Cyclic guanosine-3??5?-monophosphate induced diuresis in rats

Oßwald, H.; Yakobs, O. E.

doi:10.1007/bf00501123

Cited by 15 publications

(6 citation statements)

References 16 publications

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“…Consequently, in this respect, intracellular signal transduction is significantly different in the efferent ducts from their homologue, the proximal kidney tubules. In the latter, both cAMP [26][27][28][29][30] and cGMP [31] inhibit fluid reabsorption at about the same concentrations.…”

Section: Discussionmentioning

confidence: 93%

“…It has been established that both cyclic adenosine 3Ј,5Ј-monophosphate (cAMP) and cyclic guanosine 3Ј,5Ј-monophosphate (cGMP) are involved in regulating fluid transport in a number of other tissues. Both stimulate fluid secretion in intestines of humans [21] and rats [22][23][24][25], causing diarrhoea, and both inhibit fluid reabsorption in the proximal tubules of the kidney of a number of vertebrate species [26][27][28][29][30][31]. However, cAMP alone activates fluid secretion in canine pancreatic [32] and gallbladder epithelium [33], equine sweat glands [34], rat submandibular acinar cells [35], frog retinal pigment epithelium [36], and insect salivary glands [37,38], but activates fluid absorption in lung aveolar epithelium [39,40].…”

Section: Introductionmentioning

confidence: 91%

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Signal Transduction in the Ductuli Efferentes Testis of the Rat: Inhibition of Fluid Reabsorption by Cyclic Adenosine 3′, 5′-Monophosphate1

Man

Clulow

Jones

2003

Biology of Reproduction

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It is important to identify the signal transduction pathway involved in the regulation of fluid reabsorption by the ductuli efferentes of the testis because they reabsorb most of the fluid leaving the testis and are essential for male fertility. Microperfusion studies of the ducts in vivo showed that 0.1 or 1.0 mM dibutyryl (db)-cGMP in the perfusate had no effect on fluid reabsorption, but 0.1 mM db-cAMP significantly reduced fluid reabsorption, 0.25 mM abolished reabsorption, and 0.5-1.0 mM caused secretion. The inhibitory effect of db-cAMP was reversible. Although the presence of db-cAMP in the perfusate did not affect the concentration of Na+ in the collectate, the concentrations of K(+) and Cl(-) increased, indicating that their transport is at least partly regulated by cAMP. Including the phosphodiesterase inhibitor pentoxifylline in the perfusate decreased fluid reabsorption by the ducts in a dose-dependent manner, and it also increased the concentration of cAMP (5.5-fold) in collectate. Pentoxifylline also increased the production of cAMP (4-fold) by ducts incubated in vitro. It is concluded that cAMP, but probably not cGMP, is an intracellular messenger regulating fluid reabsorption in the efferent ducts.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 91%

Signal Transduction in the Ductuli Efferentes Testis of the Rat: Inhibition of Fluid Reabsorption by Cyclic Adenosine 3′, 5′-Monophosphate1

Man

Clulow

Jones

2003

Biology of Reproduction

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“…Cyclic GMP (cGMP) appears to be the second messenger for the acute action of ANP in the kidney (2, 4). Several investigators have demonstrated that ANP stimulates cGMP production by the kidney (2,4-6) and that the diuretic and natriuretic effects of ANP can be mimicked in vivo by infusion of cGMP (7).…”

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confidence: 99%

Four-Hour Atrial Natriuretic Peptide Infusion in Conscious Rats: Effects on Urinary Volume, Sodium, and Cyclic GMP

1988

Experimental Biology and Medicine

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Atrial natriuretic peptide (ANP) is released from the cardiac atria in response to acute volume loads; when infused acutely ANP causes diuresis and natriuresis. Cyclic GMP (cGMP) appears to be the second messenger for ANP in the kidney. The role that ANP plays in the long-term regulation of salt and water balance is unclear, however, since resistance to ANP's natriuretic and diuretic activity develops during prolonged administration. The purpose of the present study is to examine the relationship between the rate of cGMP excretion in response to ANP and the development of resistance to ANP's diuretic and natriuretic activity. Following a 30-min baseline period of infusion of Ringer's solution conscious rats received ANP at 15 pg/kg/hr ( n = 6) or Ringer's alone (n = 5) for 240 min. ANP-infused rats had a significant diuresis and natriuresis during the first hour of infusion; urinary cGMP excretion also increased compared to baseline. By 120 min after initiating the infusion in ANP-rats urinary volume and sodium excretion had declined to values not significantly different from those of baseline or control. In contrast, urinary cGMP excretion remained elevated for the duration of the ANP infusion, whether compared to baseline values or the control group. Resistance to the diuretic and natriuretic activity of ANP is not a result of mechanisms that involve cGMP generation.

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“…Struyenberg et al (15) demon strated an increase of intracellular pH of isolated tubules after treatment with acetazol amide. In addition, the increased cGMP levels at 100 mg/kg acetazolamide may contribute in part to the observed diuresis since cGMP itself leads to a marked diuresis in the rat (10).…”

Section: Discussionmentioning

confidence: 99%

Effects of Acetazolamide and Changes of Acid-Base Balance on the Content of Cyclic Nucleotides in the Rat Kidney

Oßwald¹,

Hawlina²

1979

Pharmacology

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Changes in tissue levels of cyclic adenosine 3’:5’-monophosphate (cAMP) and cyclic guanosine 3’:5’-monophosphate (cGMP) in the rat kidney in response to acid-base changes and administration of acetazolamide were measured. cAMP was determined according to the method described by Gilman and cGMP by radioimmunoassay. 1 mg/kg acetazolamide increased bicarbonate excretion 100-fold over the control values to 2.52 ± 0.5 mEq/min (mean ± SEM; n = 6), but did not influence cGMP and cAMP tissue content. 10 and 100 mg/kg acetazolamide increased cGMP tissue levels to 0.277 ± 0.048 and 0.482 ± 0.07 pmol/mg dry weight in comparison to 0.192 ± 0.04 in the controls, whereas no changes in cAMP levels occurred. Chronic as well as acute metabolic alkalosis induced an increase of cGMP levels (0.26 ± 0.03 and 0.29 ± 0.06 pmol/mg), whereas chronic metabolic and acute respiratory acidosis lowered cGMP levels to 0.14 ± 0.02 and 0.13 ± 0.02 pmol/mg. cAMP tissue levels were not affected by changes in acid-base balance. The data could suggest that cGMP participates in the regulation of acid-base balance and renal effects of acetazolamide.

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Cyclic guanosine-3??5?-monophosphate induced diuresis in rats

Cited by 15 publications

References 16 publications

Signal Transduction in the Ductuli Efferentes Testis of the Rat: Inhibition of Fluid Reabsorption by Cyclic Adenosine 3′, 5′-Monophosphate1

Signal Transduction in the Ductuli Efferentes Testis of the Rat: Inhibition of Fluid Reabsorption by Cyclic Adenosine 3′, 5′-Monophosphate1

Four-Hour Atrial Natriuretic Peptide Infusion in Conscious Rats: Effects on Urinary Volume, Sodium, and Cyclic GMP

Effects of Acetazolamide and Changes of Acid-Base Balance on the Content of Cyclic Nucleotides in the Rat Kidney

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