Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves

Silva-Netto, C. R.; Jackson, Rudolph S.; Colindres, Rómulo E.

doi:10.1152/ajprenal.1986.250.2.f322

Cited by 7 publications

(8 citation statements)

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“…The denervation was accomplished by cutting all visible nerves along the renal artery and by stripping both renal artery and hilum of all nerve bundles. Immediately thereafter, the renal artery was surrounded with a cotton pledget that had absorbed a 1o (vol/vol) phenol solution in absolute ethanol (36)(37)(38) Carotid-aortic deafferented rats (n = 8) had significantly lower (P < 0.001) plasma ANP concentrations under basal conditions than the sham-operated rats (n = 7) (Fig. 1) (Fig.…”

Section: Methodsmentioning

confidence: 99%

Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion.

Antunes‐Rodrigues

Machado

Andrade

et al. 1992

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

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Our previous studies have shown that stimulation of the anteroventral third ventricle (AV3V) region of the brain increases atrial natriuretic peptide (ANP) release, whereas lesions of the AV3V region or median eminence of the tuber cinereum block the release of ANP caused by blood volume expansion. These results suggest that participation of the central nervous system is critical to this response. The role of baroreceptors in the response was evaluated in the current research by studying the response of plasma ANP to blood volume expansion induced by intravenous injection of hypertonic saline solution (0.3 M NaCl, 2 ml/100 g of body weight, over 1 min) in conscious, freely moving male rats. Plasma samples were assayed for ANP by radioimmunoassay. In sham-operated rats, blood volume expansion induced a rapid increase in plasma ANP: the concentration peaked at 5min and remained elevated at 15 min after saline injection. One week after deafferentation of the carotid-aortic baroreceptors, basal plasma ANP concentrations were highly significantly decreased on comparison with values of sham-operated rats; plasma ANP levels S min after blood volume expansion in the deafferented rats were greatly reduced. Unilateral right vagotomy reduced resting levels of plasma ANP but not the response to blood volume expansion; resting concentrations of plasma ANP and responses to expansion were normal in bilaterally vagotomized rats. In rats that had undergone renal deafferentation, resting levels of ANP were normal but the response to blood volume expansion was significantly suppressed. The evidence indicates that afferent impulses via the right vagus nerve may be important under basal conditions, but they are not required for the ANP release induced by blood volume expansion. In contrast, baroreceptor impulses from the carotid-aortic sinus regions and the kidney are important pathways involved in the neuroendocrine control of ANP release. The evidence from these experiments and our previous stimulation and lesion studies indicates that the ANP release in response to volume expansion is mediated by afferent baroreceptor input to the AV3V region, which mediates the increased ANP release via activation of the hypothalamic ANP neuronal system. Atrial natriuretic peptide (ANP), which is primarily localized to the atrial myocytes, plays an important role in control of body fluid homeostasis by decreasing salt and water intake and increasing salt and water excretion (1-7). When the blood volume is expanded-for example, by intravenous injection of saline solution-ANP is released into the circulation and induces natriuresis, in part by direct action on the kidneys (8, 9). Natriuresis is also promoted by direct suppression of the release of aldosterone from the adrenal glomerulosa by ANP (1). ANP also inhibits the release of renin from the juxtaglomerular apparatus of the kidneys (10, 11), which decreases the release of angiotensin II, further decreasing the release of aldosterone. Since angiotensin II is an important mediator of sa...

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Section: Methodsmentioning

confidence: 99%

Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion.

Antunes‐Rodrigues

Machado

Andrade

et al. 1992

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

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“…These effects are only partially due to the release of neurohypophysial hormones, since the administration of OT and AVP promoted a further effect of LHA stimulation (479). Silva-Netto et al (478) have also shown the natriuretic effect of carbachol stimulation of the LHA in rats with intact or denervated kidneys. The control values for Na ϩ excretion were significantly higher in rats with denervated kidneys, consistent with the previously described "denervation diuresis" (114, 115, 119).…”

Section: Role Of ␣-Adrenergic and Cholinergic Receptors In Controlmentioning

confidence: 98%

Neuroendocrine Control of Body Fluid Metabolism

Antunes‐Rodrigues

Castro

Elias

et al. 2004

Physiological Reviews

397

310

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Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+ receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

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“…In addition, other authors have demonstrated that the central injection of carbachol in duces a natriuretic response that is not me diated by a rise in arterial pressure [9]. These authors have presented evidence that a hor monal factor is responsible for the increase in sodium excretion, at least with hypotha lamic injections [10].…”

Section: Discussionmentioning

confidence: 98%

Renal Function during Onset of Carbachol-Induced Hypertension in Conscious Rats

1990

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This study evaluated the changes in renal function that occur during the early phases of chronic infusion of carbachol into the lateral ventricle in conscious rats. Infusion of 1.0 µg/h of carbachol i.c.v. resulted in a prompt pressor response with mean arterial pressure rising 20 mm Hg within 15 min. The pressure remained elevated for the duration of a 2-hour infusion. Carbachol infusion at 0.5 µg/h induced a similar elevation in blood pressure, but the onset was delayed, reaching significance only after 30–60 min. The higher dose of carbachol was associated with a marked and sustained natriuresis, with sodium excretion increasing from 2.1 ± 0.3 to 5.3 ± 1.0 µEq/100 g min after 2 h, compared to 2.0 ± 0.5 and 1.8 ± 0.3 µEq/100g min in vehicle-infused control animals. Sodium excretion did not change significantly in animals infused with carbachol at 0.5 µg/h. There were no significant changes in glomerular filtration rate in any of the groups. Plasma levels of atrial natriuretic peptide (ANP) were not altered significantly by ventricular infusion of carbachol (188 ± 99 before vs. 83 ± 17 pg/ml after infusion). It is concluded that the pressor response to central carbachol infusion is not dependent on retention of sodium and water. The natriuresis observed with carbachol infusion can be dissociated from the pressor response, and is not mediated by ANP.

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Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves

Cited by 7 publications

References 0 publications

Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion.

Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion.

Neuroendocrine Control of Body Fluid Metabolism

Renal Function during Onset of Carbachol-Induced Hypertension in Conscious Rats

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