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PubMed1975

Impermeability of rabbit erythrocytes to prostaglandins.

Washed rabbit erythrocytes were suspended in Tris-electrolyte buffer containing [3H]prostaglandin (PG) E1, F1alpha, F2alpha, or A1 and one 14C-labeled compound such as sucrose. After up to 24 h of incubation, aliquots of centrifuged, packed cells and supernatant were oxidized and the 3H and 14C samples were counted. The mean sucrose space of the packed cell was 7.4%. After 1 min the E1, F1alpha, and F2alpha spaces were 16, 15.4, and 10.0%, respectively, and showed no increase even after 24 h of incubation at either 23 or 5 degrees C. At 23 degrees C the initial (0.5 min) PGA1 and thiourea spaces were 94 and 75%, respectively, whence the PGA1, but not the thiourea, space declined, reaching 30% at 4 h. The large initial uptake of PGA1 was eliminated at 5 degrees C, while it was accentuated at pH 6.8 or at a PGA1, concentration of 10(-3) M. 14C-Labeled arachidonic, octanoic, and other non-PG fatty acids gave apparent distribution spaces of 140-300%. These results show that PG's can partition into rabbit erythrocyte membranes, but the intracellular volume of the erythrocytes is not freely accessible to these autacoids. The implications of the finding that some cell membranes are impermeable to prostaglandins are discussed.

Animals↗
PubMed2006

Isoprostane-induced airway hyperresponsiveness is dependent on internal Ca2+ handling and Rho/ROCK signaling.

We previously reported the ability of isoprostanes to induce airway hyperresponsiveness (AHR). In this study, we examined the signaling mechanisms underlying that phenomenon with the standard muscle bath technique. Responses to a threshold concentration of carbachol (CCh, 3 x 10(-9) M) were significantly augmented by pretreatment for 20 min with 8-isoprostaglandin E(2) (15-E(2t)-IsoP, 10(-6) M): this AHR was obliterated in tissues pretreated with the selective Rho kinase (ROCK) inhibitor Y-27632 added 20 min before isoprostane, but not by cyclopiazonic acid (CPA). Increasing the CCh concentration to 3 x 10(-8) M (still considerably less than the half-maximally effective concentration of CCh) evoked larger contractions that were also augmented significantly by 15-E(2t)-IsoP: this AHR was completely abolished in tissues pretreated with CPA as well as those pretreated with Y-27632. We noted, however, that Y-27632 and CPA profoundly effect baseline tone and the cholinergic response per se, which confounds the interpretation of the data summarized above. We therefore modified the protocol by using combinations of CCh and blocker (CPA, Y-27632, or nifedipine) that were equieffective. In this way, we found that AHR could not be demonstrated under conditions in which Rho/ROCK signaling or Ca(2+) release was abolished (by Y-27632 and CPA, respectively). Likewise, other autacoids that act through G protein-coupled receptors via Rho/ROCK and Ca(2+) release (serotonin, histamine) mimicked this effect of isoprostane, whereas bradykinin did not. We conclude that isoprostane-induced AHR is mediated in part through an action on Rho/ROCK signaling. This novel finding may contribute to a better understanding of the mechanisms underlying AHR and asthma.

Amides↗
PubMed2001

Prostanoid receptors: ontogeny and implications in vascular physiology.

Prostanoids exert significant effects on circulatory beds. They play a role in the response of the vasculature to adjustments in perfusion pressure and oxygen and carbon dioxide tension, and they mediate the actions of numerous factors. The role of prostanoids in governing circulation of the perinate is suggested to surpass that in the adult. Prostanoids are abundantly generated in the perinate. They have been implicated in autoregulation of blood flow as studied in brain and eyes. Prostaglandins are also dominant regulators of ductus arteriosus tone. The effects of these autacoids are mediated through specific G protein-coupled receptors. In addition to the pharmacological characterization of the prostanoid receptors, important advances in understanding the biology of these receptors have been made in the last decade. Their cloning and the development of animals with disrupted genes of these receptors have been very informative. The involvement of prostanoid receptors in the developing subject, especially on brain and ocular vasculature and on ductus arteriosus, has also begun to be investigated; the expression of these receptors changes with development. Some but not all of the ontogenic changes in these receptors are attributed to homologous regulation. Interestingly, in the process of elucidating their effects, functional perinuclear prostaglandin E2 receptors have been uncovered. This article reviews prostanoid receptors and addresses implications on the developing subject with attention to vascular physiology.

