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

Saad, Wilson Abrão; Camargo, Laa; Saad, W. A.

doi:10.1159/000137967

Cited by 15 publications

(3 citation statements)

References 18 publications

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“…The autoradiographic localization of [3]clonidine binding to non-adrenergic sites was similar to, but distinct from, α 2 -adrenergic receptors in human brain (31). Prazosin is effective in blocking the natriuretic and kaliuretic response to the α 1 -adrenoceptor agonist phenylephrine (32). The present study shows that injection of prazosin into the MSA did not modify the inhibitory responses induced by ANGII injected into the 3rdV on sodium, potassium and water excretion.…”

Section: Discussionsupporting

confidence: 57%

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

Saad

Guarda

Camargo

et al. 2002

Braz J Med Biol Res

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We investigated the role of α-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na + , K + and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/µl) increased water intake (12.5 ± 1.7 ml/120 min). Clonidine (20 nmol/ µl) injected into the MSA reduced the ANGII-induced water intake (2.9 ± 0.5 ml/120 min). Pretreatment with 80 nmol/µl yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 ± 0.4 and 3.1 ± 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGIIinduced water intake (0.2 ± 0.1 and 0.2 ± 0.1 ml/120 min, respectively). ANGII reduced Na + (23 ± 7 µEq/120 min), K + (27 ± 3 µEq/120 min) and urine volume (4.3 ± 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of α 1 -and α 2 -antagonists decreased ANGII-induced water intake, and abolished the Na + , K + and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal α 1 -and α 2 -adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII. Correspondence

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Section: Discussionsupporting

confidence: 57%

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

Saad

Guarda

Camargo

et al. 2002

Braz J Med Biol Res

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“…In line with this working model, brain slice electrophysiological recordings of NE-responsive PVN neurons revealed that the excitatory effect of NE is mimicked by α 1 agonist phenylephrine (PHE), while the inhibitory effect of NE is mimicked by α 2 agonist clonidine (Wellman et al, 1993). Similar co-localization and antagonistic actions are observed in other brain regions, including NTS, DMV and VMH, suggesting that this mutual antagonistic mode of action of α 1 and α 2 -AR is generalized across different brain regions (Young and Kuhar, 1980;Saad et al, 1984;Feldman and Felder, 1989). Antagonistic action between α 1 and α 2 receptors on feeding is versatile and tightly regulated.…”

Section: Hypothalamic α-Adrenergic Receptors In Cardiometabolic Regulationmentioning

confidence: 82%

Hypothalamic GPCR Signaling Pathways in Cardiometabolic Control

Deng

Grobe

et al. 2021

Front. Physiol.

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Obesity is commonly associated with sympathetic overdrive, which is one of the major risk factors for the development of cardiovascular diseases, such as hypertension and heart failure. Over the past few decades, there has been a growing understanding of molecular mechanisms underlying obesity development with central origin; however, the relative contribution of these molecular changes to the regulation of cardiovascular function remains vague. A variety of G-protein coupled receptors (GPCRs) and their downstream signaling pathways activated in distinct hypothalamic neurons by different metabolic hormones, neuropeptides and monoamine neurotransmitters are crucial not only for the regulation of appetite and metabolic homeostasis but also for the sympathetic control of cardiovascular function. In this review, we will highlight the main GPCRs and associated hypothalamic nuclei that are important for both metabolic homeostasis and cardiovascular function. The potential downstream molecular mediators of these GPCRs will also be discussed.

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“…The potential contributions of the central nervous system and kidneys in these models of chronic stress hypertension are suggested by studies of acute environmental stress. Acute exposure to air jet stress leads to antinatriuresis and an increase in renal sympathetic nerve activity that is much greater in nephrine into the ventromedial hypothalamus, lateral hypothalamus, septal area, or 3rd cerebral ventricle of conscious rats; this natriuresis is prevented by ai-adrenoceptor antagonists and is potentiated by a 2 -adrenoceptor antagonists (Camargo et al, 1976;Morris et al, 1977;Pillar et al, 1977;Saad et al, 1984). In contrast, an antinatriuresis follows the injection of isoproterenol into the lateral hypothalamus, septal area, or 3rd cerebral ventricle; this antinatriuresis is abolished by ft, 2 -or ft-, but not ft-adrenoceptor antagonists (Morris et al, 1977;Pillar et al, 1977;Camargo et al, 1979).…”

mentioning

confidence: 99%

Hypothalamic beta 2-adrenoceptor control of renal sympathetic nerve activity and urinary sodium excretion in conscious, spontaneously hypertensive rats.

Koepke¹,

Jones²,

DiBona³

1986

Circulation Research

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SUMMARY. The contributions of /Si-, B^-, and a 2 -adrenoceptors in the posterior hypothalamus to the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from environmental stress (air jet) in conscious spontaneously hypertensive rats were examined. Air stress increased mean arterial pressure and renal sympathetic nerve activity (54% from 7.0 ± 0.7 integrator resets/min), and decreased urinary sodium excretion (44% from 2.7 ± 0.4 ^Eq/min per 100 g body weight). After bilateral injection of ICI 118,551 OS2-adrenoceptor antagonist) into the posterior hypothalamus of the same spontaneously hypertensive rats, air stress had no effect on renal sympathetic nerve activity (8% from 4.8 ± 0.7 integrator resets/min) or urinary sodium excretion (2% from 5.2 ± 0.8 /lEq/min per 100 g body weight), but still increased mean arterial pressure. Bilateral injection of isoproterenolol (/9-adrenoceptor agonist) into the posterior hypothalamus enhanced the renal sympathetic nerve activity and urinary sodium excretion (but not mean arterial pressure) responses to air stress. Air stress had no effect on renal sympathetic nerve activity or urinary sodium excretion when ICI 118,551 was given into the posterior hypothalamus before isoproterenol. Atenolol (/Ji-adrenoceptor antagonist) had no effect on the renal responses to air stress when given alone or before isoproterenol. Similarly, ICI 118,551 administered into the lateral hypothalamus or lateral cerebral ventricle, or guanabenz (a 2 -adrenoceptor agonist) given into the posterior hypothalamus, had no effects on the renal or mean arterial pressure responses to air stress. Thus, /3 2 -adrenoceptors in the posterior hypothalamus mediate the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress in conscious spontaneous hypertensive rats. (Circ Res 58: 241-248, 1986)

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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

Cited by 15 publications

References 18 publications

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

Hypothalamic GPCR Signaling Pathways in Cardiometabolic Control

Hypothalamic beta 2-adrenoceptor control of renal sympathetic nerve activity and urinary sodium excretion in conscious, spontaneously hypertensive rats.

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