Effects of renal receptor stimulation on neurons within the ventrolateral medulla of the cat

Vizzard, Margaret A.; Standish, A.; Ammons, W. S.

doi:10.1152/ajpregu.1993.265.2.r290

Cited by 7 publications

(8 citation statements)

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“…13 Afferent neural information from renal sensory receptors has been shown to influence the activity of neurons at different levels of the neuraxis. 14, 17–19, 40–44 Furthermore, ARN stimulation has also been shown to activate the PVN. 14, 17, 20 In addition, a time course study examining inducible transcription factors in the PVN found that expression of neuronal activity marker cFOS was rapidly increased after ARN stimulation.…”

Section: Discussionmentioning

confidence: 99%

Renal Denervation Improves Exaggerated Sympathoexcitation in Rats With Heart Failure

Patel

Liu

et al. 2016

Hypertension

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Renal denervation (RDN) has been postulated to reduce sympathetic drive during heart failure (HF), but the central mechanisms are not completely understood. The purpose of the present study was to assess the contribution of neuronal nitric oxide synthase (nNOS) within the paraventricular nucleus (PVN) in modulating sympathetic outflow in rats with HF that underwent RDN. HF was induced in rats by ligation of the left coronary artery. Four weeks after surgery, bilateral RDN was performed. Rats with HF had an increase in FosB-positive cells in the PVN with a concomitant increase in urinary excretion of norepinephrine and both of these parameters were ameliorated after RDN. nNOS-positive cells immunostaining, diaphorase staining, and nNOS protein expression were significantly decreased in the PVN of HF rats, findings that were ameliorated by RDN. Microinjection of nNOS inhibitor L-NMMA into the PVN resulted in a blunted increase in lumbar sympathetic nerve activity (ΔLSNA: 11 ± 2 vs. 24 ± 2%) in HF than in sham group. This response was normalized after RDN. Stimulation of afferent renal nerve (ARN) produced a greater activation of PVN neurons in rats with HF. ARN stimulation elicited a greater increase in LSNA in rats with HF compared to sham rats (ΔLSNA: 45 ± 5 vs. 22 ± 2%). These results suggest that intact renal nerves contribute to the reduction of nNOS in the PVN, resulting in activation of the neurons in the PVN of rats with HF. RDN restores nNOS and thus attenuates the sympathoexcitation commonly observed in HF.

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Section: Discussionmentioning

confidence: 99%

Renal Denervation Improves Exaggerated Sympathoexcitation in Rats With Heart Failure

Patel

Liu

et al. 2016

Hypertension

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“…Available physiological and c-fos labeling evidence indicates that neurons in the ventrolateral medulla can respond to bilateral noxious somatic stimulation (Sotgiu, 1986;Arita et al, 1988;Smith and Day, 1994;Jones and Blair, 1995;Pan et al, 1999), renal afferent mechanoreceptors and chemoreceptors (Vizzard et al, 1992(Vizzard et al, , 1993, colorectal distension (Ness et al, 1998), intraarterial injection of CO 2 -saturated saline (Arita et al, 1988) and other cardiovascular and electrolyte challenges (Dun et al, 1993;Murphy et al, 1994;Hochstenbach and Ciriello, 1995;Dayas et al, 2001), muscular activity (Li et al, 1997;Wilson and Hand, 1997), and bilateral cutaneous cooling (A.D.C., unpublished observations). Furthermore, the A1 cell group within the ventrolateral medulla appears to be critical for hypothalamic responses to physiologically stressful stimulation (Day and Sibbald, 1990;Sawchenko et al, 1996;Palkovits et al, 1999).…”

Section: Functional Significance Of Spinomedullary Inputmentioning

confidence: 99%

Differentiation of lamina I spinomedullary and spinothalamic neurons in the cat

Andrew

Krout

Craig

2003

J of Comparative Neurology

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We characterized spinomedullary neurons that project to the ventrolateral portion of the medulla that receives lamina I terminations in two sets of experiments in the cat. First, their distribution was examined using single unilateral iontophoretic injections of cholera toxin subunit B. The injection sites were characterized by microelectrode recordings from nociceptive- and thermoreceptive-specific units, indicative of lamina I input. The spinomedullary neurons were symmetrically distributed bilaterally, predominantly (63-69%) in lamina I but also in laminae V-VIII and the thoracic lateral horn (intermediolateral cell column). In horizontal sections, spinomedullary lamina I neurons included all three main morphological types described earlier. Second, spinomedullary and spinothalamic neurons were compared in retrograde double-labeling experiments. Different combinations of tracers were injected in the right thalamus and the left or right ventrolateral medulla (guided by recordings). The numbers of spinomedullary and spinothalamic neurons on the left side were comparable, and the segmental and laminar distributions were similar, except that a greater proportion of spinomedullary neurons originated from thoracic segments. However, the proportion of double-labeled neurons was consistently approximately 1%, indicating that spinomedullary and spinothalamic pathways arise from separate subpopulations. Spinomedullary neurons were more ventrally located within lamina I than spinothalamic neurons. A significantly greater proportion of spinomedullary neurons had fusiform somata (49% vs. 36%). These observations indicate that lamina I is the major source of spinal input to this portion of the ventrolateral medulla, that the projection includes several morphological types of inputs, and that this projection is distinct from the spinothalamic projection. These findings are consistent with the concept that lamina I projections constitute an ascending homeostatic afferent pathway relating the physiological condition of the body.