Animals↗
PubMed2003

Loop diuretics: from the Na-K-2Cl transporter to clinical use.

The diuretic response to loop diuretics in various disease states has consistently been found to be subnormal. One of the key determinants of the degree of diuretic response is the functional integrity of the sodium-potassium-chloride transporter in the loop of Henle. Studies in animal models suggest that expression/activity of the transporter may be affected by factors such as altered natural splicing events of NKCC2 (the gene encoding for the renal transporter), renal prostanoids, vasopressin, and other autacoids. We have reviewed the pharmacokinetics and pharmacodynamics of loop diuretics in health and in edematous disorders for which they are used. On the basis of evidence reviewed in this paper, we propose that altered expression or activity of the sodium-potassium-chloride transporter in the loop of Henle, in conjunction with events occurring in other segments of the nephron, possibly accounts for the altered diuretic response to these agents. Thus the modulators of this altered expression/activity could serve as important therapeutic targets for alternative diuretic regimens in these conditions.

Animals↗
PubMed2005

Kidney oxygen consumption, carbonic anhydrase, and proton secretion.

Oxygen consumed by the kidney (Q(O(2))) is primarily obligated to sodium reabsorption (T(Na)). The relationship of Q(O(2)) to T(Na) (Q(O(2))/T(Na)) may be altered by hormones and autacoids. To examine whether Q(O(2))/T(Na) depends on the mechanism of sodium reabsorption, we first evaluated the effects on Q(O(2)) and Q(O(2))/T(Na) of benzolamide (BNZ), a proximal diuretic that works by inhibiting membrane carbonic anhydrase. During BNZ infusion in anesthetized rats, Q(O(2)) increased by 50% despite a 25% decline in T(Na). However, BNZ failed to increase Q(O(2))/T(Na) when given along with the adenosine A1 receptor blocker, DPCPX, which inhibits basolateral Na-bicarbonate cotransport (NBC1), or EIPA, which inhibits sodium-hydrogen exchange (NHE). Incubating freshly harvested rat proximal tubules with BNZ also caused Q(O(2))to increase by 62%, an effect that was prevented by blocking the apical NHE3 with S3226. Blocking NBC1 or NHE3 in the proximal tubule will have opposite effects on cell pH, but both maneuvers should reduce active chloride transport. In conclusion, inhibiting membrane carbonic anhydrase in the proximal tubule increases Q(O(2)) and reduces the energy efficiency of sodium reabsorption by the kidney. This is not purely due to shifting the burden of reabsorption to a more expensive site downstream from the proximal tubule. Instead, increased cost may be incurred within the proximal tubule as the result of increased active chloride transport.

Animals↗
PubMed2002

Two-photon excitation fluorescence imaging of the living juxtaglomerular apparatus.

Recently, multiphoton excitation fluorescence microscopy has been developed that offers important advantages over confocal imaging, particularly for in vivo visualization of thick tissue samples. We used this state-of-the-art technique to capture high-quality images and study the function of otherwise inaccessible cell types and complex cell structures of the juxtaglomerular apparatus (JGA) in living preparations of the kidney. This structure has multiple cell types that exhibit a complex array of functions, which regulate the process of filtrate formation and renal hemodynamics. We report, for the first time, on high-resolution three-dimensional morphology and Z-sectioning through isolated, perfused kidney glomeruli, tubules, and JGA. Time-series images show how alterations in tubular fluid composition cause striking changes in single-cell volume of the unique macula densa tubular epithelium in situ and how they also affect glomerular filtration through alterations in associated structures within the JGA. In addition, calcium imaging of the glomerulus and JGA demonstrates the utility of this system in capturing the complexity of events and effects that are exerted by the specific hypertensive autacoid angiotensin II. This imaging approach to the study of isolated, perfused live tissue with multiphoton microscopy may be applied to other biological systems in which multiple cell types form a functionally integrated syncytium.

Angiotensin II↗
PubMed2004

Luminal flow induces eNOS activation and translocation in the rat thick ascending limb.

