Effect of global and regional sympathetic blockade on arterial pressure during water deprivation in conscious rats.
Forty-eight hours of water deprivation (WD) in conscious rats results in a paradoxical increase in mean arterial pressure (MAP). Previous studies suggest this may be due to increased sympathetic nerve activity (SNA). However, this remains to be investigated in conscious, freely behaving animals. The purpose of this study was to determine, in conscious rats, the role of the sympathetic nervous system (SNS) in mediating WD-induced increases in MAP and to identify which vascular beds are targeted by increased SNA. Each rat was chronically instrumented with a radiotelemetry transmitter to measure MAP and heart rate (HR) and an indwelling venous catheter for plasma sampling and/or drug delivery. MAP and HR were continuously measured during a 2-day baseline period followed by 48 h of WD and then a recovery period. By the end of the WD period, MAP increased by ∼15 mmHg in control groups, whereas HR did not change significantly. Chronic blockade of α(1)/β(1)-adrenergic receptors significantly attenuated the WD-induced increase in MAP, suggesting a role for global activation of the SNS. However, the MAP response to WD was unaffected by selective denervations of the hindlimb, renal, or splanchnic vascular beds, or by adrenal demedullation. In contrast, complete adrenalectomy (with corticosterone and aldosterone replaced) significantly attenuated the MAP response to WD in the same time frame as α(1)/β(1)-adrenergic receptor blockade. These results suggest that, in conscious water-deprived rats, the SNS contributes to the MAP response and may be linked to release of adrenocortical hormones. Finally, this sympathetically mediated response is not dependent on increased SNA to one specific vascular bed.
The Graduate Program in Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Britta J
BJ
Veitenheimer
William C
WC
Engeland
Pilar A
PA
Guzman
Gregory D
GD
Fink
John W
JW
Osborn
D000302:Adrenal Cortex / Q000294:innervation / Q000502:physiology / Q000601:surgery; D000315:Adrenalectomy; D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003243:Consciousness / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007668:Kidney / Q000294:innervation / Q000502:physiology; D008297:Male; D009994:Osmolar Concentration; D011224:Prazosin / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology*; D014868:Water Deprivation / Q000502:physiology*
D058668:Adrenergic alpha-1 Receptor Antagonists; D013565:Sympatholytics; C041226:Terazosin; D011224:Prazosin