剂d(CH2)5Tyr(Me)-AVP评估血管加压素的作用。通过分级静脉推注血管紧张素II、血管加压素和去氧肾上腺素来测定全动物血管反应性和心脏压力感受器反射敏感性。高血压大鼠在血管加压素受体阻断前后对自主神经阻断的动脉血压降低均过度。血浆中去甲肾上腺素的表观释放率显著增加27%。单独给予d(CH2)5Tyr(Me)-AVP时不影响动脉血压。然而，在神经节阻断后，血管加压素系统的抑制在正常血压和高血压大鼠中均引起类似的血压下降。肾包裹大鼠和假手术动物对去氧肾上腺素、血管紧张素II和血管加压素的动脉血压剂量反应效应相似；然而，高血压大鼠的心脏压力感受器反射敏感性受到抑制。这些研究表明，慢性高钠肾包裹性高血压中动脉血压的维持与交感神经系统功能增强有关。
