Effect of atriopeptin II on Ca influx, contractile behavior and cyclic nucleotide content of cultured neonatal rat myocardial cells

McCall, David; Fried, T. A.

doi:10.1016/0022-2828(90)91116-o

Cited by 32 publications

(18 citation statements)

References 35 publications

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“…Previously it was shown that ANF activates guanylate cyclase in heart and increases the cytoplasmic concentration of cGMP (Cramb et al, 1987;Anand-Srivastava et al, 1989;Rugg et al, 1989;McCall and Fried, 1990), a finding confirmed in the present study. We propose that the increase in cGMP causes shrinkage of myocytes by inhibiting Na+/K+/2C1-cotransport.…”

Section: Discussionsupporting

confidence: 91%

“…In the present study, the ANF-induced increase in cGMP was well maintained in isolated ventricular myocytes for 20 min. This is consistent with the observation that cGMP in ventricular muscle is elevated after a 30-min exposure to ANF (McCall and Fried, 1990). In contrast, in the presence of the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine (IBMX, 1 raM) and reduced extracellular Ca 2+ (0.5 mM), ventricular cGMP levels are reported to begin to decrease after exposure to ANF for ~ 10 rain but remain significantly greater than control at 20 min (Cramb et al, 1987).…”

Section: Is Cgmp the Second Messenger For Anf-induced Myocyte Shrinkage?supporting

confidence: 88%

“…Interpretation of the results presented up to this point depends in part on previous descriptions of the effects of ANF (Cramb et al, 1987;Anand-Srivastava et al, 1989;Rugg et al, 1989;McCall and Fried, 1990), LY83583 (Schmidt et al, 1985;MacLeod and Diamond, 1986), and M&B22948 (Lugnier et al, 1983;Brunkhorst et al, 1989;Weishaar et al, 1990) on cGMP levels in heart. Therefore, 125I-cGMP radioimmunoassay was used to confirm that the key elements of previous findings were applicable to isolated ventricular myocytes under the present experimental conditions.…”

Section: Effects Of Anf Ly83583 and Mandb22948 On Cgmp Levels In Myocmentioning

confidence: 80%

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Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Clemo

Feher

Baumgarten

1992

The Journal of General Physiology

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Previously we showed that atrial natriuretic factor (ANF) decreases cardiac cell volume by inhibiting ion uptake by Na+/K+/2CI-cotransport. Digital video microscopy was used to study the role of guanosine 3',5'-monophosphate (cGMP) in this process in rabbit ventricular myocytes. Each cell served as its own control, and relative cell volumes (volumetest/volumeco,trol) were determined. Exposure to 10 IxM 8-bromo-cGMP (8-Br-cGMP) reversibly decreased cell volume to 0.892 -0.007; the EDs0 was 0.77 +-0.33 tzM. Activating guanylate cyclase with 100 IxM sodium nitroprusside also decreased cell volume to 0.889 ---0.009. In contrast, 8-bromo-adenosine 3',5'-monophosphate (8-Br-AMP; 0.01-100 tzM) neither altered cell volume directly nor modified the response to 8-Br-cGMP. The idea that cGMP decreases cell volume by inhibiting Na+/K+/2C1-cotransport was tested by blocking the cotransporter with 10 I~M bumetanide (BUM) and removing the transported ions. After BUM treatment, 10 IxM 8-Br-cGMP failed to decrease cell volume. Replacement of Na ÷ with N-methyl-D-glucamine or C1-with methanesulfonate also prevented 8-Br-cGMP from shrinking cells. The data suggest that 8-Br-cGMP, like ANF, decreases ventricular cell volume by inhibiting Na+/K+/2C1-cotransport. Evidence that ANF modulates cell volume via cGMP was also obtained. Pretreatment with 10 IzM 8-Br-cGMP prevented the effect of 1 IzM ANF on cell volume, and ANF suppressed 8-Br-cGMP-induced cell shrinkage. Inhibiting guanylate cyclase with the quinolinedione LY83583 (10 tzM) diminished ANF-induced cell shrinkage, and inhibiting cGMP-specific phosphodiesterase with M&B22948 (Zaprihast; 100 IzM) amplified the volume decrease caused by a low dose of ANF (0.01 I~M) approximately fivefold. In contrast, neither 100 I~M 8-Br-cAMP nor 50 tzM forskolin affected the response to ANF. The effects of ANF, LY83583, and M&B29948 on cGMP levels in isolated ventricular myocytes were confirmed by 125I-cGMP radioimmunoassay. These data argue that ANF shrinks cardiac cells by increasing intracellular cGMP, thereby inhibiting Na+/K+/2C1-cotransport. Basal cGMP levels also appear to modulate cell volume.

