Natriuresis, kaliuresis and diuresis in the rat following microinjections of carbachol into the septal area

Saad, Wilson Abrão; Camargo, Laa; Netto, Cincinato Rodrigues Silva; Gentil, C; Antunes‐Rodrigues, José; Covian, Miguel R.

doi:10.1016/0091-3057(75)90006-4

Cited by 34 publications

(7 citation statements)

References 19 publications

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“…A natriuresis has previously been reported in response to acute injections of carbachol into the cerebral ventricles [7], the septal area [8], or the lateral hypothalamus [9]. The present results extend these findings to the ventricular infusion of low doses of carbachol.…”

Section: Discussionsupporting

confidence: 88%

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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Section: Discussionsupporting

confidence: 88%

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

1990

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“…Increased natriuresis has been shown to oc cur after lesion of the paraventricular nucleus [10], posterior hypothalamus [4] and preoptic area [11]. Cholinergic stimulation of several hypothalamic [18] and ventricular [6] areas and of regions in the septal area [16] caused increased urinary excretion of sodium and potassium. The adrenergic pathways of the septal area in the regulation of electrolyte and water excretion demonstrated that the stimu lating and inhibitory effects are mediated by a-and (3-adrenoceptors, repectively [1].…”

Section: Introductionmentioning

confidence: 99%

Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Saad¹,

Camargo²,

Saad³

1984

Pharmacology

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The effects of sodium and potassium excretion after intrahypothalamic administration of two α-adrenoceptor agonists and the effect of α-adrenoceptor antagonists were studied in groups of rats. Prazosin was equally effective at blocking the natriuretic and kaliuretic responses to the α₁-adrenoceptor agonist phenylephrine and the mixed α₁/α₂-adrenoceptor agonist noradrenaline, while yohimbine which acts preferentially on α₂-adrenoceptors was effective in potentiating these responses. These results suggest the presence of two types of α-adrenoceptors for the modulation of ventromedial hypothalamic pathways that interfere with the regulation of the two cations: stimulation of α₁-adrenoceptors facilitates, while stimulation of adrenoceptors inhibits the excretion of the ions.

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“…jection of norepinephrine or hypertonic saline; these results suggest that a hormonal pathway mediates the effects ofthese stimuli on sodium excretion (7). Since we have shown that the cholinergic, adrenergic, or osmotic stimulation of tissue adjacent to the 3V induces natriuresis and kaliuresis (5)(6)(7)(8)(9)(10)(11) and since ANP is localized in these structures (19), in the present experiments, we determined if the effects on sodium excretion of stimulation and ablation of the AV3V region might be mediated, at least in part, by altered ANP release.…”

mentioning

confidence: 96%

“…Cholinergic or adrenergic stimulation of the medial septal area, medial preoptic area, anterior lateral hypothalamus, and subfornical organ as well as the anterior portion of the third ventricle (AV3V) induces a dose-related natriuresis accompanied by a lesser kaliuresis (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Thus, considerable evidence indicates that the medial preoptic area, anterior lateral hypothalamus, subfornical organ, AV3V, habenula, stria medullaris, supraoptic nucleus, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (12,13,17).…”

mentioning

confidence: 99%

Role of the hypothalamus in the control of atrial natriuretic peptide release.

Baldissera

Menani

Santos

et al. 1989

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

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Stimulation of the region antero-ventral to the third cerebral ventricle (AV3V) by a cholinergic drug, carbachol, and lesions of the AV3V have been demonstrated in previous studies to either augment or decrease sodium excretion, respectively. Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Consequently, to evaluate a possible role of brain ANP in evoking the changes in renal sodium excretion that follow stimulations or lesions of the AV3V, we determined the effect of injection of carbachol into the AV3V of rats on the concentration of plasma ANP and its content in several neural tissues, the pituitary gland, lungs, and atria. Conversely, the effect of lesions in the AV3V on plasma ANP and the content of the polypeptide in the various organs was determined. Injection of carbachol into the AV3V produced the expected natriuresis, which was accompanied within 20 min by a dramatic rise in the plasma ANP concentration and a rise in ANP content in the medial basal hypothalamus, the neurohypophysis, and particularly the anterior hypophysis but without alterations in the content of ANP in the lungs or the right or left atrium. Conversely, there was a dramatic decline in plasma ANP at both 24 and 120 hr after the AV3V lesions had been placed. This was accompanied by a slight decline in the content of the peptide in the lungs. There was no change in its content in the right atrium at 24 hr after lesions, but there was a significant increase at 120 hr. There was a small decline in the content in the left atrium at 24 hr, followed by a rebound to slightly elevated levels at 120 hr. These small changes contrasted sharply with the dramatic decline in content of the peptide in the medial basal hypothalamus, median eminence, neurohypophysis, choroid plexus, anterior hypophysis, and olfactory bulb. These declines persisted or became greater at 120 hr; except in the olfactory bulb in which the decline was no longer significant. The dramatic increase in plasma ANP after carbachol stimulation of the AV3V that was accompanied by marked elevations in content of the peptide in basal hypothalamus and neuro-and adenohypophysis suggests that the natriuresis resulting from this stimulation is brought about at least in part by release of ANP from the brain. Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. In view of the much larger quantities of the peptide stored in the atria, it is still possible that changes in atrial release may contribute to the alterations in plasma ANP observed after stimulation or ablation of the AV3V region; however, these results suggest that the dramatic changes in plasma ANP that followed these manipu...

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Natriuresis, kaliuresis and diuresis in the rat following microinjections of carbachol into the septal area

Cited by 34 publications

References 19 publications

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

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

Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Role of the hypothalamus in the control of atrial natriuretic peptide release.

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Natriuresis, kaliuresis and diuresis in the rat following microinjections of carbachol into the septal area

Cited by 34 publications

References 19 publications

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

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

Effects of the Application of &alpha;<sub>1</sub>and &alpha;<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Role of the hypothalamus in the control of atrial natriuretic peptide release.

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Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion