Guanosine 3',5'-monophosphate and adenosine 3',5'-monophosphate content of human umbilical artery.

Clyman, Ronald I.; Sandler, Jeffrey A.; Manganiello, Vincent C.; Vaughan, Martha

doi:10.1172/jci108002

Cited by 69 publications

(43 citation statements)

References 23 publications

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“…Results with histamine blocking agents indicate that, as in the case of cAMP, metiamide, rather than pyrilamine, diminishes increases of cGMP in glomeruli. Such a finding differs from observations on smooth muscle preparations from umbilical arteries (33) (16).…”

Section: Discussioncontrasting

confidence: 99%

“…The incubation time employed in our experiments (2 min) was relatively short, in an attempt to detect changes not only in cAMP but also in cGMP, which are known from other systems to be transient, with a rapid onset, an early peak of the response, and with subsequent fast decline in time (32)(33)(34). In control experiments, (26), allowed measurements in small quantity of tissue; high specificity of anti-cAMP and anti-cGMP antibodies allowed simultaneous measurements ofboth cyclic nucleotides in the same tissue extract excluding cross-reactivity of cyclic nucleotides.…”

Section: Discussionmentioning

confidence: 99%

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Modulation of Cyclic Nucleotides in Isolated Rat Glomeruli

et al. 1978

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A B S T R A C T Because glomerular functions are modulated by numerous humoral agents, probably acting through cyclic nucleotides, the effects of some polypeptide hormones and biogenic amines on cyclic AMP (cAMP) and cyclic 3',5'-guanosine monophosphate (cGMP) were studied in glomeruli isolated from rat renal cortex. Glomeruli and cortical tubules were prepared by a combination of sieving and density-gradient centrifugation. Under basal conditions, the contents of cAMP and cGMP in glomeruli were significantly higher than in tubules and unfractionated renal cortical tissue.Histamine caused a striking increase in cAMP in glomeruli (+A% 675±87) and, to a lesser degree, increased cAMP in tubules (+A% 103+25) or in tissue slices. This stimulation was dose-dependent in the range of 1 ,uM-1 mM histamine. Metiamide (an H2-antagonist), but not pyrilamine (an H,-antagonist) blocked the effect of histamine on cAMP, which indicates that histamine causes its effect via interaction with H2 receptors. Histamine caused less extensive increases in cGMP in both glomeruli and tubules. Carbamylcholine caused a marked increase in cGMP in glomeruli (+A 295±7) and a much lower increase in tubules (+A% 70+20); these effects were blocked by 1334atropine. Parathyroid hormone (1 ug/ml) increased cAMP and, to a much lesser degree, also cGMP in glomeruli. In tubules, parathyroid hormone caused nmuch more extensive increases in cAMP than in glomeruli; no changes, or rather a small decline in cGMP, was observed. Angiotensin-I1 (2 uM) markedly lowered cAMP in glomeruli (-A% -45±8) and in tubules (-A% 33±7) but had no effect on cGMP. Bradykinin (20 ,M) did not consistently influience either cAMP or cGMP in glomeruli or tubules.Present results demonstrate that cAMP and cGMP metabolism in glomeruli are controlled independently by humoral agents known to alter glomerular functions in vivo. Our findings are consistent with the view that histamine and cholinergic agents generated and (or) released locally in glomeruli or in their vicinity may play important roles as mediators of immunopathological injury of glomeruli, and that these effects are mediatecl by cAMP and (or) cGMP through interaction with H2 receptors and muscarinic receptors. Likewise, our results suggest that the effects of angiotensin-II and parathyroid hormone on glomerular dynamics may be mediated by cyclic nucleotides.Thus, we surmise that extrarenal as well as intrarenal humoral agents may play an important role in the pathology and physiology of glomeruli through mediation of either cAMP, cGMP, or both. INTRODUCTIONIt has become increasingly evident in recent years that many extrarenal and intrarenal humoral agents mraymodulate diverse aspects of glomerular function (1). For example, the administration of agents such as para- thyroid hormone (PTH)' (2), angiotensin (3, 4), bradykinin, acetylcholine (5,6), and others (1) causes changes in glomerular microcirculation, hydraulic permeability, or in the ultrafiltration properties of glomerular membrane. Perhaps more importantly,...

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Modulation of Cyclic Nucleotides in Isolated Rat Glomeruli

et al. 1978

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“…They therefore suggested that the umbilical arteries may have a poor relaxant response to cyclic GMP-mediated vascular relaxation. It has also been suggested that cyclic GMP accumulation in umbilical vessels induced by acetylcholine and histamine, may be associated with vascular contraction rather than relaxation (Clyman et al, 1975). Our results demonstrate that the umbilical and chorionic plate arteries do relax by cyclic GMP-mediated mechanisms although not as efficiently as other vessels under similar experimental conditions.…”

Section: Cyclic Gmp Accumulationmentioning

confidence: 99%

Characterization and actions of human umbilical endothelium derived relaxing factor

Chaudhuri

Buga

Gold

et al. 1991

British J Pharmacology

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A bioassay cascade superfusion technique was utilized to study the properties of endothelium derived relaxing factor (EDRF) from human umbilical vein (HUV) and compare its actions on umbilical, chorionic plate and bovine pulmonary arterial strips. Histamine (1 μm), bradykinin (1 μm) and A‐23187 (0.3 μm, 1 μm) but not acetylcholine (1 μm) released EDRF. The non‐innervated human foetoplacental vessels, i.e., umbilical and chorionic plate arteries, do relax to EDRF by a guanosine 3′: 5′‐cyclic monophosphate (cyclic GMP)‐mediated mechanism. The sensitivity of the human umbilical arterial strips to EDRF was less than that of the chorionic plate arterial strips. Bovine pulmonary arterial strips were the most sensitive to the relaxant actions of human umbilical EDRF.

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“…23 In our tests, no relaxation effect could be obtained with histamine on umbilical preparations mounted for isometric tension recording in the presence or absence of indomethacin and contracted with serotonin. However, Clymann et al 24 reported marked increases in cGMP levels in the human umbilical arteries in response to low concentrations of histamine, an effect that is also mediated by an H,-receptor mechanism, while they obtained only moderate increases in cGMP in response to serotonin and acetylcholine at high concentrations. This would indicate that EDRF also induces increased cGMP levels in the umbilical vessels but that there is only a poor response of these vessels to cGMP in contrast to other vascular smooth muscle cells.…”

mentioning

confidence: 98%