Increased renal nerve activity in cardiac failure: arterial vs. cardiac baroreflex impairment

1995 ◽  
Vol 268 (1) ◽  
pp. R112-R116 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Normal Control ◽  
Cardiac Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Cardiac failure is characterized by increased renal sympathetic nerve activity that is associated with an impairment of both arterial and cardiac baroreceptor reflex function. These reflex dysfunctions are in the afferent limb at the level of the peripheral baroreceptors. This study sought to define the relative quantitative magnitude of the defects in arterial and cardiac baroreceptor function in cardiac failure. Renal sympathetic nerve activity was measured in anesthetized normal control rats and rats with cardiac failure (left coronary ligation) during sequential random order sinoaortic denervation and vagotomy to interrupt afferent input from the arterial and cardiac baroreceptors, respectively. Increases in renal sympathetic nerve activity after individual or combined sinoaortic denervation and vagotomy were less (P < 0.05 for both) in cardiac failure than in normal control rats in both order sequences (42 +/- 5 vs. 87 +/- 8%; 44 +/- 5 vs. 108 +/- 7%). In cardiac failure rats, vagotomy produced lesser increases (P < 0.05 for both) in renal sympathetic nerve activity than sinoaortic denervation in both order sequences (10 +/- 4 vs. 32 +/- 5%; 13 +/- 2 vs. 30 +/- 5%). The relative magnitude of impaired cardiac baroreceptor reflex function that is associated with the increased renal sympathetic nerve activity of cardiac failure is greater than that of impaired arterial baroreceptor reflex function.

Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats

1999 ◽  
Vol 277 (1) ◽  
pp. H8-H14 ◽  
Author(s):  
Yoshihide Fujisawa ◽  
Naoko Mori ◽  
Kouichi Yube ◽  
Hiroshi Miyanaka ◽  
Akira Miyatake ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Saline Group ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), in conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but significantly increased HR and RSNA by 88 ± 12 beats/min and 67 ± 12%, respectively. Intravenous infusion of l-NAME (50 μg ⋅ kg−1⋅ min−1) significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 ± 7 beats/min and 26 ± 12%, respectively). Pretreatment ofl-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses induced byl-NAME (92 ± 6 beats/min and 64 ± 10%, respectively).l-NAME by itself did not alter the baroreceptor reflex control of HR and RSNA. Hemorrhage increased the plasma vasopressin concentration, and its increment in thel-NAME-treated group was significantly higher than that in the 0.9% saline group. Pretreatment with the vascular arginine vasopressin V1-receptor antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced byl-NAME (54 ± 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch. It can be assumed that NO modulated the baroreflex function by altering the secretion of vasopressin induced by hemorrhage.

High-NaCl diet reduces cardiac vagal afferent nerve response to volume expansion

1987 ◽  
Vol 252 (4) ◽  
pp. R687-R692
Author(s):  
G. F. Dibona ◽  
L. L. Sawin
Keyword(s):  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Afferent Nerve ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Vagal Afferent ◽  
Renal Sympathetic

To localize the mechanism by which high dietary NaCl intake decreases the reflex inhibitory effects of intravenous volume expansion on efferent renal sympathetic nerve activity, experiments were performed in anesthetized normal rats prepared for separate examination of the afferent and efferent limbs of the cardiopulmonary baroreceptor reflex. When left ventricular end-diastolic pressure, an index of left heart filling pressure, was progressively increased by intravenous isotonic saline administration in sinoaortic-denervated rats, the increase in cardiac vagal afferent nerve activity was less in rats consuming high compared with normal dietary NaCl intake. During electrical stimulation of the central vagus nerve in sinoaortic-denervated rats, the decreases in efferent renal sympathetic nerve activity were similar in rats consuming high and normal dietary NaCl intake. Thus the effect of high dietary NaCl intake to decrease overall cardiopulmonary baroreceptor reflex gain during intravenous volume expansion is located in the afferent limb of the reflex arc.

Partial renal ischemia elicits heterogeneous control of renal sympathetic nerve activity to ischemic and nonischemic regions of the kidney

2006 ◽  
Vol 290 (2) ◽  
pp. R322-R330 ◽  
Author(s):  
Kiyoshi Shimizu ◽  
Kanji Matsukawa ◽  
Jun Murata ◽  
Hirotsugu Tsuchimochi ◽  
Ishio Ninomiya
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Ischemia ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Ischemic Region ◽  
Nerve Bundles ◽  
Renal Sympathetic

We tested the hypothesis that renal sympathetic nerve activity (RSNA) to the ischemic and nonischemic regions responded differently during partial ischemia of the kidney in pentobarbital-anesthetized cats. The renal artery divides into two branches at the front of the renal hilus: one branch perfuses predominantly the dorsal half of the kidney, and the other perfuses its ventral half. We identified the innervated area of a renal nerve bundle by supramaximal electrical stimulation and subsequently determined the changes in RSNA in response to occlusion of either renal arterial branch for 3 min. RSNA to the nonischemic region of the kidney gradually decreased by 23 ± 4% during partial renal ischemia, whereas RSNA to the ischemic region of the same kidney showed no significant change. Crushing either all renal nerve bundles or only the renal nerve bundles terminated to the ischemic region abolished the decrease in RSNA to the nonischemic region. Furthermore, intra-arterial administration of a prostaglandin synthesis inhibitor (meclofenamate, 4 mg/kg) abolished the decrease in RSNA to the nonischemic region of the kidney. Following spinal transection at the level of T7, the inhibitory response in RSNA to the nonischemic region disappeared, whereas the RSNA to the ischemic region was markedly augmented by 47 ± 17%. Thus it is likely that renal chemoreceptors activated during renal partial ischemia elicit heterogeneous control of renal sympathetic outflows to the ischemic and nonischemic regions of the same kidney, which may be determined by a net output between the supraspinal inhibitory and spinal excitatory reflexes.

Renal neurohormonal and vascular responses to dynamic exercise in humans

1991 ◽  
Vol 70 (5) ◽  
pp. 2279-2286 ◽  
Author(s):  
B. Tidgren ◽  
P. Hjemdahl ◽  
E. Theodorsson ◽  
J. Nussberger
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Plasma Concentrations ◽  
Dynamic Exercise ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Effects of graded supine dynamic exercise (30, 60, and 80-90% of maximal physical capacity, i.e., work loads of 69, 132, and 188 W) on renal vascular resistance (RVR); renal sympathetic nerve activity [assessed by the renal venous overflow of norepinephrine (NE)]; renal overflows of dopamine (DA), immunoreactive neuropeptide Y (NPY-LI), and renin; as well as plasma concentrations of angiotensin-(1-8)-octapeptide (ANG II) were evaluated in eight healthy male volunteers. Exercise evoked stimulus-dependent and marked elevations of RVR, arterial NE, epinephrine (Epi), and DA. RVR increased by 140% and the renal overflows of NE and DA increased by 1,331 and 179%, respectively, at 188 W. A net removal of NPY-LI at rest turned into a small net renal overflow, which correlated with increases in RVR at 188 W. Increases in renin release (+1,200% at 188 W) correlated with increases in renal NE and DA overflows and with arterial Epi levels. Arterial ANG II levels increased stimulus dependently (by 264% at 188 W) and correlated more closely with increases in RVR than did other variables. Thus dynamic exercise is a potent stimulus for renal nerve activation in humans, and renal sympathetic nerve activity may contribute to increased RVR both directly (NE and, at exhaustive work loads, possibly NPY) and indirectly (via renin-mediated ANG II formation).

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.

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