Literature DB >> 7028623

Effect of intracerebroventricular captopril on vasopressin and blood pressure in spontaneously hypertensive rats.

J T Crofton, R W Rockhold, L Share, B C Wang, Z P Horovitz, M Manning, W H Sawyer.   

Abstract

In conscious, unrestrained spontaneously hypertensive rats (SHR), mean arterial blood pressure (MAP) increased from a pretreatment value of 150 +/- 4 to 179 +/- 7mm Hg within 10 min (p less than 0.01) following an intracerebroventricular (i.c.v.) injection of captopril (2 mg/kg body weight), and the plasma vasopressin concentration was increased eightfold (p less than 0.01). MAP than fell to 131 +/- 5 mm Hg at 120 minutes (p less than 0.01), and plasma vasopressin concentration returned to pretreatment levels. The initial increase in MAP was due in large part to increased plasma vasopressin levels since this increase was reduced 50% by pre-treatment with a specific antagonist of the pressor action of vasopressin. The reduction in MAP at 120 minutes in captopril-treated rats may been nonspecific, since a similar effect was observed in SHR given an i.c.v. injection of a control solution. In (Wistar-Kyoto) WKY rats, i.c.v. captopril was without a statistically significant effect on MAP, but the plasma vasopressin concentration increased three-fold (p less than 0.01). These findings may reflect an increased sensitivity of the control system for vasopressin release in the SHR.

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Year:  1981        PMID: 7028623     DOI: 10.1161/01.hyp.3.6_pt_2.ii-71

Source DB:  PubMed          Journal:  Hypertension        ISSN: 0194-911X            Impact factor:   10.190


  1 in total

1.  Neuron-specific (pro)renin receptor knockout prevents the development of salt-sensitive hypertension.

Authors:  Wencheng Li; Hua Peng; Eamonn P Mehaffey; Christie D Kimball; Justin L Grobe; Jeanette M G van Gool; Michelle N Sullivan; Scott Earley; A H Jan Danser; Atsuhiro Ichihara; Yumei Feng
Journal:  Hypertension       Date:  2013-11-18       Impact factor: 10.190

  1 in total

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