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) acts as an autacoid to inhibit NaCl absorption in the thick ascending limb of the loop of Henle (THAL). In the vasculature, shear stress activates eNOS. We hypothesized that increasing luminal flow activates eNOS and enhances NO production in the THAL. We measured NO production by isolated, perfused THALs using a NO-sensitive microelectrode. Increasing luminal flow from 0 to 20 nl/min increased NO production by 43.1 +/- 4.1 pA/mm of tubule (n = 10, P < 0.05), and this response was blunted (92%) by the NOS inhibitor L-(omega)nitro-methylarginine (P < 0.05). We studied the effect of flow on eNOS subcellular localization. In the absence of flow, eNOS was diffusely localized throughout the cell (basolateral = 33 +/- 4%; middle = 27 +/- 3%; apical = 40 +/- 4% of total eNOS). Increasing luminal flow induced eNOS translocation to the apical membrane, as evidenced by a 60% increase in eNOS immunoreactivity in the apical membrane (from 40 +/- 4 to 65 +/- 2%; n = 6; P < 0.05). Disrupting the actin cytoskeleton with cytochalasin D (10 microM) reduced flow-induced NO production by 62% (from 37.1 +/- 3.4 to 14.0 +/- 2.4 pA/mm tubule, n = 7, P < 0.04) and blocked flow-induced eNOS translocation. Flow also increased the amount of phosphorylated eNOS (Ser1179) at the apical membrane (from 25 +/- 2 to 56 +/- 2%; P < 0.05). We conclude that increasing luminal flow induces eNOS activation and translocation to the apical membrane in THALs. These are the first data showing that flow regulates eNOS in epithelial cells. This may be an important mechanism for regulation of NO levels in the renal medulla.

Animals↗
PubMed2003

Key enzymes for renal prostaglandin synthesis: site-specific expression in rodent kidney (rat, mouse).

Prostanoids derived from endogenous cylooxygenase (COX)-mediated arachidonic acid metabolism play important roles in the maintenance of renal blood flow and salt and water homeostasis. The relative importance of COX-1 and COX-2 isoforms is under active investigation. We have performed a comprehensive histochemical analysis by comparing rat and mouse kidneys for cellular and subcellular localization of COX-1 and -2 and microsomal-type PGE synthase (PGES), the rate-limiting biosynthetic enzyme in PGE2 synthesis. A choice of different sera was compared, and the results were confirmed by antigen-retrieval techniques, in situ hybridization, RT-PCR, and the use of COX knockout mice. In the glomerulus, significant COX-1 expression was detected in a subset of mesangial cells. Along the renal tubule, the known COX-2 expression in cTAL and macula densa was paralleled by PGES staining. In the terminal distal convoluted tubule, connecting tubule, and cortical and medullary collecting ducts, a significant COX-1 signal was colocalized with PGES; COX-2 was not found in these sites. Intercalated cells were generally negative. Cortical fibroblasts were COX-1 and PGES positive in mice, whereas in rats only PGES could be reliably detected. Lipid-laden interstitial cells of the inner medulla were COX-1, -2, and PGES positive. Vascular smooth muscle cells were not stained. The present data support prominent functions of renal prostanoids, predominantly PGE2, by defining expression sites of the key enzymes for their biosynthesis in the rat and mouse. Results define the renal cell types involved in prostaglandin autacoid functions within spatially restricted sites such as the juxtaglomerular apparatus, mesangium, distal convolutions and collecting duct, and in compartments of the renal interstitium.

Animals↗
PubMed1989

Phospholipids in signal transduction of mesangial cells.

Glomerular mesangial cells respond to a variety of hormones, cytokines, and autacoids with an immediate hydrolysis of membrane phospholipids, including phosphatidylinositol, phosphatidylcholine, and phosphatidylethanolamine. Phospholipid metabolites such as inositol phosphates and diacylglycerol serve as initiating signals for subsequent intracellular events, including release of intracellular Ca2+ stores, increased conductance of the plasma membrane to various ions, changes of intracellular pH, and protein phosphorylation. The resting functional responses, including cell contraction and proliferation, are in turn regulated by simultaneous release of bioactive lipids such as eicosanoids and platelet-activating factor, which recognize receptors on both intrinsic glomerular cells and circulating, blood-borne cells. Through this complex signaling network, phospholipid metabolism plays a central regulatory role in mesangial functions in physiological conditions as well as in inflammatory or metabolic derangements of the kidney glomerulus.

