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Sympathetic activity in spontaneously hypertensive rats after spinal transection
The American Journal of Physiology
|November 1, 1982
Summary
Sympathetic hyperactivity in spontaneously hypertensive rats (SHR) may originate from spinal cord or ganglia. Larger adrenal nerve responses in SHR suggest spinal systems contribute to adrenomedullary hyperexcitability.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Hypertension Research
Background:
- Spontaneous hypertension in rats (SHR) is characterized by sympathetic hyperactivity.
- The precise origin of this sympathetic overactivity, whether central or peripheral, remains incompletely understood.
Purpose of the Study:
- To investigate if sympathetic hyperactivity and hyperexcitability in SHR are generated at spinal and/or ganglionic levels.
- To differentiate between supraspinal and spinal/ganglionic contributions to sympathetic overactivity in SHR.
Main Methods:
- Measurements of integrated renal and adrenal nerve activity in anesthetized, paralyzed, and artificially respired SHR and Wistar-Kyoto rats (WKY).
- Spinal cord transection at C1 to eliminate supraspinal control.
- Assessment of descending sympathoexcitatory pathway effectiveness via graded spinal stimulation.
Main Results:
- Elevated spontaneous renal nerve activity was observed in SHR compared to WKY.
- While descending excitatory pathway stimulation yielded similar renal nerve responses in both groups, SHR exhibited larger adrenal nerve responses to excitatory stimulation.
- Spontaneous adrenal preganglionic nerve activity was comparable between SHR and WKY.
Conclusions:
- Spinal and/or ganglionic mechanisms contribute to the sympathetic hyperactivity observed in SHR.
- Enhanced adrenal preganglionic nerve responses to stimulation in SHR suggest a role for spinal systems in adrenomedullary hyperexcitability in spontaneous hypertension.