Role of the Renal Nerve in Glucocorticoid Hypertension.

Yoshida, Soichi; Yamada, Katsushi; Tamura, Yasushi; Yoshida, Sho

doi:10.1507/endocrj1954.35.877

Cited by 4 publications

(1 citation statement)

References 22 publications

(23 reference statements)

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“…For example, they increase glomerular filtration rate in animals and humans at physiological and pharmacological levels (1). Glucocorticoids increase urine volume (1,11,18,28,34), urinary sodium excretion (1,11,18,28,34), and potassium excretion (1, 11) and can cause negative water balance (11,28). Glucocorticoids interfere with the sodium-retaining properties of mineralocorticoids (14).…”

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confidence: 99%

Glucocorticoids increase salt appetite by promoting water and sodium excretion

Thunhorst¹,

Beltz²,

Johnson³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Glucocorticoids [e.g., corticosterone and dexamethasone (Dex)], when administered systemically, greatly increase water drinking elicited by angiotensin and sodium ingestion in response to mineralocorticoids [e.g., aldosterone and deoxycorticosterone acetate (DOCA)], possibly by acting in the brain. In addition, glucocorticoids exert powerful renal actions that could influence water and sodium ingestion by promoting their excretion. To test this, we determined water and sodium intakes, excretions, and balances during injections of Dex and DOCA and their coadministration (DOCAϩDex) at doses commonly employed to stimulate ingestion of water and sodium. In animals having only water to drink, Dex treatment greatly increased water and sodium excretion without affecting water intake, thereby producing negative water and sodium balances. Similar results were observed when Dex was administered together with DOCA. In animals having water and saline solution (0.3 M NaCl) to drink, Dex treatment increased water and sodium excretion, had minimal effects on water and sodium intakes, and was associated with negative water and sodium balances. DOCA treatment progressively increased sodium ingestion, and both water and sodium intakes exceeded their urinary excretion, resulting in positive water and sodium balances. The combination of DOCAϩDex stimulated rapid, large increases in sodium ingestion and positive sodium balances. However, water excretion outpaced total fluid intake, resulting in large, negative water balances. Plasma volume increased during DOCA treatment and did not change during treatment with Dex or DOCAϩDex. We conclude that increased urinary excretion, especially of water, during glucocorticoid treatment may explain the increased ingestion of water and sodium that occurs during coadministration with mineralocorticoids. thirst; urine volume; dexamethasone; deoxycorticosterone acetate; food intake SYSTEMICALLY ADMINISTERED mineralocorticoids, such as aldosterone and deoxycorticosterone acetate (DOCA), stimulate vigorous sodium ingestion by activating mineralocorticoid receptors in the brain. Glucocorticoids, such as corticosterone, greatly increase this salt appetite response when coadministered with mineralocorticoids (2,17,33,35). Systemically administered glucocorticoids also increase water drinking in response to peripheral and central administration of ANG II (9, 27). The potentiation of salt appetite and thirst by glucocorticoids has been postulated to arise from glucocorticoid actions within the brain, affecting either mineralocorticoid (17, 35) or ANG II (3,6,8,22) receptors. For example, high levels of glucocorticoids are proposed to increase type I mineralocorticoid receptors and thus mineralocorticoid binding in the brain (17,35). Additionally, glucocorticoids may increase the number of ANG II receptors in the brain (22) and thereby augment the central actions of ANG II (which, in turn, may interact with mineralocorticoid receptors).Glucocorticoids also have systemic effects that could facilitate ingest...

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mentioning

confidence: 99%

Glucocorticoids increase salt appetite by promoting water and sodium excretion

Thunhorst¹,

Beltz²,

Johnson³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The Neuroendocrinology, Neurochemistry and Molecular Biology of Thirst and Salt Appetite

Johnson¹,

Thunhorst²

2007

Handbook of Neurochemistry and Molecular Neurobiology

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Effects of Itraconazole, Dexamethasone and Naringin on the Pharmacokinetics of Nadolol in Rats

Miyazaki¹,

Misaka²,

Ogata³

et al. 2013

Drug Metabolism and Pharmacokinetics

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The aim of the present study was to clarify the involvement of P-glycoprotein (P-gp) or organic anion transporting polypeptide (Oatp) 1a5 in the pharmacokinetics of nadolol (NDL), a non-metabolized hydrophilic β-adrenoceptor blocker, in rats. Pretreatment with itraconazole (ICZ, P-gp inhibitor, 50 mg/kg) for 30 min before oral administration of NDL (10 mg/kg) significantly increased the area under the plasma concentration-time curve (AUC₀₋∞)of NDL by 1.7-fold compared with control. Intragastric administration of dexamethasone (DEX, 8 mg/kg) for 4 consecutive days increased P-gp level in the intestine and the liver. In line with this, DEX pre-treatment decreased maximum plasma concentration (C(max)) of NDL by 28% of control. To inhibit the intestinal Oatp1a5, naringin (NRG, 0.145 mg/kg) was preadministered orally for 30 min before the oral administrations of NDL or celiprolol (CEL, 10 mg/kg, Oatp1a5 substrate). Although NRG markedly reduced C(max) and AUC₀₋∞ of CEL by 60% and 65% of control, respectively, little difference was observed in the plasma concentration of NDL between NRG and control. These results suggest that P-gp is greatly involved in the pharmacokinetics of NDL, while the involvement of Oatp1a5 in the pharmacokinetics of NDL may be less than that of celiprolol in rats.

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Role of the Renal Nerve in Glucocorticoid Hypertension.

Cited by 4 publications

References 22 publications

Glucocorticoids increase salt appetite by promoting water and sodium excretion

Glucocorticoids increase salt appetite by promoting water and sodium excretion

The Neuroendocrinology, Neurochemistry and Molecular Biology of Thirst and Salt Appetite

Effects of Itraconazole, Dexamethasone and Naringin on the Pharmacokinetics of Nadolol in Rats

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