کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4348955 | 1296915 | 2007 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sympathoexcitation of moxonidine in the caudal ventrolateral medulla is dependent on I1-imidazoline receptors in anesthetized rats
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Moxonidine is a second-generation centrally acting antihypertensive drug that has a high affinity for I1-imidazoline receptors (I1R). The caudal ventrolateral medulla (CVLM), an important region involved in cardiovascular activity, contains binding sites for centrally acting drugs. Our study aimed to determine the effects of moxonidine injected into the CVLM on cardiovascular activity in anesthetized rats. Unilateral microinjection of moxonidine (0.4 and 4 nmol) into the CVLM dose-dependently increased blood pressure (BP) by 8 ± 2 and 18 ± 2 mmHg and renal sympathetic nerve activity (RSNA) by 19 ± 3 and 48 ± 5% without modifying heart rate. Microinjection of the I1R/α2-adrenoceptor antagonist efaroxan (4 nmol) into the CVLM produced significant decreases in baseline BP and RSNA, but also completely abolished the increases in BP (2 ± 1 versus 18 ± 2 mmHg, P < 0.01) and RSNA (3 ± 2 versus 45 ± 10%, P < 0.01) evoked by subsequent injection of moxonidine (4 nmol). However, prior injection of yohimbine (500 pmol), a selective antagonist of α2-adrenoceptors, into the CVLM had no significant (P > 0.05) effect on the moxonidine-induced increase in BP (18 ± 2 versus 17 ± 3 mmHg) and RSNA (45 ± 10 versus 42 ± 7%). The current data suggest that moxonidine injection into the CVLM has an excitatory effect on cardiovascular activity, which is mediated by an I1R dependent mechanism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 426, Issue 2, 16 October 2007, Pages 91-96
Journal: Neuroscience Letters - Volume 426, Issue 2, 16 October 2007, Pages 91-96
نویسندگان
Li-Gang Wang, Lie Gao, Wei Wang, Wen-Jun Yuan, Wei-Zhong Wang,