Evidence for H&lt;sub&gt;2&lt;/sub&gt; Receptor Activity on Glomerular Cells

Sperk, Günther; Ratzenhofer, E; Simbruner, G.; Coradello, H; Pollak, Arnold; Lubec, Jana

doi:10.1159/000172755

Cited by 2 publications

(1 citation statement)

References 4 publications

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“…Torres et al (19) were the first to describe an H2 receptormediated, stimulatory effect of histamine on cAMP production in rat glomeruli. Studies using labeled histamine HI and H2 receptor antagonists show that both receptors are present in glomeruli (22) and that a hormone-sensitive adenylate cyclase primarily linked to the H2 receptor is present on glomerular cells (22,23 More recently, histamine has been shown to stimulate renin release by the isolated perfused rat kidney, an effect primarily mediated by an H2 receptor (24). In addition to its hemodynamic effects on the renal and other regional circulations, histamine is an important regulator of the immune-inflammatory response in many tissues (25)(26)(27).…”

Section: Introductionmentioning

confidence: 99%

Histamine modulates contraction and cyclic nucleotides in cultured rat mesangial cells. Differential effects mediated by histamine H1 and H2 receptors.

Sedor¹,

Abboud²

1985

J. Clin. Invest.

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Histamine influences the glomerular microcirculation and modulates immune-inflammatory responses. In the rat kidney, histamine is synthesized by glomeruli and stimulates cyclic nucleotide production specifically in glomeruli. We investigated the in vitro effect of histamine on cyclic nucleotide accumulation in rat cultured glomerular mesangial and epithelial cells.Histamine stimulated cyclic AMP (cAMP) accumulation in cultured mesangial cells (64.0±22.1 to 511.4±86.6 pmol/mg protein, n = 9) but had no effect on cAMP accumulation in epithelial cells. This effect was dose-dependent and timedependent. Stimulation of cAMP accumulation occurred in the range of 5 X 10' M-10' M histamine with a half maximal stimulatory effect of 2 X 10' M. Initial stimulation was noted by 30 s, and maximum stimulation was observed at 5 min. The H2 antagonist cimetidine (10-4 M) abolished the stimulatory effect of histamine (10-4 M), while equimolar concentrations of the HI antagonist diphenhydramine had no significant effect on cAMP accumulation. Moreover, the specific H2 agonist dimaprit, but not the HI agonist 2-pyridylethylamine, stimulated cAMP accumulation. Histamine had no effect on cAMP accumulation in epithelial cells or on cyclic guanosine monophosphate accumulation in epithelial or mesangial cells.Since the in vivo infusion of histamine reduces ultrafiltration coefficient and since mesangial cell contraction is thought to be responsible for the reduction in the ultrafiltration coefficient, we examined the effect of histamine on the contractile property of mesangial cells. Histamine (5 X 10'-10-4 M) contracted mesangial cells, and the HI antagonist diphenhydramine (10-4 M) but not the H2 antagonist cimetidine (10-4 M) prevented histamine (10-4 M) induced contraction. In addition, the HI agonist 2-pyridylethylamine, but not the H2 agonist dimaprit, contracted mesangial cells. Histamine and its specific agonists and antagonists induced contraction of isolated glomeruli as assessed by glomerular planar surface area in a manner parallel to their effect on mesangial cells. Cinnarizine (10-5 M), a Ca' channel blocker, or Ca', Mg++-free medium prevented histamine (10-4 M) induced mesangial cell and glomerular contraction. Thus, histamine enhances cAMP accumulation specifically in mesangial cells via an H2 receptor. In contrast, histamine

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Section: Introductionmentioning

confidence: 99%

Histamine modulates contraction and cyclic nucleotides in cultured rat mesangial cells. Differential effects mediated by histamine H1 and H2 receptors.

Sedor¹,

Abboud²

1985

J. Clin. Invest.

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Regulation of prorenin secretion in cultured human transfected juxtaglomerular cells.

Pinet¹,

Mizrahi²,

Laboulandine³

et al. 1987

J. Clin. Invest.

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The regulation of renin secretion was studied in continuous culture of human juxtaglomerular cells (JGC), which provided a permanent source of human renin production (Pinet, F., M. T. Corvol, F. Dench, J. Bourguignon, J. Feunteun, J. Menard, and P. Corvol, 1985, Proc. NatL Acad. Sci. USA,. 95% of the renin species secreted was prorenin, and therefore this study concerned primarily prorenin secretion. Renin production was stable, since the cells had been maintained in culture for more than two years. In culture, these human cells formed colonies of smooth musclelike cells, and electron microscopy showed the presence of cytoskeleton structures including myofibrils and attachment bodies. This human model was used to investigate the control of prorenin secretion in vitro at cellular level. Various pharmacological agents known to stimulate or inhibit renin secretion were tested in the cell cultures. The variations in prorenin secretion were measured in the supernatant. Forskolin, an independent receptor activator of adenylate cyclase, stimulated prorenin secretion in a dose-dependent manner and this stimulation was mediated by 3',5' cyclic-AMP (cAMP). Angiotensin II (All) was found to inhibit prorenin secretion directly in a dose-dependent manner and atrial natriuretic factor (ANF), whose effects on human JGC were characterized for the first time, was also shown to exert such inhibition. When the effects of this inhibition by All and ANF were tested on forskolin-mediated stimulation of prorenin secretion, the latter was inhibited and no change occurred in cAMP release. When JGC were treated with histamine, bradykinin, or one or two bradykinin analogues, the responses suggested that in these cells, H2-histamine receptors and kinin receptors are dependent on adenylate cyclase. One peptide, substance P., had an inhibitory effect on prorenin secretion but it was less important than All and ANF. The present results demonstrate that the adenylate cyclase system of human JGC remains intact during culture and supports the hypothesis that cAMP is the second messenger and Ca,2+ the final messenger involved in renin secretion. The cell system used here permits the evaluation of cellular responses and intracellular events in granulated cells in a human model.

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Evidence for H<sub>2</sub> Receptor Activity on Glomerular Cells

Cited by 2 publications

References 4 publications

Histamine modulates contraction and cyclic nucleotides in cultured rat mesangial cells. Differential effects mediated by histamine H1 and H2 receptors.

Histamine modulates contraction and cyclic nucleotides in cultured rat mesangial cells. Differential effects mediated by histamine H1 and H2 receptors.

Regulation of prorenin secretion in cultured human transfected juxtaglomerular cells.

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