Effects of sodium pump inhibition on the relaxation induced by synthetic Atrial Natriuretic Factor (ANF) and sodium nitroprusside

The objective of this study was to determine the direct actions of atrial natriuretic factor (ANF) on the pulmonary vascular bed and to compare these actions with those of sodium nitroprusside (SNP). The responses to incremental infusion rates of 1, 5, 10, and 50 ng.kg-1.min-1 synthetic human ANF and to 1-2 micrograms.kg-1.min-1 SNP were examined in the in situ autoperfused lung lobe of open-chest anesthetized pigs under conditions of normal and elevated pulmonary vascular tone. During basal conditions, ANF and SNP caused small but significant reductions in pulmonary artery pressure (Ppa) and pulmonary venous pressure (Ppv) with no change in lobar vascular resistance (LVR). When pulmonary vascular tone was increased by prostaglandin F2 alpha (20 micrograms/min), ANF infusion at doses greater than 1 ng.kg-1.min-1 decreased Ppa and LVR in a dose-related fashion. Infusion of 50 ng.kg-1.min-1 ANF and of 2 micrograms.kg-1.min-1 SNP maximally decreased Ppa, from 33 +/- 3 to 20 +/- 2 mmHg (P less than 0.001) and from 31 +/- 4 to 18 +/- 1 mmHg (P less than 0.001), respectively. At these doses, ANF reduced systemic arterial pressure by only 11.5 +/- 3% compared with 34 +/- 4% decreased with SNP (P less than 0.001). The results indicate that ANF, similarly to SNP, exerts a direct potent vasodilator activity in the porcine pulmonary vascular bed, which is dependent on the existing level of vasoconstrictor tone.

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Leukotriene D4 inhibits atrial natriuretic factor-dependent cGMP production in rat glomerulus

AJP Renal Physiology ◽

10.1152/ajprenal.1989.256.1.f95 ◽

1989 ◽

Vol 256 (1) ◽

pp. F95-F99

Author(s):

Y. Terada ◽

K. Tomita ◽

N. Yoshiyama ◽

T. Shiigai ◽

F. Marumo

Keyword(s):

Sodium Nitroprusside ◽

Guanylate Cyclase ◽

Atrial Natriuretic Factor ◽

Soluble Guanylate Cyclase ◽

Leukotriene D4 ◽

Isolated Glomeruli ◽

Cgmp Production ◽

Natriuretic Factor ◽

Isolated Rat ◽

Atrial Natriuretic

The effects of leukotriene D4 (LTD4) on guanosine 3',5'-cyclic monophosphate (cGMP) production induced by atrial natriuretic factor (ANF) or sodium nitroprusside (SNP) were investigated in isolated rat glomeruli. First, the isolated glomeruli were preincubated in Krebs-Ringer buffer containing 3-isobutyl-1-methylxanthine for 10 min, then incubated with varying concentrations of ANF, SNP, and LTD4 for 3 min. cGMP content was determined by radioimmunoassay. cGMP production (fmol.glomerulus-1.3 min-1) was not increased by LTD4. cGMP accumulation was increased by ANF (1 microM) and SNP (100 microM) remarkably from 0.19 +/- 0.09 to 3.24 +/- 0.21 (n = 7, mean +/- SE), and from 0.19 +/- 0.09 to 3.67 +/- 0.47 (n = 4), respectively. The increase in cGMP production by ANF was significantly and dose-dependently inhibited by LTD4 (P less than 0.05). Maximum suppression was observed at the concentration of 100 nM (from 3.06 +/- 0.33 to 1.43 +/- 0.09; P less than 0.05). However, LTD4 caused no significant change in the level of cGMP production induced by SNP. Second, particulate or soluble guanylate cyclase from glomeruli were similarly investigated. ANF selectively activated particulate guanylate cyclase and the response was selectively inhibited by LTD4 from 9.07 +/- 1.79 fmol.micrograms-1.3 min-1 (n = 6) to 4.70 +/- 0.70 (n = 6, P less than 0.05). These results suggest the site where LTD4 has effect on cGMP production induced by ANF was the particulate guanylate cyclase system, but not the soluble guanylate cyclase system.

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Atrial Natriuretic Factor Potentiates the Human Forearm Vasoconstrictor Response to Sympathetic Stimulation

Clinical Science ◽

10.1042/cs0860275 ◽

1994 ◽

Vol 86 (3) ◽

pp. 275-283 ◽

Cited By ~ 5

Author(s):

Tim L. Th. A. Jansen ◽

Dr Paul Smits ◽

Jacques W. M. Lenders ◽

Marie-Cécile G. S. Jacobs ◽

Jacques Willemsen ◽

...

Keyword(s):

Sodium Nitroprusside ◽

Negative Pressure ◽

Atrial Natriuretic Factor ◽

Lower Body Negative Pressure ◽

Sympathetic Stimulation ◽

Lower Body ◽

Natriuretic Factor ◽

Vasoconstrictor Response ◽

Forearm Vascular Resistance ◽

Atrial Natriuretic

1. Atrial natriuretic factor has been suggested to affect human sympathetic nervous system activity. The interaction between atrial natriuretic factor and the sympathetic nervous system has not been fully elucidated yet, but may occur at different sites. We studied this modulator effect at the level of the forearm vascular bed: the forearm vasoconstrictor response was examined after α-adrenergic sympathetic stimulation in healthy subjects during the loco-regional administration of atrial natriuretic factor, sodium nitroprusside and placebo. As a sympathetic stimulation test, the technique of the lower body negative pressure (–20 mmHg) was used. 2. Lower body negative pressure increased the forearm vascular resistance by +37 ± 8% during concomitant intra-arterial infusion of placebo (n = 10). During a predilator state achieved by infusion of atrial natriuretic factor (10 ng min−1 100 ml−1 forearm volume) into the brachial artery, lower body negative pressure subsequently induced a forearm vasoconstrictor response of +153 ± 22% (P < 0.05 versus placebo), whereas this was +64 ± 14% when predilatation was achieved by infusion of an equipotent vasodilator dose of sodium nitroprusside (P > 0.1 versus placebo; P < 0.05 versus atrial natriuretic factor). The potentiation of the forearm vasoconstrictor response to lower body negative pressure by atrial natriuretic factor only occurred in the experimental and not in the contralateral arm. According to calculations on simultaneously sampled arterial and venous plasma catecholamine concentrations, the augmented forearm vasoconstrictor response seemed not to be caused by an increased release of noradrenaline. 3. In a second experiment (n = 10), we demonstrated that atrial natriuretic factor did not alter the forearm vasoconstrictor response to the intra-arterial administration of exogenous noradrenaline, thereby excluding a postsynaptic modulation by atrial natriuretic factor. In the presence of atrial natriuretic factor, the subsequent infusion of two dosages of noradrenaline (0.1 and 1.0 ng min−1 100 ml−1 forearm volume) increased the forearm vascular resistance by +118 ± 29% and +387 ± 79%, respectively, whereas these numbered +129 ± 18% and + 316 ± 41% when atrial natriuretic factor was replaced by an equipotent dose of sodium nitroprusside. 4. We conclude that atrial natriuretic factor potentiates the forearm vasoconstrictor response to α-adrenergic sympathetic stimulation in man, and that this effect may be located at the level of the forearm vascular bed. This potentiation cannot be explained by an increased vascular α-adrenergic sensitivity. More detailed studies are needed to analyse the effects of atrial natriuretic factor on local noradrenaline kinetics to elucidate influences on sympathetic neurotransmission.

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Effects of angiotensin II on plasma atrial natriuretic factor in nonpregnant and pregnant ewes

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y95-082 ◽

1995 ◽

Vol 73 (5) ◽

pp. 644-650 ◽

Cited By ~ 3

Author(s):

L. Fan ◽

D. Javeshghani ◽

S. Mukaddam-Daher ◽

Z. Guan ◽

B. S. Nuwayhid ◽

...

Keyword(s):

Angiotensin Ii ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Sodium Nitroprusside ◽

Atrial Natriuretic Factor ◽

Natriuretic Factor ◽

Pregnant Sheep ◽

Nitroprusside Infusion ◽

Atrial Natriuretic

The release of atrial natriuretic factor (ANF) is primarily determined by atrial stretch, but may also be modulated by circulating angiotensin II (AngII). During pregnancy, the circulating concentrations of both ANF and AngII are increased. To further define possible effects of AngII on ANF release, four doses of AngII (0.5, 5, 20, 40 ng∙kg−1∙min−1) were intravenously infused into five nonpregnant and five pregnant (105–140 days of gestation) ewes alone and during the simultaneous infusion of sodium nitroprusside at doses sufficient to abolish the pressor effects of AngII. Mean arterial pressure (MAP) was increased from 80 ± 2 to a maximum of 121 ± 5 mmHg (1 mmHg = 133.3 Pa) in nonpregnant ewes (p < 0.01) and from 79 ± 2 to 116 ± 4 mmHg in pregnant ewes (p < 0.01) over the range of AngII infusion. MAP was unaltered during AngII plus nitroprusside infusion, averaging 78 ± 3 mmHg in nonpregnant ewes and 80 ± 2 mmHg in pregnant ewes. Basal ANF was higher (p < 0.01) in pregnant sheep than in nonpregnant sheep. With AngII infusion alone, plasma ANF was increased from 13 ± 2 to 42 ± 4 fmol/mL in nonpregnant ewes (p < 0.01) and from 23 ± 5 to 72 ± 16 fmol/mL in pregnant ewes (p < 0.01). However, during AngII plus nitroprusside infusion, the increases in plasma ANF observed were completely abolished in both nonpregnant and pregnant ewes. These results suggest that AngII does not have a direct stimulatory effect on ANF release but rather that the increase in plasma ANF is a consequence of the pressor effects of AngII. This response does not appear to be altered during ovine pregnancy.Key words: angiotensin II, atrial natriuretic factor, nitroprusside, mean arterial pressure.

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