Nonuniform sympathetic nerve responses to intravenous hypertonic saline infusion

Weiss, Mark L.; Claassen, Dale E.; Hirai, Tadakazu; Kenney, Michael J.

doi:10.1016/0165-1838(95)00108-5

Cited by 92 publications

(113 citation statements)

References 13 publications

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“…In this regard, barodenervation or prevention of the ANG II-evoked increase in ABP does enhance thirst and acutely increases sympathetic outflow (Robinson and Evered, 1987;Schreihofer et al, 2000;Stocker et al, 2001Stocker et al, , 2002Xu and Sved, 2002;Stocker et al, 2004). To the extent it has been examined, similar observations have been reported during increases in plasma osmolality (Weiss et al, 1996;Chen and Toney, 2001;Stocker et al, 2001Stocker et al, , 2002. Due to these functional observations, an attractive hypothesis arises that the ability of ANG II and hyperosmolality to evoke appropriate physiological responses depends upon the prevailing level of ABP and/or blood volume.…”

Section: Discussionmentioning

confidence: 89%

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Stocker

Toney

2007

Brain Research

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The goal of the present study was to determine the effect of activating vagal afferent fibers on the discharge of median preoptic (MnPO) neurons responsive to peripheral angiotensin II (ANG II) and osmotic inputs. Vagal afferents were activated by electrical stimulation of the proximal end of the transected cervical vagus nerve (3 pulses, 100 Hz, 1 ms, 100-500 μA). Of 21 MnPO neurons, 19 were antidromically activated from the hypothalamic paraventricular nucleus (PVH) (latency: 10.3 ±1.3 ms, threshold: 278±25 μA). MnPO-PVH cells had an average spontaneous discharge of 2.1±0.4 Hz. Injection of ANG II (150 ng) and/or hypertonic NaCl (1.5 Osm/L, 100 μl) through the internal carotid artery significantly (P<0.01) increased the firing rate of most 84%). Vagus nerve stimulation significantly (P<0.01) decreased discharge (−73±9%) in 10 of 16 (63%) neurons with an average onset latency of 108±19 ms. Among the remaining 6 MnPO-PVH neurons vagal activation either increased discharge (177±100%) with a latency of 115±15 ms (n=2) or had no effect (n=4). Pharmacological activation of chemosensitive vagal afferents with phenyl biguanide produced an increase (n=3), decrease (n=2), or no change (n=6) in discharge. These observations indicate that a significant proportion of ANG II-and/or osmo-sensitive MnPO neurons receive convergent vagal input. Although the sensory modalities transmitted by the vagal afferents to MnPO-PVH neurons are not presently known, the presence of inhibitory and excitatory vagalevoked responses indicates that synaptic processing by these cells integrates humoral and visceral information to subserve potentially important cardiovascular and body fluid homeostatic functions.

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Section: Discussionmentioning

confidence: 89%

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Stocker

Toney

2007

Brain Research

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“…Acute increases in OSM rapidly elevate BP and sympathetic nerve activity to specific beds, [3][4][5] and more chronic increases in plasma OSM, such as during water deprivation, seem to sustain this rapid sympathoexcitation. 6 Moreover, recent studies suggest that increased OSM contributes to sympathoexcitation in at least one model of salt-sensitive hypertension, the deoxycorticosterone-treated rat consuming excess salt (DOCA-salt) rat.…”

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confidence: 99%

Central Action of Increased Osmolality to Support Blood Pressure in Deoxycorticosterone Acetate–Salt Rats

O'Donaughy

Brooks

2006

Hypertension

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Abstract-To test the hypothesis that increased osmolality contributes to hypertension in deoxycorticosterone acetate (DOCA)-salt-hypertensive rats by acting in the brain, DOCA-salt and Sham-salt rats were instrumented with bilateral, nonoccluding intracarotid and femoral catheters. Two weeks prior, rats were uninephrectomized and received subcutaneous implants with or without DOCA (65 mg) and began drinking salt water (1% NaCl and 0.2% KCl). DOCA-salt rats (nϭ28) exhibited elevated blood pressure (159Ϯ4 mm Hg; PϽ0.05) and heart rate (392Ϯ10 bpm; PϽ0.05) compared with Sham-salt animals (nϭ5; blood pressure: 107Ϯ5 mm Hg; heart rate: 355Ϯ10 bpm). Bilateral intracarotid infusion of hypotonic fluid (osmolality: Ϸ40 mOsm/L), which lowers osmolality of blood to the brain by Ϸ2%, rapidly decreased blood pressure in DOCA-salt rats (Ϫ22Ϯ4 mm Hg after 15 minutes; PϽ0.05; nϭ7) but not Sham-salt rats (2Ϯ2 mm Hg; nϭ5). Hypotonic fluid infused intravenously did not lower blood pressure (0Ϯ2 mm Hg) in DOCA-salt rats (nϭ7). In DOCA-salt rats pretreated with a V 1 vasopressin antagonist (Manning compound, 5 g, IV), intracarotid hypotonic infusion still decreased blood pressure (Ϫ10Ϯ3 mm Hg; PϽ0.05; nϭ9), but the response was smaller (PϽ0.05). Finally, in DOCA-salt rats (nϭ4) pretreated with the V 1 antagonist and the ganglionic blocker hexamethonium, decreasing osmolality of blood to the brain did not reduce blood pressure. These data indicate that, in DOCA-salt rats, hypertonicity acts in the brain to support blood pressure, in part by stimulating vasopressin secretion and in part by stimulating another rapidly reversible mechanism, likely the sympathetic nervous system. Key Words: hypertension, sodium-dependent Ⅲ central nervous system Ⅲ hypertension, mineralocorticoid Ⅲ sodium Ⅲ sympathetic nervous system Ⅲ vasopressin I ncreasing evidence supports a role for body fluid osmolality (OSM) in the regulation of blood pressure (BP) and sympathetic nerve activity (for reviews see References 1,2 ). Acute increases in OSM rapidly elevate BP and sympathetic nerve activity to specific beds, 3-5 and more chronic increases in plasma OSM, such as during water deprivation, seem to sustain this rapid sympathoexcitation. 6 Moreover, recent studies suggest that increased OSM contributes to sympathoexcitation in at least one model of salt-sensitive hypertension, the deoxycorticosterone-treated rat consuming excess salt (DOCA-salt) rat. More specifically, DOCA-salt rats exhibit hypertension and elevated OSM and/or NaCl levels, 7-10 and normalization of OSM results in profound decreases in BP and lumbar sympathetic nerve activity. 8 However, the site at which OSM is sensed to trigger sustained sympathoexcitation in DOCA-salt rats has not been identified.Osmoreceptors are present in numerous organs, including the liver, kidney, and brain, but significant indirect evidence implicates the brain in this action. First, forebrain circumventricular organs contain osmoreceptors that are exquisitely sensitive to minute changes in OSM. 11 Second, forebrain...

