Carbidopa Does Not Affect the Renal Response to Atrial Natriuretic Factor in Man

1989 ◽  
Vol 77 (3) ◽  
pp. 281-285 ◽  
Author(s):  
Helen M. Lewis ◽  
M. R. Wilkins ◽  
M. J. Kendall ◽  
M. R. Lee
Keyword(s):  
Atrial Natriuretic Factor ◽  
Similar Increase ◽  
Double Blind ◽  
Renal Response ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Urinary Dopamine ◽  
Renal Dopamine ◽  
Factor Concentration ◽  
Atrial Natriuretic

1. The dependence of atrial natriuretic factor on renal dopamine for its renal effects in man was examined in 10 healthy volunteers using the dopa decarboxylase inhibitor carbidopa. 2. Each volunteer attended on two occasions, and received an infusion of atrial natriuretic factor (4 pmol min−1 kg−1) for 60 min after pretreatment with either placebo or carbidopa orally. These were administered in random, double-blind fashion. 3. A similar increase in plasma atrial natriuretic factor concentration was seen after atrial natriuretic factor infusion on both visits. 4. Infusion of atrial natriuretic factor produced a small unsustained rise in urinary dopamine excretion. This increase in urinary dopamine excretion was blocked by carbidopa with no effect on the natriuresis. 5. Urinary guanosine 3′:5′-cyclic monophosphate excretion increased in response to the atrial natriuretic factor infusion whether placebo or carbidopa was given. Guanosine 3′:5′-cyclic monophosphate, but not dopamine, may be a mediator of the renal response to atrial natriuretic factor in man.

Inhibitory effect of atrial natriuretic factor on sympathetic ganglionic neurotransmission in humans

1995 ◽  
Vol 269 (2) ◽  
pp. R406-R412 ◽  
Author(s):  
J. S. Floras
Keyword(s):  
Atrial Natriuretic Factor ◽  
Muscle Sympathetic Nerve Activity ◽  
Acetylcholinesterase Inhibitor ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Inhibitory Effect ◽  
Double Blind Study ◽  
Double Blind ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

I have previously documented an inhibitory effect of atrial natriuretic factor (ANF) on postganglionic muscle sympathetic nerve activity (MSNA) in normal subjects that was consistent with either a central or ganglionic sympathoinhibitory action. To test the latter hypothesis, I examined, in seven young normotensive men, the effect of saline (as vehicle) and ANF (50 micrograms, then 50 ng.kg-1.min-1), given on 2 separate days according to a random double-blind study design, on blood pressure, heart rate, and MSNA before and after ganglionic neurotransmission was stimulated with edrophonium (ED; 12 mg iv), a rapidly reversible acetylcholinesterase inhibitor without central nervous system effects, and during subsequent augmentation of central sympathetic outflow by a cold pressor test (CPT). In five of these subjects, the protocol was replicated during nitroprusside infusion (0.4 micrograms.kg-1.min-1). ED increased MSNA during vehicle (P < 0.005) and nitroprusside (P < 0.003) but not during ANF infusion. The sympathoneural response to the combined stimuli of ED and CPT was also attenuated by ANF compared with either saline or nitroprusside infusions. Conclusions were that 1) postganglionic MSNA is increased by ED, 2) this facilitative effect of ED is attenuated by ANF, and 3) modulation of ganglionic neurotransmission is one mechanism for the relative sympatho-inhibition observed when ANF is infused at this dose.

Vasopressin inhibits diuresis induced by water immersion in humans

1992 ◽  
Vol 73 (3) ◽  
pp. 932-936 ◽  
Author(s):  
S. Farrow ◽  
G. Banta ◽  
S. Schallhorn ◽  
R. May ◽  
A. Mers ◽  
...  
Keyword(s):  
Placebo Group ◽  
Atrial Natriuretic Factor ◽  
Water Immersion ◽  
Urine Osmolality ◽  
Plasma Aldosterone ◽  
Plasma Aldosterone Concentration ◽  
Natriuretic Factor ◽  
V2 Receptor ◽  
Factor Concentration ◽  
Atrial Natriuretic

We tested the hypothesis that 1-desamino-8-D-arginine vasopressin (DDAVP), a V2-receptor agonist, could inhibit the diuresis induced by water immersion in humans. Water and electrolyte excretion, plasma atrial natriuretic factor concentration, and plasma aldosterone concentration were measured initially and after 3 h of water immersion in 13 healthy sodium-replete men given either placebo or 20 micrograms of intranasal DDAVP. Guanosine 3′,5′-cyclic monophosphate and urea excretion and urine osmolality were also determined. DDAVP inhibited the diuresis induced by water immersion in men: 758 +/- 168 (SE) ml/3 h in the placebo group vs. 159 +/- 28 ml/3 h in the DDAVP group (P less than 0.05). After 3 h of water immersion, plasma atrial natriuretic factor concentrations were increased from 11 +/- 2 to 20 +/- 4 pg/ml in the placebo group and from 14 +/- 2 to 33 +/- 4 pg/ml in the DDAVP group (P less than 0.05). Plasma aldosterone concentrations were decreased from 98 +/- 18 to 45 +/- 6 pg/ml in the placebo group (P less than 0.05) and from 54 +/- 17 to 25 +/- 5 pg/ml in the DDAVP group (P less than 0.05). Despite these changes in aldosterone and atrial natriuretic factor concentrations, which should increase sodium excretion, DDAVP decreased the natriuresis induced by water immersion in humans: 56 +/- 8 meq Na+/3 h in the placebo group vs. 36 +/- 6 meq Na+/3 h in the DDAVP group (P less than 0.05). DDAVP may be used to prevent the diuresis associated with central redistribution of blood volumes that occur during water immersion.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of Na-K-Cl cotransport in endothelial cells by atrial natriuretic factor

