Lesion of A2 noradrenergic neurons with nanoinjections of anti-DβH-saporin into the NTS.

<p>Number and average (mean ± S.E.M.) of TH-positive cells in 40-µm-thick sections from the dorsal (A) and the ventrolateral medulla (B). Sections were taken from 1.9 mm rostral to the obex to 1.9 mm caudal to the obex in animals submitted to A2 or sham lesions. Bilateral nanoinjections of anti-DβH-saporin into the NTS produced a loss of TH-containing neurons in this area (A2 group, loss = 70%; C2 group, loss = 34%), in the RVLM (C1 group, loss = 11%) and in the CVLM (A1 group, loss = 16%). † p<0.05 compared with sham lesion.</p

Baseline values for body weight, MAP, HR, RBF, RVC and RSNA in sham and A2 lesioned rats.

<p>Values are means ± S.E.M. b.wt., body weight; MAP, mean arterial pressure; HR, heart rate; RBF, renal blood flow; RVC, renal vascular conductance; ∫RSNA, integrate of renal sympathetic nerve activity.</p

Effects of A2 noradrenergic neuron lesions on baroreceptor reflexes.

<p>Post-systolic averages of arterial pressure (AP) and renal sympathetic nerve activity (SNA) waves (A) and coherence values between AP and SNA power spectrum (B) before hypertonic saline infusion in sham and A2-lesioned rats.</p

Typical examples.

<p>Digitized record of cardiovascular and sympathetic responses induced by hypertonic saline infusion in sham (A) and A2-lesioned rats (B). ABP = arterial pressure, RBF = renal blood flow, RSNA = renal sympathetic nerve activity (RSNA), hexameth. = hexamethonium.</p

Effects of A2 noradrenergic neuron lesions on cardiovascular and autonomic responses induced by hypernatremia.

<p>Effects of infusion of hypertonic saline (3 M NaCl, 1.8 ml·Kg⁻¹ body weight) on mean arterial pressure (Δ MAP; A), heart rate (Δ HR; B), renal blood flow (Δ RBF; C), renal vascular conductance (Δ RVC; D) and renal sympathetic nerve activity (Δ RSNA; E) in sham and A2-lesioned rats. The bars indicate the moment of hypertonic saline infusion. Error bars indicate S.E.M. * p<0.05 compared with baseline; † p<0.05 compared with sham lesion.</p

Lesions of A1 noradrenergic neurons after nanoinjections of anti-DβH-saporin into the CVLM.

<p>The number and average (mean ± S.E.M.) of TH-positive cells in 40-µm-thick sections of the dorsal (A) and ventrolateral medulla (B). Sections from animals that were submitted to A1 lesions or sham were taken from 1.9 mm rostral to the obex to 1.9 mm caudal to the obex. Bilateral nanoinjections of anti-DbH-saporin into the CVLM produced a loss of TH-containing neurons in this area (A1 group, loss  = 81%). However, in the RVLM (C1 group, loss  = 10%) and NTS (A2/C2 groups, loss < 0%), this loss was either decreased or not evident, respectively. ^† compared with sham, p<0.05.</p

Photomicrography of the nitrocellulose membrane with marking of TH in the MnPO and cortex.

<p>Molecular analysis of noradrenergic neurotransmission of the A1 group of the CVLM region for MnPO with marking for TH (circle) by the Dot Blot technique in sham and anti-DβH-saporin-treated rats. Photomicrographs of a coronal section of a brain showing withdrawal of the tissue mass from the MnPO (circle) and cortex (arrows; B).</p

Baroreceptor sensitivity and chemoreflex response.

<p>Baroreflex sensitivity(BS; A) expressed by changes in the heart rate (HR) and mean arterial pressure (MAP) that were induced by phenyleprine infusion in sham and A1-lesioned rats. p<0.05. Changes in MAP (B) and HR (C) induced by intravenous potassium cyanide infusion.</p

Sodium and blood hemoglobin concentrations in plasma. Mean

<p>± S.E.M. of plasma sodium (A) and blood hemoglobin concentrations (B) at baseline and as a response to HS infusion in sham and A1-lesioned rats. * different from baseline; † different from sham at the same time point; for both, p<0.05.</p

Typical examples.

<p>Digitized record of cardiovascular responses that were induced by hypertonic saline infusion in sham (A) and A1-lesioned rats (B). Arterial blood pressure (ABP), mean arterial pressure (MAP), and heart rate (HR).</p