Animals↗
PubMed1990

Differences in synergistic actions of vasopressin and deoxycorticosterone in rat and rabbit CCD.

We examined the time course of changes in osmotic water permeability (Pf, micron/s), lumen-to-bath 22Na+ flux (Jl----b, pmol.min-1.mm-1), and transepithelial voltage (VT, mV) in response to arginine vasopressin (AVP) in isolated perfused rat and rabbit cortical collecting ducts (CCD). CCDs were isolated from "normal" (untreated) animals and animals 4-14 days after an intramuscular depot injection of deoxycorticosterone pivalate (DOC; 35 mg/rabbit, 5 mg/rat). In the normal rat CCD, 220 pM AVP added to the bathing solution increased Pf from approximately 0 to 981 +/- 120, Jl----b from 24 +/- 5 to 62 +/- 9, and VT from -0.7 +/- 0.6 to -4.0 +/- 0.6 (mean +/- SE; P less than 0.05). The effect of AVP on Pf in DOC-treated rats was not significantly different, but the effects on Jl----b and VT were greater. Jl----b rose from a control value of 78 +/- 16 to 192 +/- 14 with AVP, and VT hyperpolarized from -4.2 +/- 1.6 to -12.2 +/- 0.4. All of these effects of AVP in the normal and DOC-treated rat CCD persisted for greater than or equal to 90-150 min. In DOC-treated rabbit tubules, AVP caused a stable increase in Pf from 9 +/- 6 to 800 +/- 199, which was significantly greater than in normal tubules (379 +/- 32). In the normal rabbit CCD we confirmed previous observations that AVP produces only a transient increase in Na+ absorption and VT; Jl----b increased from 76 +/- 4 to 96 +/- 7 during the period 15-25 min after AVP addition but subsequently fell to 80 +/- 6; VT transiently hyperpolarized from -55 +/- 7 to -64 +/- 8 at 3-8 min after AVP and then fell to -54 +/- 9. In DOC-treated rabbit CCDs, AVP produced no change whatsoever in Jl----b, which was not significantly different from the control value of 99 +/- 7, nor in VT, which was -68 +/- 8 mV. These results indicate fundamental differences in the response of the rat and rabbit CCD to AVP and the presence or absence of synergistic interactions with mineralocorticoids, which may relate to their differing response to other autacoids.

Animals↗
PubMed1991

Hormonal mediators of amino acid-induced glomerular hyperfiltration in humans.

It has been speculated that glucoregulatory hormones and/or renal autacoids mediate the increase in glomerular filtration rate (GFR) induced by the administration of protein or amino acids. Because infusion of a mixture of amino acids (AA mix), but not of branched-chain amino acids (BCAA) alone, increases GFR, we performed a crossover study in seven normal subjects in which the glomerular hemodynamic effects of separate 3-h infusions of these two amino acid solutions were compared with changes in potential mediators of this response, i.e., glucoregulatory hormones, renin, vasodilatory prostaglandins (PGs), and guanosine 3',5'-cyclic monophosphate (cGMP). As expected, infusion of the AA mix but not BCAA resulted in a prompt and sustained increase in GFR. Both infusions caused a significant increase in plasma insulin, whereas glucagon increased only with the AA mix. Plasma growth hormone was initially unchanged with both infusions but increased after 2 h of BCAA. Neither infusion significantly increased the urinary excretion of PGE2, 6-keto-PGF1 alpha, or cGMP. Both infusions resulted in a small but significant decrease in plasma renin activity. Infusion of BCAA but not the AA mix resulted in a progressive decrease in plasma glucose and potassium concentrations and an increase in renal sodium reabsorption that may have resulted from stimulation of insulin secretion that was not counterbalanced by a simultaneous increase in glucagon. Thus only changes in glucagon exhibited a significant temporal relationship with changes in GFR, lending further support to a role for glucagon as a mediator of amino acid-induced glomerular hyperfiltration.

Adult↗
PubMed1991

Thromboxane stimulates synthesis of extracellular matrix proteins in vitro.

