Hemodynamic responses to paraventricular nucleus disinhibition with bicuculline in conscious rats

Martin, Douglas; Haywood, Joseph R.

doi:10.1152/ajpheart.1993.265.5.h1727

Cited by 54 publications

(65 citation statements)

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“…Furthermore, parvocellular neurons of the PVN project to regions of the CNS that control sympathetic outflow (36), including the rostral ventrolateral medulla, the dorsomedial medulla, and the spinal intermediolateral cell column (26,36,39). Numerous studies support the concept that neuronal projections from autonomic neurons in the PVN can modulate the activity of sympathetic nerves (27,28). Such data demonstrate that the PVN is an important central site where information concerning the level of blood-borne ANG II is processed and may play a significant role in mediating the attenuated renal SNA response to acute VE when circulating ANG II is chronically infused.…”

Section: Discussionmentioning

confidence: 99%

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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In this study the hypothesis was tested that chronic infusion of ANG II attenuates acute volume expansion (VE)-induced inhibition of renal sympathetic nerve activity (SNA). Rats received intravenous infusion of either vehicle or ANG II (12 ng·kg −1 ·min −1 ) for 7 days. ANG II-infused animals displayed an increased contribution of SNA to the maintenance of mean arterial pressure (MAP) as indicated by ganglionic blockade, which produced a significantly (P < 0.01) greater decrease in MAP (75 ± 3 mmHg) than was observed in vehicle-infused (47 ± 8 mmHg) controls. Rats were then anesthetized, and changes in MAP, mean right atrial pressure (MRAP), heart rate (HR), and renal SNA were recorded in response to right atrial infusion of isotonic saline (20% estimated blood volume in 5 min). Baseline MAP, HR, and hematocrit were not different between groups. Likewise, MAP was unchanged by acute VE in vehicle-infused animals, whereas VE induced a significant bradycardia (P < 0.05) and increase in MRAP (P < 0.05). MAP, MRAP, and HR responses to VE were not statistically different between animals infused with vehicle vs. ANG II. In contrast, VE significantly (P < 0.001) reduced renal SNA by 33.5 ± 8% in vehicle-infused animals but was without effect on renal SNA in those infused chronically with ANG II. Acutely administered losartan (3 mg/kg iv) restored VEinduced inhibition of renal SNA (P < 0.001) in rats chronically infused with ANG II. In contrast, this treatment had no effect in the vehicle-infused group. Therefore, it appears that chronic infusion of ANG II can attenuate VE-induced renal sympathoinhibition through a mechanism requiring AT 1 receptor activation. The attenuated sympathoinhibitory response to VE in ANG II-infused animals remained after arterial barodenervation and systemic vasopressin V 1 receptor antagonism and appeared to depend on ANG II being chronically increased because ANG II given acutely had no effect on VE-induced renal sympathoinhibition. Keywordssympathetic nerve activity; cardiopulmonary reflex; body fluid balance; arterial baroreceptor reflex Numerous studies have investigated interactions between circulating ANG II and the arterial baroreceptor reflex. Whereas recent studies indicate that an acute increase in circulating ANG II can attenuate the increase in sympathetic nerve activity (SNA) that follows arterial baroreceptor unloading (34), chronic increases of ANG II have been repeatedly demonstrated to reset arterial baroreflex control of SNA (4, 6). The latter effect may permit SNA to rise relative to the prevailing level of arterial pressure. In addition to the arterial Copyright © 2003 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript baroreflex, the cardiopulmonary baroreflex is also an important determinant of sympathetic outflow as well as sodium and water balance. However, the extent to which chronic increases of ANG II might interact with this reflex to modify the SNA response to volume expansion (VE) is not known. This is surprising given that norma...

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Section: Discussionmentioning

confidence: 99%

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…12 Recently, in our laboratory, we have observed that interventions that raise MCFP by approximately 1 mm Hg are also associated with an increase in CO of approximately 10% to 15%. 26,32 Thus, changes in MCFP can have a significant impact on CO. In the present study, we observed a difference in MCFP that ranged from 1.2 to 1.7 mm Hg, which is of sufficient magnitude to have significantly elevated CO.…”