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“…An intravenous infusion of hypertonic saline elevates BP and lumbar SN discharge but reduces renal SN discharge (37). It is difficult to directly determine cardiac SN activity under conscious conditions in diseased animals.…”

Section: Discussionmentioning

confidence: 99%

“…Kamiya et al (11) reported that muscle SN activity parallels the renal and cardiac SN activity in response to baroreceptor pressure changes in anesthetized rabbits. In contrast, others have reported that central or peripheral stimuli cause selective and differential influences on the SN activity of each organ in anesthetized and conscious animals (13,36,37).Previous studies have shown that cardiovascular recovery from stress plays an important role in the pathogenesis of hypertension and is a predictor of overall mortality (1, 5). Sustained increases in SN activity after transient stress may accelerate cardiovascular damage.…”

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confidence: 94%

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Transient hypercapnic stress causes exaggerated and prolonged elevation of cardiac and renal interstitial norepinephrine levels in conscious hypertensive rats

Sobajima

Nozawa

Nakadate

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The responses of sympathetic nerve activity to transient stress can be exaggerated in salt-sensitive (SS), hypertensive subjects. Cardiac and renal interstitial norepinephrine (iNE) levels during and after transient hypercapnia were investigated in conscious SS rats. Dahl SS and salt-resistant (SR) 6-wk-old rats were fed a high-salt diet, and at 12 wk iNE levels in the heart and kidney were determined using microdialysis with probes inserted in the left ventricular (LV) wall and kidney. A telemetry system determined blood pressure and heart rate (HR) in separate animals. After recovery from the operation, data were collected before, during, and after exposure to normoxic 10% CO 2 for 25 min under unanesthetized conditions. The plasma NE concentrations at baseline did not differ between the two strains. Both cardiac and renal iNE levels were much higher in SS rats than in SR rats at baseline as well as during hypercapnic stress. After stress, the markedly increased iNE levels of SS rats were prolonged in the LV as well as in the kidney. During hypercapnic stress, HR decreased in both SS and SR rats, while sudden increases in HR immediately after the withdrawal from stress were followed by its slower reduction in SS rats compared with SR rats. In conclusion, transient hypercapnic stress causes exaggerated and prolonged elevation of iNE levels in the heart as well as in kidneys of SS animals. salt-sensitive; interstitial norepinephrine; hypercapnia CENTRAL SYMPATHOEXCITATION and renal fluid retention may be involved in the development of salt-sensitive (SS) hypertension. Transient environmental or mental stress in SS animals and subjects causes a greater increase in blood pressure (BP) and renal sympathetic nerve (SN) activity and greater antinatriuresis compared with salt-resistant (SR) animals and subjects (2,3,9,16). Hypertension is also accompanied by increased chemoreflex sensitivity (29, 33) and, therefore, hypoxic and/or hypercapnic stress could augment SN activity in SS hypertensive subjects complicated by sleep apnea syndrome. Thus, the enhanced SN responsiveness to stress may play a role in the high morbidity or mortality of SS hypertensive subjects. However, it remains unclear whether the augmented response of renal SN activity to transient stress occurs in parallel to the response in other organs, especially in the heart, because it is difficult to directly determine cardiac SN activity in conscious animals. Kamiya et al. (11) reported that muscle SN activity parallels the renal and cardiac SN activity in response to baroreceptor pressure changes in anesthetized rabbits. In contrast, others have reported that central or peripheral stimuli cause selective and differential influences on the SN activity of each organ in anesthetized and conscious animals (13,36,37).Previous studies have shown that cardiovascular recovery from stress plays an important role in the pathogenesis of hypertension and is a predictor of overall mortality (1, 5). Sustained increases in SN activity after transient stress may accel...

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Nonuniform sympathetic nerve responses to intravenous hypertonic saline infusion

Cited by 92 publications

References 13 publications

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Central Action of Increased Osmolality to Support Blood Pressure in Deoxycorticosterone Acetate–Salt Rats

Transient hypercapnic stress causes exaggerated and prolonged elevation of cardiac and renal interstitial norepinephrine levels in conscious hypertensive rats

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