The vasoconstrictor eicosanoid thromboxane plays an important role in the pathogenesis of several renal diseases. As an autacoid, its local release alters blood flow and induces platelet aggregation. We report a direct stimulatory effect of thromboxane on extracellular matrix protein production and gene expression in vitro. Treatment of two cell types, differentiated mouse teratocarcinoma cells (F9+) and human glomerular mesangial cells, with two different thromboxane analogues resulted in increased production of components of the extracellular matrix including fibronectin and the basement membrane proteins laminin and type IV collagen. These responses to thromboxane were not the result of a mitogenic effect of thromboxane nor the result of an increase in total cellular protein. The increased production of extracellular matrix proteins was, at least in part, due to an increase in the steady-state level of mRNA for these genes. Furthermore, the effect of thromboxane was markedly inhibited by cotreatment with a thromboxane-receptor antagonist. These results suggest a new potential role for thromboxane as a mediator of the sclerotic and fibrotic responses to injury.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

EGF and PGE2 inhibit rabbit CCD Na+ transport by different mechanisms: PGE2 inhibits Na(+)-K+ pump.

The rabbit cortical collecting duct absorbs Na+ by a transport system comprised of an apical membrane Na+ channel and a basolateral membrane Na(+)-K(+)-adenosinetriphosphatase. The rate of Na+ absorption across this epithelium is acutely inhibited by several hormones and autacoids including epidermal growth factor (EGF) and prostaglandin E2 (PGE2). We used electrophysiological analysis to determine which Na+ transport mechanism is primarily regulated in response to EGF and PGE2. We used concentrations of EGF and PGE2 that inhibited Na+ absorption to a comparable degree. We assessed the effects of these agents on Na+ transport primarily by the calculated equivalent current; the validity of this indicator was verified using simultaneous tracer flux measurements. EGF and PGE2 had different effects on the intracellular electrophysiological parameters. EGF (in the presence of a cyclooxygenase inhibitor) hyperpolarized the apical membrane voltage in a manner analogous to the Na(+)-channel blocker amiloride, reduced the transepithelial conductance, and increased the fractional resistance of the apical membrane. In comparison, PGE2 depolarized the apical membrane voltage in a manner analogous to the Na(+)-K+ pump inhibitor ouabain, and caused no significant changes in transepithelial conductance or apical membrane conductance. The finding that EGF hyperpolarized the apical membrane indicates that this agent attenuates Na+ absorption by reducing apical Na+ entry due to a decrease in the magnitude of the apical membrane Na+ conductance. In contrast, the electrophysiological changes produced by PGE2 indicate primary inhibition of the basolateral Na(+)-K+ pump following PGE2 treatment.

Amiloride↗
PubMed1993

Hormonal regulation of inner medullary collecting duct sodium transport.

The inner medullary collecting duct (IMCD) is the final arbiter of renal Na+ excretion, and Na+ transport in this segment is controlled by a wide variety of hormones and renal autacoids. This review examines the mechanisms of IMCD Na+ transport and its regulation using results obtained from micropuncture and microcatheterization studies in the intact animal, as well as data from isolated perfused tubules, freshly prepared cell suspensions, and cultured IMCD cells. Where appropriate, results from closely related tissues such as the cortical collecting duct and model urinary epithelia are examined. Na+ reabsorption in this segment occurs predominantly via apical amiloride-sensitive Na+ channels and basolateral Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase). Although there is some evidence for the activities of other transporters such as Na(+)-K(+)-2Cl- and Na-Cl cotransporters and Na+/H+ exchanger, their role in Na+ homeostasis remains undefined. Mineralocorticoids augment the activities of both apical Na+ channels and basolateral Na(+)-K(+)-ATPase by a variety of complex mechanisms. Prostaglandin E2 inhibits Na(+)-K(+)-ATPase and appears to mediate the actions of several peptide hormones, including endothelin, interleukin-1, and atrial natriuretic peptide [ANP-(31-67)]. Several peptides in the ANP family [ANP-(99-126), urodilatin, and brain natriuretic peptide] bind to guanylate cyclase-linked receptors, leading to inhibition of apical Na+ channel function. These mechanisms of regulation of IMCD Na+ transport likely play important roles in total body Na+ balance in health and disease.

