Adrenergic control of cAMP generation in rat inner medullary collecting tubule cells

Teitelbaum, Isaac; Strasheim, A.; Berl, Tomás

doi:10.1038/ki.1989.34

Cited by 21 publications

(16 citation statements)

References 23 publications

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“…Although some evidence suggests that NE is capable of inhibiting the hydro-osmotic effects of vasopressin intrarenally (23)(24)(25)(26)(27), results from the present study do not support the concept that an intrarenal mechanism is the major factor responsible for NE-induced diuresis in conscious dogs. For example, if NE inhibited vasopressin-induced renal water reabsorption in conscious dogs, urine flow should have increased during NE infusion, regardless of the prevailing arterial blood pressure.…”

Section: Discussioncontrasting

confidence: 99%

Contribution of Plasma Vasopressin Concentration and Blood Pressure to Norepinephrine-Induced Diuresis in Conscious Dogs

Zhu

Leadley

1993

Experimental Biology and Medicine

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Infusion of norepinephrine (NE) into humans and experimental animals induces diuresis by mechanisms that are not completely understood. Two series of experiments were performed to determine whether changes in plasma levels of vasopressin or changes in mean arterial pressure (MAP) are important-factors in NE-induced diuresis in conscious dogs. First, plasma vasopressin (PAVP) levels were measured in normal and cardiac-denervated conscious dogs during a 30-min intravenous infusion of NE (0.5 micrograms.kg-1.min-1). When NE was administered to normal dogs, urine flow increased from 0.3 +/- 0.1 to 0.9 +/- 0.4 ml/min. PAVP did not decrease, in spite of increases in mean arterial pressure (from 103 +/- 4 to 123 +/- 6 mm Hg) and left atrial pressure (from 5.2 +/- 0.9 to 8.6 +/- 1.4 mm Hg). The same dose of NE infused into cardiac-denervated dogs significantly increased urine flow (from 0.2 +/- 0.1 to 0.8 +/- 0.3 ml/min) and MAP (from 107 +/- 5 to 147 +/- 10 mm Hg), and decreased PAVP (from 1.8 +/- 0.3 pg/ml to 1.2 +/- 0.3 pg/ml). In the second series of experiments, NE was infused into cardiac-denervated dogs for 40 min. During the final 20 min of NE infusion, nitroprusside was infused to offset the pressor effect of NE by returning MAP to the initial control level. Urine flow increased during the first 20 min in which NE alone was given; however, when MAP was returned to the control level by nitroprusside infusion, urine flow also returned to the control level. PAVP increased from a control value of 3.6 +/- 0.6 to 18.9 +/- 3.8 pg/ml 15 min after the NP infusion had begun. We conclude that a decrease in PAVP is not required to elicit diuresis during NE infusion in normal conscious dogs and that the pressor effect of NE appears to play a major role in NE-induced diuresis.

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Section: Discussioncontrasting

confidence: 99%

Contribution of Plasma Vasopressin Concentration and Blood Pressure to Norepinephrine-Induced Diuresis in Conscious Dogs

Zhu

Leadley

1993

Experimental Biology and Medicine

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“…Higher activities were expected and found in monolayer cultures which were 100% viable, and these levels were maintained throughout 14 days in culture, diminishing slightly at 21 days. The rapid formation of cAMP with arginine vasopressin in microdissected collecting tubules of various species with arginine vasopressin has been reported by several investigators [43, 44]. Stimulation of cAMP formation in these monolayers once again is confirmatory evidence of the collecting duct origin of these cells.…”

Section: Discussionsupporting

confidence: 56%

Isolation, Culture and Characterization of Human Renal Proximal Tubule and Collecting Duct Cells

Trifillis¹

1999

Nephron Exp Nephrol

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The complexity and heterogeneity of the human nephron with regard to cell types make well-defined in vitro systems of renal cells valuable for studies of the pathogenetic mechanisms involved in nephrotoxicity. In our laboratory renal proximal tubule cells (PTC) and collecting duct cells (CDC) have been isolated, cultured and characterized from cadaver kidneys (postmortem time <24 h) for use in studies of renal cytotoxicity induced by therapeutics and bacteria. PTC seeded at 10⁶ cells/ml formed confluent monolayers within 7 days. Histochemical markers were used to determine the origin of the cell cultures. Cells were negative for factor VIII, positive for cytokeratin and γ-glutamyltransferase (GGT), and bound winged pea lectin. CDC, isolated from the renal papillae, formed monolayers within 14 days of seeding. CDC were negative for factor VIII and GGT, positive for cytokeratin and bound peanut lectin. PTC and CDC isolates and cultures exhibited typical epithelial cell ultrastructure: cell junctions, intermediate filaments, microvilli, and numerous mitochondria. The morphological and histochemical evidence confirms that PTC and CDC can be isolated and cultured for use in in vitro studies.

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“…Studies were performed in Krebs-Ringer's buffer, pH 7.4, at 300 mOsm/kg H20 in the presence of 0.5 mM isobutylmethylxanthine to inhibit phosphodiesterase. Incubation with effector solutions and subsequent determinations of cAMP and protein were performed as reported previously (7,9). Results are expressed as fmol cAMP/Mg protein.…”

Section: Methodsmentioning

confidence: 99%

Vasopressin-stimulated phosphoinositide hydrolysis in cultured rat inner medullary collecting duct cells is mediated by the oxytocin receptor.

Teitelbaum

1991

J. Clin. Invest.

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Studies were performed to identify the receptor that mediates AVP-stimulated phosphoinositide (PI) hydrolysis in cultured rat inner medullary collecting tubule (RIMCT) cells. While the selective V1 receptor agonist [Ho1, Phe2, Orn8] VT has no effect on inositol trisphosphate (IP3) production over the range of 10(-13)-10(-7) M, the selective V2 receptor agonist VDAVP stimulates IP3 production in dose-dependent fashion. Oxytocin stimulates IP3 production in dose-dependent fashion as well. AVP-stimulated phospholipase C activity is not inhibited by the V1 receptor antagonist d(CH2)5Tyr(Me)AVP(10(-7) M) but is eliminated by the V2 receptor antagonist d(CH2)5DTyr(Et)VAVP (10(-7) M). Similarly, the response to oxytocin is eliminated by the V2 receptor antagonist. The selective oxytocin receptor agonist [Thr4, Gly7] oxytocin does not stimulate cAMP production in RIMCT cells but does promote PI hydrolysis. The selective oxytocin receptor antagonist desGlyNH2d(CH2)5[Tyr(Me)-Thr4]OVT (10(-7) M) does not inhibit AVP-stimulated cAMP production but eliminates IP3 production in response to AVP or the V2 receptor agonist VDAVP. These studies demonstrate that AVP or a V2 receptor agonist stimulate PI hydrolysis in cultured RIMCT cells via occupancy of the oxytocin receptor.

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Adrenergic control of cAMP generation in rat inner medullary collecting tubule cells

Cited by 21 publications

References 23 publications

Contribution of Plasma Vasopressin Concentration and Blood Pressure to Norepinephrine-Induced Diuresis in Conscious Dogs

Contribution of Plasma Vasopressin Concentration and Blood Pressure to Norepinephrine-Induced Diuresis in Conscious Dogs

Isolation, Culture and Characterization of Human Renal Proximal Tubule and Collecting Duct Cells

Vasopressin-stimulated phosphoinositide hydrolysis in cultured rat inner medullary collecting duct cells is mediated by the oxytocin receptor.

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