On a Dual Role for Clonidine Stimulation of the Ventromedial Nucleus of the Hypothalamus in Sodium and Potassium Renal Excretions of Rats

Saad, Wilson Abrão; Camargo, Gabriela; Camargo, Luiz Antônio de Arruda

doi:10.1159/000139440

Cited by 2 publications

(2 citation statements)

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“…The diuresis produced by the central administration of clonidine has been attributed to the inhibition of vasopressin release (35) and natriuresis has been attributed to renal sympathoinhibition (34,36). The present results suggest that the facilitatory effect of clonidine on natriuresis and kaliuresis is mediated by the activation of α 1 -adrenoceptors and the inhibitory effects are mediated by α 2A -adrenoceptors (37). Circumventricular structures present excitatory and inhibitory mechanisms responsible for regulating the renal sodium, potassium and water excretion (29).…”

Section: Discussionmentioning

confidence: 63%

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: Discussionmentioning

confidence: 63%

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 addition, GABA in the central nervous system may modulate vasopressin, a humoral substance involved in cardiovascular regulation in the body. Intracerebroventricular or intravenous application of GABA markedly decreases the plasma level of vasopressin (33,39). Therefore, it appears that central GABA exerts its cardiovascular effect through both autonomic and humoral pathways.…”

mentioning

confidence: 99%

Reduced endogenous GABA-mediated inhibition in the PVN on renal nerve discharge in rats with heart failure

Kun

Patel

2002

American Journal of Physiology-Regulatory, Integrative and Comp

127

144

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One characteristic of heart failure (HF) is increased sympathetic activation. The paraventricular nucleus (PVN) of the hypothalamus (involved in control of sympathetic outflow) has been shown to have increased neuronal activation during HF. This study examined the influence of endogenous GABA input (inhibitory in nature) into the PVN on renal sympathetic nerve discharge (RSND), arterial blood pressure (BP), and heart rate (HR) in rats with HF induced by coronary artery ligation. In alpha-chloralose- and urethane-anesthetized rats, microinjection of bicuculline (a GABA antagonist) into the PVN produced a dose-dependent increase in RSND, BP, and HR in both sham-operated control and HF rats. Bicuculline attenuated the increase in RSND and BP in HF rats compared with control rats. Alternatively, microinjection of the GABA agonist muscimol produced a dose-dependent decrease in RSND, BP, and HR in both control and HF rats. Muscimol was also less effective in decreasing RSND, BP, and HR in HF rats than in control rats. These results suggest that endogenous GABA-mediated input into the PVN of rats with HF is less effective in suppressing RSND and BP compared with control rats. This is partly due to the post-release actions of GABA, possibly caused by altered function of post-synaptic GABA receptors in the PVN of rats with HF. Reduced GABA-mediated inhibition in the PVN may contribute to increased sympathetic outflow, which is commonly observed during HF.

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On a Dual Role for Clonidine Stimulation of the Ventromedial Nucleus of the Hypothalamus in Sodium and Potassium Renal Excretions of Rats

Cited by 2 publications

References 0 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

Reduced endogenous GABA-mediated inhibition in the PVN on renal nerve discharge in rats with heart failure

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