Abstract
This study investigated the cellular basis for the enhanced ganglionic responsiveness
to NK1 agonists in the spontaneously hypertensive rat (SHR) in comparison to their normotensive
counterpart, the Wistar–Kyoto (WKY) rat. Rats for in vivo studies were anesthetized
with pentobarbital and treated with chlorisondamine (10.5 μmol/kg). Extracellular
recordings from the external carotid nerve showed a greater responsiveness of decentralized
SHR superior cervical ganglia (SCG) to intravenous injection of SP (32 nmol/kg). Blood
pressure and heart rate were increased in SHRs, whereas WKY rats responded with a
decrease in blood pressure and only slight tachycardia. Membrane properties of SCG
neurons, as shown by intracellular microelectrode recordings, were similar between
strains. Picospritzer application of the NK1 agonist GR-73632 (100 μM, 1 s) evoked slow depolarization and increased neuron excitability.
Spontaneous firing was evoked only in some neurons. Depolarization amplitudes were
similar between strains; however, the NK1 agonist depolarized a greater number of neurons in hypertensive rats. In conclusion,
SHRs are more responsive to ganglion stimulation by NK1 agonists due to a greater number of responsive cells within the SCG rather than an
enhanced responsiveness of individual neurons.
Keywords
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Article info
Publication history
Accepted:
January 3,
2002
Received in revised form:
December 23,
2001
Received:
October 8,
2001
Identification
Copyright
© 2002 Elsevier Science B.V. Published by Elsevier Inc. All rights reserved.
