Role of calcium ions in kinin‐induced chloride secretion

Cuthbert, A. W.; Halushka, Perry V.; Margolius, Harry S.; Spayne, J. A.

doi:10.1111/j.1476-5381.1984.tb10797.x

Cited by 23 publications

(17 citation statements)

References 26 publications

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“…Kinin reacts with receptors in the basolateral aspect of the cell which result in the activation of a calcium channel. The blocking effects of verapamil (Cuthbert et al, 1984) and Co2, (Manning et al, 1982) formation under calcium-free conditions may be evidence for (b). The reason why iPGE2 generation is unaffected is unknown but possibly it is derived by a different route (see Bareis et al, 1983) or at a different cellular location.…”

Section: Possible Involvement Ofcyclic Amp In the Responses To Kininsmentioning

confidence: 99%

“…The effect on chloride secretion is sensitive to indomethacin, suggesting the involvement of eicosanoid formation in kinin action (Cuthbert & Margolius, 1982). In the preceding paper (Cuthbert et al, 1984) we have studied, in some detail, the dependence upon calcium of the chloride secretory process. Here we concentrate on correlations between biophysical and biochemical events following addition of kinin.…”

Section: Introductionmentioning

confidence: 99%

“…In the previous paper (Cuthbert et al, 1984) we showed that the actions of both kinins and PGE2 on SCC in rat colon were potentiated by inhibiting phosphodiesterase with isobutylmethylxanthine (IBMX). Determination of cyclic AMP content of tissues following addition of kinins was made to obtain direct evidence for or against the involvement of adenylate cyclase.…”

Section: Possible Involvement Ofcyclic Amp In the Responses To Kininsmentioning

confidence: 99%

“…0.3 ptEq for kallidin (1 AM) (Table 1, Cuthbert et al, 1984). The undoubted instability of PGI2 is a complicating factor in making these comparisons, so some experiments were done with carbacyclin, a stable analogue of PGI2.…”

Section: Possible Involvement Ofcyclic Amp In the Responses To Kininsmentioning

confidence: 99%

“…Tissues were bathed in Krebs-Henseleit solution of the composition given in the previous paper (Cuthbert et al, 1984). This solution had a pH of 7.4 when gassed with 95 % 02: 5 % CO2 at 37?C.…”

Section: Solutionsmentioning

confidence: 99%

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Mediators of the secretory response to kinins

Cuthbert

Halushka

Margolius

et al. 1984

British J Pharmacology

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1 The output of immunoreactive (i) 6 keto prostaglandin Fl, (i6ketoPGF1,). iPGE2 and ithromboxane B2 (iTXB2) from isolated colonic epithelium of the rat into the apical and basolateral bathing solution has been measured. In some instances tissues were also voltage clamped at 0 mV to measure short circuit current (SCC). 2 Kallidin (lysylbradykinin) stimulated the output of all three eicosanoids, specifically from the basolateral face of the tissue. The output was similar whether or not the tissues were short circuited. 3 Both the SCC response and eicosanoid output were dependent upon the concentration of kallidin, but not in a strictly proportional manner, there being relatively more eicosanoid output at submaximal kinin concentrations. 4 Indomethacin, 5 JiM, abolished the eicosanoid output, in response to kinin, while some part of the SCC response remained. 5 Calcium removal from the basolateral bathing fluid severely attenuated the SCC response, reduced the output of i6ketoPGFp, to half, but left the output of iPGE2 unchanged. In the presence or absence of calcium it is probable that sufficient PGE material is released to cause part of the SCC changes seen with kinin. 6 Kinin and PGE1 increased the cyclic AMP content of intact epithelia, provided a phosphodiesterase inhibitor was added at the same time.7 It is proposed that kinin causes an increase in calcium influx at the basolateral pole of the tissue. This calcium is necessary for the production of some eicosanoids and the subsequent generation of cyclic AMP, which then increases apical chloride permeability. In addition, calcium may facilitate entry of chloride through the basolateral face of the cells by activating a cotransport mechanism.

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Section: Possible Involvement Ofcyclic Amp In the Responses To Kininsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Possible Involvement Ofcyclic Amp In the Responses To Kininsmentioning

confidence: 99%

Section: Possible Involvement Ofcyclic Amp In the Responses To Kininsmentioning

confidence: 99%

Section: Solutionsmentioning

confidence: 99%

See 3 more Smart Citations

Mediators of the secretory response to kinins

Cuthbert

Halushka

Margolius

et al. 1984

British J Pharmacology

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Immunophysiology of Intestinal Electrolyte Transport

Powell

1991

Comprehensive Physiology

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Tissue Kallikrein–Kinin System

Clements

2000

Comprehensive Physiology

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The sections in this article are: Historical Perspectives Kallikrein–Kinin Systems Plasma Kallikrein–Kinin System Tissue Kallikrein–Kinin System Components of the Tissue Kallikrein–Kinin System Tissue Kallikrein Kallikrein Inhibitors: Kallistatin Kininogens Kinins and Peptidase Metabolism Kinin Receptors Tissue Kallikrein–Kinin System and Electrolyte and Water Balance in the Kidney Localization of Kallikrein–Kinin System Components Interrelationship of Renin–Angiotensin and Kallikrein–Kinin Systems Regulatory and Mediatory Factors Kinins and Electrolyte Transport Prostaglandins and Other Intracellular Mediators Tissue Kallikrein–Kinin System and Electrolyte Transport in Other Tissues Colon and Intestinal Epithelia Other Epithelia Overview

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Role of calcium ions in kinin‐induced chloride secretion

Cited by 23 publications

References 26 publications

Mediators of the secretory response to kinins

Mediators of the secretory response to kinins

Immunophysiology of Intestinal Electrolyte Transport

Tissue Kallikrein–Kinin System

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