Abstract

The caudal medulla of the rat was mapped for cardiovascular sensitive regions by recording changes in mean arterial pressure (MAP) and heart rate evoked by microinjections of l-glutamate (1 nmol/50 nl). Using this technique to selectively activate cell soma in the brainstem, a new pressor area in the caudal ventrolateral medulla has been identified. Several sites located approximately 1–1.5 mm posterior to the caudal medullary depressor zone were found where l-glutamate evoked pressor responses of 10–45 mm Hg. The most responsive area was located just dorsal to the lateral aspect of the lateral reticular nucleus at the level of the pyramidal decussation and the caudalmost pole of the inferior olives. Pressor responses at this site averaged 37 ± 2mm Hg. Changes in heart rate were inconsistent and both tachycardia and bradycardia were observed. Increases in arterial pressure elicited from the caudal pressor area (CPA) were abolished by ganglionic blockade. Pressor responses evoked from the CPA were also eliminated after functional inactivation of vasopressor neurons in the rostral ventrolateral medulla (RVM) was produced by microinjections of muscimol. Inhibition of CPA neurons by microinjections of GABA had no effect on MAP while GABA markedly reduced MAP when injected into the RVM. These studies demonstrate that a circumscribed region of the caudal ventrolateral medulla contains a population of ‘vasopressor’ neurons distinct from those located in the rostral medulla. No evidence was obtained to suggest that neural activity in the CPA contributes to the maintenance of arterial pressure. The precise functional role of the CPA in central cardiovascular regulation remains to be determined.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.