کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4329333 1614212 2008 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Enhanced response from the caudal pressor area in spontaneously hypertensive rats
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Enhanced response from the caudal pressor area in spontaneously hypertensive rats
چکیده انگلیسی

The caudal pressor area (CPA), located in the caudal extension of the ventrolateral medulla, tonically activates the rostral ventrolateral medulla (RVLM) vasomotor neurons and regulates arterial pressure (AP) in normotensive animals. It is well established that sympathoexcitatory outflow from the RVLM in spontaneously hypertensive rats (SHR) is elevated compared to normotensive animals. Several studies have reported different cardiovascular responses to pharmacological alteration of the RVLM in SHR. Although the CPA may be one of the sources of presympathoexcitatory influence to the RVLM vasomotor drive in normotensive animals, it is unclear whether hypertensive animals such as SHR differ in their response to vasomotor drive evoked from the CPA. In this study, we examined whether sympathoexcitatory influence evoked from the CPA is enhanced in SHR. Local injection of glutamate into the CPA of chloralose-anesthetized male SHR elicited a substantially greater pressor response than in Wistar–Kyoto (WKY) rats, whereas the pressor response evoked by local injection of glutamate into the RVLM was the same in both strains. Furthermore, injection of glycine into the CPA decreased blood pressure to a greater extent in SHR than in WKY rats. These results suggest that the sympathoexcitatory influence of the CPA is enhanced in SHR. Therefore, the enhancement of sympathoexcitatory vasomotor drive evoked from the CPA may, at least in part, support elevated AP and regulate sympathetic tone in this hypertensive model.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1227, 28 August 2008, Pages 89–95
نویسندگان
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