Section: Discussionmentioning

confidence: 99%

Venous Tone in the Developmental Stages of Spontaneous Hypertension

1998

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Abstract-The initial stages of hypertension in the spontaneously hypertensive rat (SHR) are characterized by an increase in cardiac output. Venous capacitance plays an important role in the control of cardiac output. This study tested the hypothesis that venous tone is elevated in the developmental stages of spontaneous hypertension. Male SHR or normotensive Wistar-Kyoto (WKY) rats were instrumented for the measurement of arterial pressure (FAP) and intrathoracic vena caval pressure (FVP). A latex-tipped catheter was advanced into the right atrium via the jugular vein. Mean circulatory filling pressure (MCFP), an index of integrated venomotor tone, was calculated as MCFPϭFVPϩ(FAPϪFVP)/VAR. FAP and FVP were recorded after 5 seconds of right atrial balloon inflation. The venous to arterial compliance ratio (VAR) was estimated as 76 for WKY and 106 for SHR. Mean arterial pressure (MAP), heart rate, and MCFP were recorded in conscious rats of 4 to 6 and 8 to 10 weeks of age. In 4-to 6-week-old rats, both MAP and MCFP were significantly elevated in the SHR (MAP, 129Ϯ6 mm Hg; MCFP, 6.6Ϯ0.4 mm Hg) compared with the age-matched WKY (MAP, 91Ϯ6 mm Hg; MCFP, 5.4Ϯ0.4 mm Hg), whereas heart rate was not significantly different. The elevations in MAP (SHR, 144Ϯ4 mm Hg; WKY, 102Ϯ3 mm Hg) and MCFP (SHR, 7.7Ϯ0.3 mm Hg; WKY, 6.0Ϯ0.2 mm Hg) in SHR were exaggerated at 8 to 10 weeks of age. After ganglionic blockade (chlorisondamine; 10 mg/kg), the differences in MCFP were no longer statistically significant between SHR and WKY at both 4 to 6 weeks of age (3.9Ϯ0.2 versus 4.0Ϯ0.3 mm Hg) and 8 to 10 weeks of age (5.0Ϯ0.3 versus 4.3Ϯ0.3 mm Hg, respectively). The differences in MAP at 4 to 6 weeks of age (79Ϯ7 versus 67Ϯ5 mm Hg, respectively) also were not statistically significant after ganglionic blockade. However, a significant difference in MAP between strains remained after ganglionic blockade in 8-to 10-week-old rats (90Ϯ5 versus 63Ϯ3 mm Hg, respectively). These findings indicate that venous tone is increased via autonomic effector systems during the developmental stages of spontaneous hypertension. These data also suggest that autonomic mechanisms predominate at very early stages, whereas nonautonomic mechanisms assume more importance in maintaining the elevated MAP as hypertension progresses. (Hypertension. 1998;31[part 1]:139-144.)

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“…autonomic parameters, such as blood pressure and heart rate (Martin et al, 1991;Martin and Haywood, 1993). The cellular populations in the PVH that are responsive to BMI microinjection have not yet been defined.…”

Section: Effects Of Gaba Antagonism On Pvh Activitymentioning

confidence: 99%

Neurotransmitter Regulation of Cellular Activation and Neuropeptide Gene Expression in the Paraventricular Nucleus of the Hypothalamus

2002

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Norepinephrine (NE), glutamate (Glu), and GABA have been identified as important neurotransmitters governing neuroendocrine mechanisms represented in the paraventricular nucleus of the hypothalamus (PVH). Microinjection studies were used to compare the efficacy of these transmitter mechanisms in stimulating PVH output neurons. Local administration of NE provoked an increase in plasma corticosterone levels and Fos induction in the both the parvocellular and magnocellular divisions of the nucleus. This treatment also stimulated a robust increase in corticotropin-releasing factor (CRF) heteronuclear (hn) RNA in the parvocellular PVH and a more subtle, although reliable, increase in arginine vasopressin (AVP) hnRNA in this same compartment. Local administration of the GABA A receptor antagonist bicuculline methiodide (BMI) resulted in increased plasma corticosterone and, in contrast to NE treatment, Fos induction limited primarily to the parvocellular PVH.BMI elicited marked increases in both CRH and AVP hnRNAs within the parvocellular division of the nucleus. Over a wide range of concentrations, Glu failed to produce reliable increases in corticosterone secretion and induced only weak activational responses limited primarily to non-neurosecretory regions of the PVH. Local Glu administration did, however, provoke Fos induction in identified GABAergic neurons immediately adjoining the PVH, suggesting that the muted response to Glu may be a consequence of concurrent activation of local inhibitory interneurons. These results support a differential involvement of adrenergic, glutamatergic and GABAergic mechanisms in regulating neurosecretory populations of the PVH and suggest that involvement of local circuit neurons must be carefully considered in the interpretation of microinjection studies.

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Hemodynamic responses to paraventricular nucleus disinhibition with bicuculline in conscious rats

Cited by 54 publications

References 0 publications

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Venous Tone in the Developmental Stages of Spontaneous Hypertension

Neurotransmitter Regulation of Cellular Activation and Neuropeptide Gene Expression in the Paraventricular Nucleus of the Hypothalamus

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