The role of central muscarinic and nicotinic receptors in the regulation of sodium and potassium renal excretion

Saad, Wilson Abrão; Camargo, Laa; Graeff, Frederico Guilherme; Silva-Neto, C.R.; Antunes‐Rodrigues, José; Covian, Miguel R.

doi:10.1016/0306-3623(76)90051-3

Cited by 17 publications

(13 citation statements)

References 5 publications

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“…Plasma ANP concentrations increased significantly and maximally at 20 min after 3V injection of carbachol and ,,(8) (8) I, (5) remained elevated at 40 min (Fig. 2).…”

Section: Resultsmentioning

confidence: 98%

“…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: 99%

“…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).…”

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confidence: 99%

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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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“…Plasma ANP concentrations increased significantly and maximally at 20 min after 3V injection of carbachol and ,,(8) (8) I, (5) remained elevated at 40 min (Fig. 2).…”

Section: Resultsmentioning

confidence: 98%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

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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“…These findings are reiterated by a study showing that impaired pelvic neurokinin expression associated with responsiveness of renal sensory receptors in 16-wk old LP offspring are conducive to excess renal reabsorption of sodium and development of hypertension in this programmed model [8]. Otherwise, investigators have demonstrated that administration of adrenergic agonists into different cerebral sites elicits a substantial increase in renal sodium excretion accompanied by decreasing arterial pressure [10,[16][17][18]21]. Thus, we hypothesized that enhanced blood pressure in maternal low-protein intake offspring is associated at least in part, with changes in renal neural activity and reduced urinary sodium excretion that may relate to imbalanced central adrenergic receptors modulation.…”

Section: Discussionmentioning

confidence: 99%

“…It has long been known that there is an association between the CNS and the control of water and salt excretion by the kidneys [1,13,14]. Adrenergic stimulation of the septal area, lateral hypothalamus, subfornical organ, and the anterior region of the third ventricle induces dose-related natriuresis accompanied by, but to a lesser extent, kaliuresis [9,[15][16][17][18][19][20][21]. On the other hand, studies have shown that electrolytic lesion of the hypothalamic regions in conscious rats reduces salt intake, and the pressor response to cholinergic and noradrenergic microinjection into the median preoptic nucleus [22].…”

Section: Introductionmentioning

confidence: 99%

Effect of intracerebroventricular epinephrine microinjection on blood pressure and urinary sodium handling in gestational protein-restricted rat adult male offspring

Gontijo

Bôer

Custódio

et al. 2018

Preprint

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Background. In this study, we hypothesized that blunting of the natriuresis response to intracerebroventricularly (i.c.v.) microinjected adrenergic agonists are involved in the development of hypertension in maternal low-protein (LP) intake offspring. Methods. Stainless steel cannula was stereotaxically implanted into the right lateral ventricle, by use of techniques reported elsewhere and after that, was evaluated the effect of i.c.v. injection of adrenergic agonists, at increasing concentrations, and of α1 and α2-adrenoceptor antagonists on blood pressure and urinary sodium handling in LP offspring relative to age-matched, normal (NP) protein intake group. Results. We confirmed that epinephrine (Epi) microinjected into the lateral ventricle (LV) of conscious NP rats leads to enhanced natriuresis followed by a reduction in arterial pressure. This response was associated with increased proximal and post-proximal sodium excretion accompanied by an unchanged glomerular filtration rate. The current study showed in both, NP and LP offspring that natriuretic effect of Epi injection into the LV was abolished by prior local microinjection of an α1adrenoceptor antagonist (prazosin). Conversely, LV α2-adrenoceptor antagonist (yohimbine) administration potentiated the action of epinephrine. The LV yohimbine pretreatment normalized urinary sodium excretion and reduced the blood pressure in LP compared with age-matched NP offspring. Conclusion. These are, as far as we are aware, the first results showing the role of central adrenergic receptors interaction on hypertension pathogenesis in maternal protein-restricted fetal programming offspring. The study also provides good evidence of the existence of central nervous system adrenergic mechanisms consisting of α1 and α2-adrenoceptors, which works reciprocally on the control of renal sodium excretion and blood pressure. Although the precise mechanism of the different natriuretic response of NP and LP rats is still uncertain, these results led us to speculate that inappropriate neural adrenergic pathways might have significant effects on tubule sodium transport, resulting in the inability of the kidneys to control hydrosaline balance, and, consequently, an increase in blood pressure.3

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Altered urinary sodium excretion response after central cholinergic and adrenergic stimulation of adult spontaneously hypertensive rats

et al. 2015

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In this study, we hypothesized that blunting of the natriuresis response to intracerebroventricularly (i.c.v.) microinjected cholinergic and adrenergic agonists is involved in the development of hypertension in spontaneously hypertensive rats (SHR). We evaluated the effect of i.c.v. injection of cholinergic and noradrenergic agonists, at increasing concentrations, and of muscarinic cholinergic and α1 and α2-adrenoceptor antagonists on blood pressure and urinary sodium handling in SHR, compared with age-matched Wistar Kyoto rats (WR). We confirmed that CCh and NE microinjected into the lateral ventricle (LV) of conscious rats leads to enhanced natriuresis. This response was associated with increased proximal and post-proximal sodium excretion accompanied by an unchanged rate of glomerular filtration. We showed that cholinergic-induced natriuresis in WR and SHR was attenuated by previous i.c.v. administration of atropine and was significantly lower in the hypertensive strain than in WR. In both groups the natriuretic effect of injection of noradrenaline into the LV was abolished by previous local injection of an α1-adrenoceptor antagonist (prazosin). Conversely, LV α2-adrenoceptor antagonist (yohimbine) administration potentiated the action of noradrenaline. The LV yohimbine pretreatment normalized urinary sodium excretion in SHR compared with age-matched WR. In conclusion, these are, as far as we are aware, the first results showing the importance of interaction of central cholinergic and/or noradrenergic receptors in the pathogenesis of spontaneous hypertension. These experiments also provide good evidence of the existence of a central adrenergic mechanism consisting of α1 and α2-adrenoceptors which works antagonistically on regulation of renal sodium excretion.

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The role of central muscarinic and nicotinic receptors in the regulation of sodium and potassium renal excretion

Cited by 17 publications

References 5 publications

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

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

Effect of intracerebroventricular epinephrine microinjection on blood pressure and urinary sodium handling in gestational protein-restricted rat adult male offspring

Altered urinary sodium excretion response after central cholinergic and adrenergic stimulation of adult spontaneously hypertensive rats

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