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Section: Discussionsupporting

confidence: 91%

Section: Is Cgmp the Second Messenger For Anf-induced Myocyte Shrinkage?supporting

confidence: 88%

Section: Effects Of Anf Ly83583 and Mandb22948 On Cgmp Levels In Myocmentioning

confidence: 80%

See 1 more Smart Citation

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Clemo

Feher

Baumgarten

1992

The Journal of General Physiology

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“…Measurements of cyclic GMP levels in preparations from both tissues showed that YC-1 signi®-cantly increased cyclic GMP levels in smooth muscle but not in isolated myocytes from the heart. In contrast, activation of particular guanylyl cyclase with atriopeptin II (McCall & Fried, 1990) signi®cantly increased the cyclic GMP levels in the isolated cardiomyocytes. These ®ndings suggest that sGC can be activated by YC-1 in aortic smooth muscle but not in heart muscle.…”

Section: Discussionmentioning

confidence: 85%

“…Inhibition of sGC by ODQ resulted in cyclic GMP levels of 6.5+0.5 pmol mg 71 protein (n=10) which were not di erent from unstimulated preparations (P=0.75). In parallel experiments, atriopeptin II (100 nM), an activator of particular guanylyl cyclase (McCall & Fried, 1990), increased the cyclic GMP levels to 11.5+1.4 pmol mg 71 protein (n=9) in the isolated cardiomyocytes (P50.001; Figure 4b), E ects of YC-1 on cyclic AMP levels in aortic rings and isolated cardiomyocytes weight (n=8) and 286+36 pmol mg 71 wet weight (n=8) under control conditions and after stimulation with YC-1 (30 mM), respectively. In the cardiomyocytes, the corresponding values were 49+4 pmol mg 71 protein (n=10) and 52+3 pmol mg 71 protein (n=10), respectively.…”

Section: E Ects Of Yc-1 On Cyclic Gmp Levels In Aortic Rings and Isolmentioning

confidence: 99%

Activation of soluble guanylyl cyclase by YC‐1 in aortic smooth muscle but not in ventricular myocardium from rat

Wegener

Gath

Förstermann

et al. 1997

British J Pharmacology

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1 The e ects of YC-1 (3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole), an activator of soluble guanylyl cyclase, on tension, levels of cyclic GMP and cyclic AMP, and cardiac L-type Ca 2+ -current (I Ca(L) ) were investigated in aortic smooth muscle and ventricular heart muscle from rat. 2 YC-1 (0.1 ± 30 mM) induced a concentration-dependent relaxation in aortic rings precontracted with phenylephrine (3 mM). The relaxant e ects of YC-1 were reversed by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (30 mM; ODQ), potentiated by zaprinast (10 mM) and antagonized by Rp-8-BrcGMPS (100 mM). 3 In ventricular heart muscle strips, YC-1 (30 mM) exhibited no e ects on force of contraction (F c ) in the absence or presence of either zaprinast (10 mM) or 3-isobutyl-1-methylxanthine (30 mM). F c was slightly increased by YC-1 (30 mM) in the presence of isoprenaline (100 nM), but this e ect was not in¯uenced by ODQ (30 mM). 4 Cardiac I Ca(L) was not signi®cantly a ected by YC-1 (30 mM), either in the absence or presence of isoprenaline (30 nM). 5 In aortic rings, cyclic GMP levels were increased almost 3 fold by YC-1 (30 mM); this e ect was abolished by ODQ (30 mM). In isolated ventricular cardiomyocytes, cyclic GMP levels were not a ected by YC-1 (30 mM) but almost doubled by activation of particular guanylyl cyclase with atriopeptin II (100 nM). 6 YC-1 (30 mM) did not increase cyclic AMP levels either in aortic rings or in ventricular cardiomyocytes. In contrast, isoprenaline (3 mM) increased cyclic AMP levels about two fold in both tissues. In cardiomyocytes, the e ect of isoprenaline (3 mM) was slightly enhanced by YC-1 (30 mM). 7 It is concluded that relaxation of smooth muscle preparations by YC-1 is mediated mainly by activation of soluble guanylyl cyclase and subsequent increase in cyclic GMP levels. The failure of YC-1 to a ect cardiac F c , levels of cyclic GMP, and I Ca(L) suggests that soluble guanylyl cyclase is not in¯uenced by YC-1 in rat heart muscle or only barely present in this tissue.

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Atrial Natriuretic Factor

Atlas

Maack

1992

Comprehensive Physiology

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Effect of atriopeptin II on Ca influx, contractile behavior and cyclic nucleotide content of cultured neonatal rat myocardial cells

Cited by 32 publications

References 35 publications

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Modulation of rabbit ventricular cell volume and Na+/K+/2Cl- cotransport by cGMP and atrial natriuretic factor.

Activation of soluble guanylyl cyclase by YC‐1 in aortic smooth muscle but not in ventricular myocardium from rat

Atrial Natriuretic Factor

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