Adrenergic nerves mediate the venoconstrictor response to PVN stimulation

Martin, Douglas; Egland, M.C.; Barnes, Ludwig; Vogel, Erin

doi:10.1016/j.brainres.2005.12.116

Cited by 9 publications

(11 citation statements)

References 34 publications

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“…Interestingly, in this study CVP was increased by cerebral sodium-sensitive mechanisms. The finding that inhibition of the PVN blocked this response is in accordance with previous studies describing increased venous resistance after electrical stimulation of the PVN and merits further investigation as it could be a contributing factor in the early stages of sodium induced hypertension (26).…”

Section: Discussionsupporting

confidence: 90%

Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep

Frithiof

Ramchandra²,

Hood³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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The contribution of the paraventricular nucleus of the hypothalamus (PVN) in mediating cardiovascular, renal, hormonal, and sympathetic nerve responses to increased cerebrospinal fluid (CSF) [Na(+)] was investigated in conscious sheep. Intracerebroventricular hypertonic NaCl (0.5 mol/l, 20 microl/min for 60 min) increased arterial blood pressure [AP; +13.4 (sd 2.0) mmHg, P < 0.001] and central venous pressure [CVP; +2.8 (sd 1.3) mmHg, P < 0.001], but did not significantly change heart rate or cardiac output (n = 6). Elevated CSF [Na(+)] also lowered plasma ANG II levels [-3.3 (sd 1.6) pmol/l, P = 0.004] and increased creatinine clearance [+31.5 (sd 32.7) ml/min, P = 0.03] and renal sodium excretion [+9.2 (sd 9.2) mmol/h, P = 0.003]. Lidocaine injection (1 microl, 2%) into the PVN prior to the ICV infusion had no apparent effect per se, but it abolished the AP, CVP, creatinine clearance, and ANG II responses to hypertonic NaCl, as well as reducing the increase in renal sodium excretion (n = 6). Subsequent studies were performed in conscious sheep with chronically implanted electrodes for measurement of renal sympathetic nerve activity (RSNA). The effects of ICV hypertonic NaCl on AP and RSNA were measured before and after PVN-injection of glycine (250 nmol in 500 nl artificial CSF). ICV NaCl increased AP and decreased RSNA (P < 0.001). These effects were significantly reduced by glycine (P = 0.02-0.001, n = 5). Saline injected into the PVN (n = 5) or lidocaine injected outside the PVN (n = 6) had no effect on the response to ICV hypertonic NaCl. These results indicate that the PVN is an important mediator of cerebrally induced homeostatic responses to elevated sodium concentration/hyperosmolality.

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Section: Discussionsupporting

confidence: 90%

Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep

Frithiof

Ramchandra²,

Hood³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Conversely, sympathetic or cardiovascular effects seen after microinjection of higher doses of BMI into nearby regions may well be a consequence of exciting neurons in the DMH (see DeNovellis et al, 1995). This would be particularly true in reports that have targeted the PVN with microinjections ranging from 50 pmol to as much as 2 nmol of BMI and assumed that sympathoexcitatory or cardiovascular effects noted were a consequence of disinhibiting neurons in the latter region (Martin et al, 1991;Reynolds et al, 1996;Zhang and Patel, 1998;Kenney et al, 2003;LaGrange et al, 2003;Reddy et al, 2005;Martin et al, 2006). The extent of the region activated by microinjection of 10 pmoles of BMI in this study make it highly plausible that at least some of the changes elicited by microinjection of these larger doses into the nearby PVN may be a consequence of spread or diffusion to the DMH.…”

Section: Discussionmentioning

confidence: 99%

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

et al. 2008

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Activation of neurons in the dorsomedial hypothalamus (DMH) appears to play an important role in signaling the excitation of brain regions responsible for experimental fever and for many of the physiological and behavioral changes seen in experimental stress or anxiety in rats. Here, we examined the effect of disinhibition of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in selected regions of the brain that have been implicated in anxiety and responses to stress and fever in rats. Disinhibition of the DMH resulted in dramatic increases in local Fos expression and also increased the numbers of Fos-positive neurons in the lateral septal nucleus and in both the parvocellular and magnocellular subdivisions of the paraventricular nucleus, with greater increases ipsilateral to the injection site in the DMH. However, microinjection of BMI had no significant effect on Fos expression in the bed nucleus of the stria terminalis, another forebrain area implicated in stress and anxiety. In the brainstem, disinhibition of the DMH increased Fos expression in the nucleus tractus solitarius and the ventrolateral medulla bilaterally with greater increases again ipsilateral to the site of the microinjection, and also in the midline rostral raphe pallidus. Thus, disinhibition of neurons in the DMH in conscious rats results in increases in Fos expression in selected forebrain and brainstem regions that have been implicated in stress-induced physiological changes, anxiety, and experimental fever.

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“…Electrical or chemical PVN stimulation with N-methyl-Daspartic acid has been reported to increase MAP, HR and renal sympathetic nerve activity (Kannan et al, 1989;Li et al, 2001). The microinjection of bicuculline, a GABA-A receptor antagonist, into the PVN of either anesthetized or unanesthetized rats also increased MAP, HR and sympathetic nerve activity, thus suggesting a tonic PVN influence on the autonomic activity (Chen et al, 2003;Martin et al, 2006;Schlenker et al, 2001;Zhang and Patel, 1998).…”

Section: Introductionmentioning

confidence: 97%

Paraventricular nucleus modulates autonomic and neuroendocrine responses to acute restraint stress in rats

Busnardo

Tavares

Resstel

et al. 2010

Autonomic Neuroscience

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The paraventricular nucleus of the hypothalamus (PVN) has been implicated in several aspects of neuroendocrine and cardiovascular control. The PVN contains parvocellular neurons that release the corticotrophin release hormone (CRH) under stress situations. In addition, this brain area is connected to several limbic structures implicated in defensive behavioral control, as well to forebrain and brainstem structures involved in cardiovascular control. Acute restraint is an unavoidable stress situation that evokes corticosterone release as well as marked autonomic changes, the latter characterized by elevated mean arterial pressure (MAP), intense heart rate (HR) increases and decrease in the tail temperature. We report the effect of PVN inhibition on MAP and HR responses, corticosterone plasma levels and tail temperature response during acute restraint in rats. Bilateral microinjection of the nonspecific synaptic blocker CoCl(2) (1 mM/100 nL) into the PVN reduced the pressor response; it inhibited the increase in plasma corticosterone concentration as well as the fall in tail temperature associated with acute restraint stress. Moreover, bilateral microinjection of CoCl(2) into areas surrounding the PVN did not affect the blood pressure, hormonal and tail vasoconstriction responses to restraint stress. The present results show that a local PVN neurotransmission is involved in the neural pathway that controls autonomic and neuroendocrine responses, which are associated with the exposure to acute restraint stress.

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Adrenergic nerves mediate the venoconstrictor response to PVN stimulation

Cited by 9 publications

References 34 publications

Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep

Hypothalamic paraventricular nucleus mediates sodium-induced changes in cardiovascular and renal function in conscious sheep

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

Paraventricular nucleus modulates autonomic and neuroendocrine responses to acute restraint stress in rats

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