Animals↗
PubMed1993

Short-term regulation of renal Na-K-ATPase activity: physiological relevance and cellular mechanisms.

Sodium-potassium-activated adenosinetriphosphatase (Na-K-ATPase; the Na:K pump), located at the basolateral domain of epithelial cells, provides the driving force for active sodium and potassium translocation and for the secondary active transport of other solutes across the renal tubules. Short-term regulation of renal Na-K-ATPase activity (i.e., not reflecting changes in its biosynthesis rate) provides an important mechanism of modulating tubule transport and thus the final Na and K urinary excretion. Recent studies have provided abundant evidence that such regulation is effected by complex functional networks that are specific for different nephron segments and involve distinct and often mutually interacting intracellular signal transduction pathways. The effects of hormones and autacoids linked to alterations in cell adenosine 3',5'-cyclic monophosphate and consequently of protein kinase A, in the levels and distribution of protein kinase C, or in the generation of various eicosanoids provide examples of rapid Na:K pump activity modulation by the mechanisms mentioned above. In this review we assess the roles of specific intracellular messengers and the manner in which they, and especially protein kinases, might interact with the pump in the short-term regulation of its activity; also, we examine the emerging evidence supporting the participation of the cytoskeleton in this process.

Animals↗
PubMed1994

Hereditary and acquired defects in signaling through the hormone-receptor-G protein complex.

Extracellular signals reach the interior of cells as second messengers through intermediary transducers located within or closely associated with the plasma membrane. One of the most common pathways involves the interaction of the extracellular signaling element with a membrane-bound receptor and guanine nucleotide-binding regulatory protein (G protein). Inherited and acquired defects that alter the function of the first messenger (hormone, neurotransmitter, autacoid, or paracrine substance) or either of the transducing components (G protein-coupled receptor or G protein) can lead to defective signaling and, ultimately, disease. Clinically relevant examples of defects of all three of those signaling components have recently been described. These can take the form of inherited or sporadic mutations of the genes encoding the various signaling components, or of neutralizing antibodies against those components. The purpose of this review is to summarize how acquired or inherited defects in each of those pathways might lead to diseases.

Animals↗
PubMed1989

Serotonin increases excitability of rabbit C-fiber neurons by two distinct mechanisms.

Serotonin (5-HT) increases impulse activity in visceral afferent C-fibers in vivo. A 5-HT-induced membrane depolarization may partially account for this effect. Here, we examined the potential contribution of an additional mechanism to the 5-HT-mediated increase in impulse activity. Approximately 40% of rabbit visceral C-fiber neurons exhibit a protracted (greater than 3 s) spike afterhyperpolarization (AHPslow) that is a major determinant of repetitive firing properties in these neurons. Intracellular recording methods were applied to rabbit nodose ganglion neurons in vitro to assess whether 5-HT could increase excitability through effects on the AHPslow. Results revealed a concentration-dependent 5-HT-mediated depression of the AHPslow amplitude and duration that was accompanied by decreased accommodation of action potential firing. Experiments with 5-HT receptor antagonists further showed that this autacoid depressed the AHPslow through a different 5-HT receptor subtype than that subserving the 5-HT-induced depolarization. Thus the AHPslow represents a distinct locus where 5-HT can increase the impulse activity of these visceral C-fiber afferents.

Animals↗
PubMed2006

Transduction mechanisms in airway sensory nerves.

The induction of action potentials in airway sensory nerves relies on events leading to the opening of cation channels in the nerve terminal membrane and subsequent membrane depolarization. If the membrane depolarization is of sufficient rate and amplitude, action potential initiation will occur. The action potentials are then conducted to the central nervous system, leading to the initiation of various sensations and cardiorespiratory reflexes. Triggering events in airway sensory nerves include mechanical perturbation, inflammatory mediators, pH, temperature, and osmolarity acting through a variety of ionotropic and metabotropic receptors. Action potential initiation can be modulated (positively or negatively) through independent mechanisms caused mainly by autacoids and other metabotropic receptor ligands. Finally, gene expression of sensory nerves can be altered in adult mammals. This neuroplasticity can change the function of sensory nerves and likely involve both neurotrophin and use-dependent mechanisms. Here we provide a brief overview of some of the transduction mechanisms underlying these events.

Action Potentials↗