Tonic inhibition of renal response to vasopressin by a pertussis toxin substrate

Jeffries, William B.; Fallet, Rachel W.; Gong, Gordon; Dreal, P Van; Pettinger, William A.

doi:10.1152/ajprenal.1988.255.6.f1107

Cited by 3 publications

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“…In previous studies, both pertussis-toxin-sensitive and -insensitive effects of adrenaline have been reported: adrenaline binding and stimulation of phosphorylase in hepatocytes [24], as well as adrenaline binding and stimulation of phosphoinositide hydrolysis and prostaglandin E2 formation in MDCK cells [25], were found to be insensitive to pretreatment with pertussis toxin. On the other hand, noradrenaline-induced inhibition of Ca 2+ channels in dorsal root ganglion neurons [26], adrenaline-induced inhibition of adenylate cyclase [27][28][29][30][31], inhibition of insulin secretion [32,33] and stimulation of phosphoinositide turnover [34] have been reported to be blocked by pertussis toxin.…”

Section: Discussionmentioning

confidence: 99%

Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

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Paulmichl

Wöll

et al. 1991

Biochemical Journal

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The effects of adrenaline on the potential difference across the cell membrane, on formation of inositol phosphates and on intracellular Ca2+ ([Ca2+]i) were analysed in cells without or with pretreatment with pertussis toxin or phorbol 12-myristate 13-acetate (PMA). In untreated cells, adrenaline leads to a sustained hyperpolarization, a stimulation of Ins(1,4,5)P3 and Ins(1,3,4,5,)P4 formation and a transient increase in [Ca2+]i from 78 +/- 7 to 555 +/- 43 nM, followed by a plateau of 260 +/- 23 microM. In the absence of extracellular Ca2+ the effect of adrenaline on both potential difference and [Ca2+]i is transient. In cells pretreated with pertussis toxin, the effects of adrenaline on InsP3 and [Ca2+]i are still preserved, but the effect on potential difference is transient. In cells pretreated with PMA, the effect of adrenaline on InsP3 formation is severely decreased and that on [Ca2+]i abolished, whereas a transient hyperpolarizing effect is still present. This transient hyperpolarization is abolished by additional pretreatment with pertussis toxin. The observations suggest that adrenaline hyperpolarizes the cell membrane of MDCK cells by several distinct mechanisms. First, adrenaline stimulates the formation of InsP3 and InsP4, which at least in part accounts for the release of intracellular Ca2+ and the entry of Ca2+ from the extracellular fluid. Stimulation of phospholipase C is not mediated by pertussis-toxin-sensitive G-proteins, but apparently is inhibited by activation of protein kinase C. Second, adrenaline hyperpolarizes the cell membrane by a mechanism independent from increase in [Ca2+]i which is sensitive to pertussis toxin but is, at least in part, insensitive to PMA.

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Section: Discussionmentioning

confidence: 99%

Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

Pfeilschifter

Paulmichl

Wöll

et al. 1991

Biochemical Journal

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Renal ?-adrenergic receptors and genetic hypertension

Jackson

Insel

1993

Pediatr Nephrol

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The hypothesis has been proposed that an increase in the number of renal alpha-adrenergic receptors may contribute to the pathogenesis of genetic hypertension. Herein we review recent findings regarding expression of renal alpha 1 (alpha 1a, alpha 1b)- and alpha 2 (alpha 2a, alpha 2b)-adrenergic subtypes and we provide an updated revision of the above-stated hypothesis. Enhancement in receptor number or in post-receptor components responsible for alpha 1- and alpha 2-adrenergic-mediated sodium reabsorption in proximal tubule may contribute to sodium retention and an elevation in blood pressure. Perhaps such changes contribute to the increase in blood pressure in genetically determined hypertension in humans, although direct tests of this notion have not yet been performed.

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Renal .ALPHA.2-Adrenoceptor Overexpression in Dahl Salt-Sensitive Rats. Regulation by Dietary NaCl and Dissociation from Salt-Insensitive Hypertension.

et al. 1992

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Dietary NaCI-induced changes in blood pressure and agonist and antagonist binding properties to renal a2-adrenoceptors were studied in inbred (Rapp) strains of Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats were placed on either salt-deficient (0.13% NaCI in chow) or high salt (1% NaCI solution to drink plus 0.13% NaCI chow) diets for 1 to 8 weeks. Saturation binding studies with [3H]-rauwolscine and [H]-p-aminoclonidine and competition studies with [3H]-rauwolscine and epinephrine were then performed in renal plasma membranes from each group. Systolic blood pressure rose significantly in S rats on the salt-deficient diet for 2 or more weeks, and was further increased by high salt intake, indicating that there are salt-sensitive and salt-insensitive components to the hypertension in inbred S rats. The blood pressure of R rats was unaffected by dietary NaCI content. Two or more weeks of high salt feeding significantly elevated renal a2-adrenoceptor density ([3H]-rauwolscine binding) in S but not R rats. Interestingly, NaCI restriction in weanling S rats completely prevented this increase in a2-adrenoceptor density over the course of the study. The number of hih affinity agonist binding sites (assessed with [3H] p-aminoclonidine and epinephrine displacement of [ H]-rauwolscine) was increased in S rats after high salt feeding. Removal of the high salt diet failed to reverse the NaCI-induced elevations in total and high affinity a2-adrenoceptor density in S rats. We conclude that: 1) the initiation of renal a2-adrenoceptor overexpression in Dahl S rats is entirely dependent on dietary NaCI content; 2) the overexpression of renal a2-adrenoceptors was independent of the salt-insensitive component of hypertension in S rats, precluding a causal linkage between these parameters;3) the rise in renal a2-adrenoceptors was closely paralleled by salt-sensitive increments in blood pressure, suggesting a functional relationship between these two variables; 4) In contrast to reported changes in renal a2-adrenoceptor properties following renal denervation, dietary NaCI augments the number of high affinity renal a2-adrenoceptor agonist binding sites in S rats but does not increase the proportion of these sites relative to total receptor number. (Hypertens Res 1992;15: 85-92)

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Tonic inhibition of renal response to vasopressin by a pertussis toxin substrate

Cited by 3 publications

References 0 publications

Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

Renal ?-adrenergic receptors and genetic hypertension

Renal .ALPHA.2-Adrenoceptor Overexpression in Dahl Salt-Sensitive Rats. Regulation by Dietary NaCl and Dissociation from Salt-Insensitive Hypertension.

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