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“…Further support for a possible interaction between the arterial baroreceptor and renorenal reflexes at the medullary level is derived from studies in rats showing that electrical stimulation of the afferent renal nerves decreases MAP as well as the activity of neurons in the RVLM, which have pulse-synchronous activity and which decrease their activity in response to pressor doses of intravenous phenylephrine (15). Importantly, activation of the afferent renal nerves by physiological stimuli, including increases in renal pelvic pressure and ischemia, activates neurons in the RVLM (43).…”

Section: Renorenal and Arterial Baroreflexesmentioning

confidence: 99%

“…Importantly, the activity of many of these neurons is also modulated by inputs from both the aortic and carotid sinus nerves (8). Considering the convergence of the afferent signals from the renal and carotid sinus nerves on neurons in several brain areas involved in cardiovascular control, including RVLM (4,16,40,42,43), we speculate that the lack of afferent renal nerve input to cardiovascular sensitive neurons in these areas may contribute to an impairment of arterial baroreflex control of ERSNA, eventually leading to increased MAP in conditions of high-salt diet. In this context, it is of interest that sinoaortic denervated rats are also characterized by salt-sensitive hypertension (35).…”

Section: Possible Mechanisms Involved In the Increased Arterial Pressmentioning

confidence: 99%

“…In view of these studies, we reasoned that the mechanisms involved in an impairment of the arterial baroreflex control of ERSNA in DRX rats fed high-sodium diet would be related to lack of afferent renal nerve signals to the supraspinal centers involved in cardiovascular control. There is considerable evidence for the control of ERSNA being influenced by a central interaction between the neural input from the afferent renal nerves and neural input from the arterial baroreceptors (4,16,40,43,44).We examined arterial baroreflex function in conscious rats by two different methods: 1) the pharmacological method …”

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Afferent renal denervation impairs baroreflex control of efferent renal sympathetic nerve activity

Kopp¹,

Jones²,

DiBona³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kopp UC, Jones SY, DiBona GF. Afferent renal denervation impairs baroreflex control of efferent renal sympathetic nerve activity. Am J Physiol Regul Integr Comp Physiol 295: R1882-R1890, 2008. First published October 22, 2008 doi:10.1152/ajpregu.90529.2008Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which decreases ERSNA to prevent sodium retention. High-sodium diet enhances ARNA, suggesting an important role for ARNA in suppressing ERSNA during excess sodium intake. Mean arterial pressure (MAP) is elevated in afferent renal denervated by dorsal rhizotomy (DRX) rats fed high-sodium diet. We examined whether the increased MAP in DRX is due to impaired arterial baroreflex function. In DRX and sham DRX rats fed high-sodium diet, arterial baroreflex function was determined in conscious rats by intravenous nitroprusside and phenylephrine or calculation of transfer function gain from arterial pressure to ERSNA (spontaneous baroreflex sensitivity). Increasing MAP did not suppress ERSNA to the same extent in DRX as in sham DRX, Ϫ60 Ϯ 4 vs. Ϫ77 Ϯ 6%. Maximum gain, Ϫ4.22 Ϯ 0.45 vs. Ϫ6.04 Ϯ 0.90% ⌬ERSNA/mmHg, and the maximum value of instantaneous gain, Ϫ4.19 Ϯ 0.45 vs. Ϫ6.04 Ϯ 0.81% ⌬ERSNA/mmHg, were less in DRX than in sham DRX. Likewise, transfer function gain was lower in DRX than in sham DRX, 3.9 Ϯ 0.2 vs. 6.1 Ϯ 0.5 NU/mmHg. Air jet stress produced greater increases in ERSNA in DRX than in sham DRX, 35,000 Ϯ 4,900 vs. 20,900 Ϯ 3,410% ⅐ s (area under the curve). Likewise, the ERSNA responses to thermal cutaneous stimulation were greater in DRX than in sham DRX. These studies suggest impaired arterial baroreflex suppression of ERSNA in DRX fed high-sodium diet. There were no differences in arterial baroreflex function in DRX and sham DRX fed normal-sodium diet. Impaired arterial baroreflex function contributes to increased ERSNA, which would eventually lead to sodium retention and increased MAP in DRX rats fed high-sodium diet. dorsal rhizotomy; high-sodium diet; renorenal reflexes; spontaneous baroreflex sensitivity; reflex renal nerve stimulation IN THE KIDNEY, THE MAJORITY of the renal sensory nerves are located in the renal pelvic wall (27,28,32). The afferent renal nerves project to the ipsilateral dorsal root ganglia at the T 6 -L 2 level with the majority of the cell bodies of the afferent renal nerves being at the T 9 -L 1 level (3,6,14). These nerves are activated by increases in renal pelvic pressure within the physiological range (26). The increase in afferent renal nerve activity (ARNA) produced by increased renal pelvic pressure leads to a reflex decrease in efferent renal sympathetic nerve activity (ERSNA) and a natriuresis, i.e., a renorenal reflex response (29).The responsiveness of the afferent renal nerves is enhanced by high-sodium and suppressed by low-sodium diet by a mechanism at the peripheral nerve endings (26). In conditions of increased sodium intake, the threshold for activation of the renal mechanosensory nerves is Ͻ 3 mmHg (26)...

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Effects of renal receptor stimulation on neurons within the ventrolateral medulla of the cat

Cited by 7 publications

References 0 publications

Renal Denervation Improves Exaggerated Sympathoexcitation in Rats With Heart Failure

Renal Denervation Improves Exaggerated Sympathoexcitation in Rats With Heart Failure

Differentiation of lamina I spinomedullary and spinothalamic neurons in the cat

Afferent renal denervation impairs baroreflex control of efferent renal sympathetic nerve activity

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