Role of transmitters in mediating hypothalamic control of electrolyte excretion

Morris, Mariana; McCann, S. M.; Orias, R.

doi:10.1139/y77-157

Cited by 39 publications

(21 citation statements)

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“…Injection of carbachol into the third cerebral ventricle (3V), into the medial septal area, and into several other CNS structures induces natriuresis and kaliuresis through the activation of muscarinic receptors (4)(5)(6)(7). The hypothalamic natriuretic system is also controlled by a stimulatory a1-adrenergic and an inhibitory f-adrenergic pathway.…”

mentioning

confidence: 99%

Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.

Antunes‐Rodrigues

Marubayashi²,

Favaretto³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Expansion of the blood volume induces natriuresis, which tends to return the blood volume to normal. This response is mediated at least in part by the release of atrial natriuretic peptide (ANP) into the circulation. Previous experinents have shown the participation of the anterior ventral third ventricular (AV3V) region of the hypothalamus in the ANP release that follows volume expansion. When injected into the AV3V region, the cholinergic drug carbachol induces natriuresis and the release of ANP. In the present experiments, microinjection of norepinephrine into the AV3V region induced natriuresis and an increase in plasma ANP. To determine whether cholinergic and a-adrenergic pathways are crucial to the volume expansion-induced release of ANP, certain receptor-blocking drugs were injected into the AV3V region ofconscious rats. Thirty minutes later blood volume was expanded by intravenous injection of 2.0 ml/100 g of body weight of hypertonic saline (0.3 M NaCI). Microinjection of isotonic saline (2 gd) into AV3V region of control animals 30 min prior to volume expansion had no effect on the 3-fold increase in plasma ANP concentrations measured 5 min after volume expansion. In contrast, although the receptor-blocking drugs did not alter the initial concentrations of plasma ANP 30 min later, just prior to volume expansion, blockade of muscarinic cholinergic receptors by intraventricular injection of 5 nmol (2 id) of atropine sulfate or methylatropine markedly reduced the response to volume expansion but did not obliterate it. Microinjection of the a receptor blocker phentolamine (5 nmol) into the AV3V 30 min prior to volume expansion also markedly suppressed the ANP response. Intraperitoneal (i.p.) injection of methylatropine (0.01 mmol/100 g of body weight), which does not cross the blood-brain barrier, also did not affect the basal levels of ANP 30 min after i.p. injection. But, in striking contrast with the blockade of the response to volume expansion induced by intraventricular injection of methylatropine, the response to volume expansion was markedly enhanced by i.p. injection of methylatropine. The results therefore indicate that hypothalamic muscarinic and a-adrenergic synapses are essential to release of ANP in response to volume expansion. These results are consistent with a hypothetical pathway for physiological control of ANP release which involves distension of baroreceptors within the right atria, carotid and aortic sinuses, and kidney which alters afferent input to brain stem noradrenergic neurons with axons projecting to the AV3V region. There they activate cholinergic interneurons by an a1-adrenergic synapse. The cholinergic neurons in turn stimulate ANP neurons in this brain region via muscarinic receptors. The stimulation of these neurons activates efferent pathways which induce the release of ANP.The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to...

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mentioning

confidence: 99%

Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.

Antunes‐Rodrigues

Marubayashi²,

Favaretto³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…Consistent with these findings, nanoinjection of norepinephine into the MnPO, the major source of AV3V efferents, increased renal sodium excretion (60) and ANP release, whereas acute pharmacological blockade of α1-adrenoceptors in the AV3V reduced the ANP release induced by blood volume expansion (40). Therefore, we hypothesized that noradrenergic neurotransmission from the A1 noradrenergic group to the MnPO may be involved in the cardiovascular responses to hypernatremia.…”

Section: The Anteroventral Third Ventricle Regionmentioning

confidence: 56%

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

Cravo

Lopes

Pedrino

2011

Braz J Med Biol Res

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Water deprivation and hypernatremia are major challenges for water and sodium homeostasis. Cellular integrity requires maintenance of water and sodium concentration within narrow limits. This regulation is obtained through engagement of multiple mechanisms and neural pathways that regulate the volume and composition of the extracellular fluid. The purpose of this short review is to summarize the literature on central neural mechanisms underlying cardiovascular, hormonal and autonomic responses to circulating volume changes, and some of the findings obtained in the last 12 years by our laboratory. We review data on neural pathways that start with afferents in the carotid body that project to medullary relays in the nucleus tractus solitarii and caudal ventrolateral medulla, which in turn project to the median preoptic nucleus in the forebrain. We also review data suggesting that noradrenergic A1 cells in the caudal ventrolateral medulla represent an essential link in neural pathways controlling extracellular fluid volume and renal sodium excretion. Finally, recent data from our laboratory suggest that these structures may also be involved in the beneficial effects of intravenous infusion of hypertonic saline on recovery from hemorrhagic shock.

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“…We had previously shown that cholinergic and adrenergic synapses within the hypothalamus mediated the natriuresis induced by 3V injection of hypertonic saline (15). Therefore, we evaluated their role in the ANP release evoked by volume expansion.…”

Section: Role Of Hypothalamic Anpergic Neurons In Volume Expansionindmentioning

confidence: 99%

“…Cholinergic blockade with atropine diminished the response to norepinephrine and blocked the natriuretic response to hypertonic saline. We suggested that sodium receptors in the ventricular wall (14) modify renal sodium excretion by a stimulatory pathway involving cholinergic and a-adrenergic receptors and inhibit sodium excretion by a tonically active ß-receptor pathway (15). Much later, ß-receptors were described in the hypothalamus (16) and it was shown that their levels are modified by gonadal steroids (16).…”

Section: Transmitters In the Hypothalamus: Control Of Fluid And Electmentioning

confidence: 99%

Neuroendocrine control of body fluid homeostasis

McCann

Gutkowska²,

Antunes‐Rodrigues

2003

Braz J Med Biol Res

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Angiotensin II and atrial natriuretic peptide (ANP) play important and opposite roles in the control of water and salt intake, with angiotensin II promoting the intake of both and ANP inhibiting the intake of both. Following blood volume expansion, baroreceptor input to the brainstem induces the release of ANP within the hypothalamus that releases oxytocin (OT) that acts on its receptors in the heart to cause the release of ANP. ANP activates guanylyl cyclase that converts guanosine triphosphate into cyclic guanosine monophosphate (cGMP). cGMP activates protein kinase G that reduces heart rate and force of contraction, decreasing cardiac output. ANP acts similarly to induce vasodilation. The intrinsic OT system in the heart and vascular system augments the effects of circulating OT to cause a rapid reduction in effective circulating blood volume. Furthermore, natriuresis is rapidly induced by the action of ANP on its tubular guanylyl cyclase receptors, resulting in the production of cGMP that closes Na + channels. The OT released by volume expansion also acts on its tubular receptors to activate nitric oxide synthase. The nitric oxide released activates guanylyl cyclase leading to the production of cGMP that also closes Na + channels, thereby augmenting the natriuretic effect of ANP. The natriuresis induced by cGMP finally causes blood volume to return to normal. At the same time, the ANP released acts centrally to decrease water and salt intake.

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Role of transmitters in mediating hypothalamic control of electrolyte excretion

Cited by 39 publications

References 0 publications

Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.

Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

Neuroendocrine control of body fluid homeostasis

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