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A2 noradrenergic lesions prevent renal sympathoinhibition induced by hypernatremia in rats.

Pedrino GR, Freiria-Oliveira AH, Almeida Colombari DS, Rosa DA, Cravo SL (2012) A2 noradrenergic lesions prevent renal sympathoinhibition induced by hypernatremia in rats. PLoS One 7(5):e37587. doi: 10.1371/journal.pone.0037587

Summary: It is thought that renal sympathetic nerve activity is a key component of the response to acute or chronic elevated concentrations of saline in the blood stream. The authors investigated what neurons are involved in the central control of these responses. Rats received bilateral 6.3 ng injections of anti-DBH-SAP (Cat. #IT-03) into the nucleus of the solitary tract. An equimolar amount (1.3 ng) of saporin (Cat. #PR-01) was used as a control. Loss of the A2 noradrenergic neurons altered the renal sympathetic nerve activity response to elevated saline, suggesting that these neurons help regulate the extracellular fluid compartment.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Saporin (Cat. #PR-01)