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Does the spinal cord generate functionally significant sympathetic activity in the awake rat?
1Department of Veterinary Biology, University of Minnesota, St. Paul 55108.
The American Journal of Physiology
|April 1, 1994
Summary
Sympathetic nerve activity (SNA) is not significant in rats with spinal cord transection. Adrenergic blockade causes natriuresis and decreased heart rate due to imidazoline binding, not spinally generated SNA.
Area of Science:
- Physiology
- Neuroscience
- Cardiovascular Research
Background:
- Conflicting conclusions exist on sympathetic nerve activity (SNA) in rats with cervical spinal cord transection (CST).
- Adrenergic blockade in CST rats causes natriuresis and decreased heart rate, but the underlying mechanism is debated.
Purpose of the Study:
- To determine if spinally generated SNA or nonspecific antagonist effects cause natriuresis and bradycardia in CST rats.
- To investigate the specific mechanisms behind adrenergic blockade-induced physiological changes in CST rats.
Main Methods:
- Administered adrenergic antagonists (phentolamine, propranolol) to CST rats with renal denervation, adrenalectomy, or ganglionic blockade (hexamethonium).
- Tested for nonspecific drug effects by administering combinations of adrenergic antagonists (idazoxan, prazosin, yohimbine).
Main Results:
- Renal denervation, adrenalectomy, and ganglionic blockade did not prevent the significant increase in sodium excretion or decrease in heart rate.
- Idazoxan plus propranolol reproduced the natriuresis, but prazosin, yohimbine, and propranolol did not.
- No evidence for functionally significant spinally generated SNA was found.
Conclusions:
- There is no evidence for significant spinally generated sympathetic nerve activity in conscious CST rats.
- The natriuresis observed with phentolamine administration in CST rats is attributed to imidazoline binding, not SNA.