Quantitative and sustained suppression of renal sympathetic nerve activity by left atrial distension in conscious dogs

1991 ◽  
Vol 419 (6) ◽  
pp. 610-615 ◽  
Author(s):  
Kenju Miki ◽  
Yoshiaki Hayashida ◽  
Keizo Shiraki
Keyword(s):  
Sympathetic Nerve ◽  
Left Atrial ◽  
Sympathetic Nerve Activity ◽  
Conscious Dogs ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Left Atrial Distension ◽  
Renal Sympathetic

Renal sympathetic nerve activity and renal responses during head-up tilt in conscious dogs

1989 ◽  
Vol 257 (2) ◽  
pp. R337-R343 ◽  
Author(s):  
K. Miki ◽  
Y. Hayashida ◽  
F. Tajima ◽  
J. Iwamoto ◽  
K. Shiraki
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Functional Responses ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Head Up Tilt ◽  
Renal Sympathetic

Renal sympathetic nerve activity (RSNA) was measured in conjunction with functional responses of the kidney during head-up tilt in eight conscious female dogs. A 40 degree head-up tilt resulted in a sustained increase in RSNA by 53 +/- 10% (P less than 0.05) relative to control level. Urine flow and osmolal and sodium excretions decreased significantly to a nadir of -55 +/- 4, -42 +/- 7, and -59 +/- 10%, respectively, whereas free water clearance and creatinine clearance did not change significantly during head-up tilt. The systemic arterial pressure (at kidney level) increased significantly from 110 +/- 4 to 129 +/- 6 mmHg, and central venous pressure decreased significantly from -0.7 +/- 0.5 to -7.6 +/- 0.6 mmHg. The chronic bilateral renal denervation, which was performed 2-4 wk before the experiment, abolished both the antidiuretic and antinatriuretic responses to heald-up tilt. These results indicate that an increase in RSNA plays a significant role in the decrease in urine flow and sodium excretion induced by 40 degree head-up tilt in conscious dogs.

Effects of l-carnosine on renal sympathetic nerve activity and DOCA-salt hypertension in rats

2002 ◽  
Vol 97 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Akira Niijima ◽  
Tomoko Okui ◽  
Yasuo Matsumura ◽  
Toshihiko Yamano ◽  
Nobuo Tsuruoka ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Salt Hypertension ◽  
Renal Sympathetic

Suppression of renal sympathetic nerve activity during portal vein infusion of hypertonic saline

1998 ◽  
Vol 274 (1) ◽  
pp. R97-R103 ◽  
Author(s):  
Yasuhiro Nishida ◽  
Isao Sugimoto ◽  
Hironobu Morita ◽  
Hiroshi Murakami ◽  
Hiroshi Hosomi ◽  
...  
Keyword(s):  
Portal Vein ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Venous Infusion ◽  
Portal Vein Infusion ◽  
Renal Sympathetic

Sodium ions absorbed from the intestine are postulated to act on the liver to reflexly suppress renal sympathetic nerve activity (RSNA), resulting in inhibition of sodium reabsorption in the kidney. To test the hypothesis that the renal sympathoinhibitory response to portal venous NaCl infusion involves an action of arginine vasopressin (AVP) at the area postrema, we examined the effects of portal venous infusion of hypertonic NaCl on RSNA before and after lesioning of the area postrema (APL) or after pretreatment with an AVP V1 receptor antagonist (AVPX). Rabbits were chronically instrumented with portal and femoral venous catheters, femoral arterial catheters, and renal nerve electrodes. Portal venous infusion of 9.0% NaCl (0.02, 0.05, 0.10, and 0.15 ml ⋅ kg−1 ⋅ min−1of 9.0% NaCl for 10 min) produced a dose-dependent suppression of RSNA (−12 ± 3, −34 ± 3, −62 ± 5, and 80 ± 2%, respectively) that was greater than that produced by femoral vein infusion of 9.0% NaCl (2 ± 3, −3 ± 2, −12 ± 4, and −33 ± 3%, respectively). The suppression of RSNA produced by portal vein infusion of 9.0% NaCl was partially reversed by pretreatment with AVPX (−9 ± 3, −20 ± 3, −41 ± 4, and −55 ± 4%, respectively) and by APL (−11 ± 2, −25 ± 2, −49 ± 3, and −59 ± 6%, respectively). There were no significant differences between the effects of AVPX and APL, and the effect of APL was not augmented by AVPX. These results indicate that the suppression of RSNA due to portal venous infusion of 9.0% NaCl involves an action of AVP via the area postrema.

scholarly journals Electroacupuncture and Moxibustion Decrease Renal Sympathetic Nerve Activity and Retard Progression of Renal Disease in Rats

2012 ◽  
Vol 35 (5) ◽  
pp. 355-364 ◽  
Author(s):  
Josne C. Paterno ◽  
Cássia T. Bergamaschi ◽  
Ruy R. Campos ◽  
Elisa M.S. Higa ◽  
Maria Fernanda Soares ◽  
...  
Keyword(s):  
Renal Disease ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Progression Of Renal Disease ◽  
Renal Sympathetic

scholarly journals Angiotensin receptor antagonist improves cardiac reflex control of renal sodium handling in heart failure

1998 ◽  
Vol 274 (2) ◽  
pp. H636-H641 ◽  
Author(s):  
Gerald F. Dibona ◽  
Susan Y. Jones ◽  
Linda L. Sawin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sodium Handling ◽  
Renal Sympathetic

In rats with congestive heart failure, type 1 angiotensin II receptor antagonist treatment (losartan) decreases basal renal sympathetic nerve activity and improves arterial baroreflex regulation of renal sympathetic nerve activity. This investigation examined the effect of losartan on cardiac baroreflex regulation of renal sympathetic nerve activity and renal sodium handling in rats with congestive heart failure. Losartan treatment decreased arterial pressure from 120 ± 3 to 93 ± 5 mmHg and increased the afferent (from 0.95 ± 0.21 to 2.22 ± 0.42% Δafferent vagal nerve activity/mmHg mean right atrial pressure, P < 0.05) and overall gain (from −1.14 ± 0.19 to −4.20 ± 0.39% Δrenal sympathetic nerve activity/mmHg mean right atrial pressure, P < 0.05) of the cardiac baroreflex. During isotonic saline volume loading, urinary sodium excretion increased from 2.4 ± 0.8 to 10.5 ± 1.3 μeq/min in vehicle-treated rats (excretion of 52 ± 3% of the load) and from 3.0 ± 1.0 to 15.1 ± 1.8 μeq/min in losartan-treated rats (excretion of 65 ± 4% of the load, P < 0.05). When rats were changed from a low- to a high-sodium diet, cumulative sodium balance over 5 days was 7.8 ± 0.6 meq in vehicle-treated rats and 4.2 ± 0.4 meq in losartan-treated rats ( P < 0.05). In congestive heart failure, losartan treatment improved cardiac baroreflex regulation of renal sympathetic nerve activity, which was associated with improved ability to excrete acute and chronic sodium loads.

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