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Biomedical subjects

R Boucher

Publications and source records attributed to R Boucher.

209 records · Page 12Linked to original sources

Contribution of the sympathetic nervous system to the centrally-induced pressor action of angiotensin II in rats.

1. Angiotensin II (ANG II) may increase blood pressure by central nervous system mechanisms. The involvement of the sympathetic nervous system in the centrally-induced pressor effect of ANG II in the rat was investigated. 2. Plasma noradrenaline concentrations, measured as an index of sympathetic nervous system activity, increased after intracerebroventricular (i.c.v.) injection of pressor doses of ANG II, both in normotensive and in spontaneously hypertensive rts. 3. To assess the functional significance of this, the sympathetic nervous system was inhibited by phentolamine, reserpine, and guanethidine. In phentolamine-infused rats, low doses of i.c.v. ANG II elicited a blood pressure decrease, but at maximal pressor doses, no difference between phentolamine-treated and control rats was observed. In reserpinized rats, the central pressor effect of ANG II was greater than in controls. Guanethidine pretreatment did not affect the blood pressure response to i.c.v. injected ANG II. 4. It is concluded that the central pressor effects of ANG II are accompanied by a stimulation of the sympathetic nervous system. In the rat, this stimulation may be functionally important for the initial phase of the central pressor action. This could not be established for the maximal pressor responses.

Angiotensin II↗

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

The effects of dietary sodium on the central actions of angiotensin II (AII) and on 125I-AII binding to brain membranes were investigated in rats fed a low-sodium or control diet and implanted with a permanent cannula into the lateral cerebral ventricle. Blood pressure (BP) responses to AII injections intracerebroventricularly (i.v.t.) were blunted in sodium-deficient rats compared with controls. The BP increases in response to i.v.t.-injected Carbachol were the same in the two groups. In sodium-depleted rats, water intake was lower than in controls after AII given i.v.t.; higher after 1.5% NaCl i.v.t.; and unchanged after Carbachol i.v.t. The pressor response to AII given i.v.t. was higher in spontaneously hypertensive rats (SHR) than Wistar-Kyoto (WKY) control rats. This hyperresponsiveness to central AII was abolished by feeding a low-sodium diet. Specific 125I-AII binding in vitro to brain membranes was consistently lower in sodium-depleted rats. The results suggest that sodium depletion modifies the central actions of AII. This may be related in part to changes in the binding properties of AII receptors in the brain.

Angiotensin II↗

Purification of tonin by affinity chromatography.

Tonin has been purified from rat submaxillary glands. The purification procedure included affinity chromatography on Sepharose 4B coupled to antitonin followed by DEAE chromatography and gel filtration on Sephadex G-100. Homogeneity of the purified enzyme was confirmed by Sephadex G-100 gel filtration, disc electrophoresis, and isoelectric focusing on polyacrylamide gel, immunodiffusion, and immunoelectrophoresis. The tonin was purified 11.5-fold, with 35% recovery. The purified tonin has full enzymatic or immunological activity.

Animals↗