Chemical form of dietary L-carnitine affects plasma but not tissue carnitine concentrations in male Sprague-Dawley rats.

In Experiment 1, rats (n = 54) were randomly assigned to control or one of the four sources of l-Carnitine supplemented at either 100 or 200 micromol/kg/day and were allowed to acclimate for 14 days. Following a 12-h fast, plasma samples were obtained at 0, 5, 10, 15, 30, 60, 120, 240, 480 and 720 min after l-Carnitine feeding and assayed for free l-Carnitine concentration. Plasma-free l-Carnitine levels were affected by time after treatment intake (p < 0.0001) and l-Carnitine source (p < 0.0001). The time x source interaction was not statistically significant (p = 0.99). In Experiment 2, rats (n = 54) were randomly assigned to control or one of the four sources of l-Carnitine at either 100 or 200 micromol/kg/day and were acclimated as in experiment 1. Rats were sacrificed 120 min after feeding. Samples of liver and skeletal muscle were obtained and assayed for free l-Carnitine concentration. Neither skeletal muscle (p = 0.44) or liver (p = 0.59) tissue concentrations of l-Carnitine were affected by any l-Carnitine source as compared with the control. We conclude that some differences exist in plasma concentrations of free l-Carnitine following ingestion of different chemical forms of l-Carnitine. It is unclear if these differences in the circulating concentration of free l-Carnitine translate into any physiological differences for the animal. In this study, chemical form of l-Carnitine had no effect on skeletal muscle or liver tissue concentrations of l-Carnitine in young male Wistar rats.

Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity.

Acutely increasing peripheral angiotensin II (ANG II) reduces the maximum renal sympathetic nerve activity (RSNA) observed at low mean arterial blood pressures (MAPs). We postulated that this observation could be explained by the action of ANG II to acutely increase arterial blood pressure or increase circulating arginine vasopressin (AVP). Sustained increases in MAP and increases in circulating AVP have previously been shown to attenuate maximum RSNA at low MAP. In conscious rabbits pretreated with an AVP V1 receptor antagonist, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng x kg(-1) x min(-1)) on the relationship between MAP and RSNA when the acute pressor action of ANG II was left unopposed with that when the acute pressor action of ANG II was opposed by a simultaneous infusion of sodium nitroprusside (SNP). Intravenous infusion of ANG II resulted in a dose-related attenuation of the maximum RSNA observed at low MAP. When the acute pressor action of ANG II was prevented by SNP, maximum RSNA at low MAP was attenuated, similar to that observed when ANG II acutely increased MAP. In contrast, intravertebral infusion of ANG II attenuated maximum RSNA at low MAP significantly more than when administered intravenously. The results of this study suggest that ANG II may act within the central nervous system to acutely attenuate the maximum RSNA observed at low MAP.

Angiotensin II modulation of the arterial baroreflex: role of the area postrema.

1. Resetting the operating point of the arterial baroreflex appears to be an important factor involved in determining the level of sympathetic outflow. 2. Substantial data indicate that circulating angiotensin (Ang)II can reset the arterial baroreflex to higher operating pressures. 3. This action of AngII to increase the level of sympathetic nervous system outflow relative to blood pressure may contribute to elevated mean arterial pressure (MAP) during AngII hypertension, as well as to the maintenance of MAP during low sodium states. 4. In most instances, the resetting observed during elevated peripheral AngII is dependent on the area postrema (AP). 5. Although the central mechanisms by which the arterial baroreflex resets to different operating pressures remain to be completely defined, the AP may provide a separate mechanism whereby humoral factors can modulate the operating point of the arterial baroreflex.