1989 ◽  
Vol 257 (1) ◽  
pp. C36-C44 ◽  
Author(s):  
M. E. O'Donnell
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Response ◽  
Atrial Natriuretic Factor ◽  
Second Messengers ◽  
Vasoactive Agents ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Endothelial Cell Response ◽  
Atrial Natriuretic

Many vasoactive agents have been shown to bind to specific receptors on endothelial cells. Among these is atrial natriuretic factor (ANF). Binding of ANF to endothelial cells has been demonstrated to induce elevation of intracellular guanosine 3',5'-cyclic monophosphate (cGMP). Other vasoactive agents have been shown to cause elevation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP), Ca, and diacylglycerol. However, the endothelial cell response that occurs subsequent to elevation of cGMP or other second messengers is not well understood. Recently, endothelial cells have been shown to possess a Na-K-Cl cotransport system that is stimulated by vasopressin and bradykinin and inhibited by isoproterenol. Thus it is possible that modulation of Na-K-Cl cotransport may play a role in the endothelial cell response to second messengers that are elevated by ANF and other vasoactive agents. This possibility was examined in the present study by evaluating the effects of a variety of vasoactive agents and their second messengers on endothelial cell Na-K-Cl cotransport. Cotransport was assessed as bumetanide-sensitive K influx in cultured bovine aortic endothelial cells. A number of agents were found to reduce Na-K-Cl cotransport, including ANF, acetylcholine, histamine, and norepinephrine. Cotransport was found to be stimulated by angiotensin II, as well as vasopressin and bradykinin. Na-K-Cl cotransport was also inhibited by elevation of intracellular cGMP or cAMP or by treatment of the cells with phorbol ester to activate protein kinase C. However, A23187-induced elevation of intracellular Ca caused stimulation of Na-K-Cl cotransport.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of atrial natriuretic factor-induced inhibition of rat mesangial cell mitogenesis.

1990 ◽  
Vol 259 (3) ◽  
pp. E312 ◽  
Author(s):  
R G Appel
Keyword(s):  
Atrial Natriuretic Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Maximal Response ◽  
Thymidine Uptake ◽  
Dependent Manner ◽  
Cyclic Monophosphate ◽  
3T3 Fibroblasts ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Recent observations suggest that atrial natriuretic factor (ANF) may have growth-inhibitory activity. The present studies were performed to further define this action in rat mesangial cells (which have both biological and clearance ANF receptors) and in 3T3 fibroblasts (which have only clearance ANF receptors). Both cell types were made quiescent by removal of serum and then reactivated by exposure to a serum-free defined medium. ANF inhibited [3H]thymidine uptake in a dose-dependent manner in mesangial cells (half-maximal response 10(-11) M; 47% maximal inhibitory effect) but had no effect in 3T3 fibroblasts. Exogenous 8-bromoguanosine 3',5'-cyclic monophosphate (0.1 mM) inhibited [3H]thymidine uptake by 33% in mesangial cells but had no effect in 3T3 fibroblasts. Counts in mesangial cells exposed to 0.1 mM sodium nitroprusside, which stimulates guanosine 3',5'-cyclic monophosphate (cGMP), were inhibited by 76%. However, this represented a toxic effect, because excessive trypan blue uptake was noted in this condition. Mesangial cell number after 3 days of logarithmic proliferation was reduced by 33% in cells incubated with 1.0 nM ANF compared with vehicle. Incubation of mesangial cell monolayers with ANF caused a concentration-dependent increase in intracellular cGMP accumulation. Threshold responses occurred at concentrations one order of magnitude greater than that resulting in the antimitogenic action. In 3T3 fibroblast monolayers exposed to ANF, cGMP accumulation occurred but was markedly attenuated compared with mesangial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Rate-induced increase in plasma atrial natriuretic factor can occur independently of changes in atrial wall stretch

1991 ◽  
Vol 260 (6) ◽  
pp. H1953-H1958
Author(s):  
F. Riddervold ◽  
O. A. Smiseth ◽  
C. Hall ◽  
G. Groves ◽  
C. Risoe
Keyword(s):  
Atrial Natriuretic Factor ◽  
Atrial Pacing ◽  
Similar Increase ◽  
Atrial Wall ◽  
Natriuretic Factor ◽  
Anesthetized Dogs ◽  
Left And Right ◽  
The Relationship ◽  
Different Levels ◽  
Atrial Natriuretic

Tachycardia is known to increase the plasma level of atrial natriuretic factor (ANF). The aim of the study was to determine whether such release of ANF can occur independently of increased atrial wall stretch. Seven anesthetized dogs were instrumented with pressure catheters and sonomicrometer crystals to measure left and right auricular and atrial free wall dimensions. During atrial pacing, the measured atrial dimensions were kept constant by adjusting vascular constrictors placed around the great vessel trunks. When atrial rate was increased progressively by pacing at 150, 200, and 250 min-1, plasma ANF increased from 40.8 +/- 5.4 to 43.0 +/- 6.0 (P = NS) and 103.1 +/- 17.6 (SE) pmol/l (P less than 0.05), respectively. Repeating the pacing sequence at two different levels of elevated left atrial pressure caused at each level a similar increase in plasma ANF at 250 min-1. The relationship between plasma ANF and atrial dimensions was shifted upward by pacing, such that ANF was higher for any given atrial dimension. In conclusion, pacing tachycardia elevates plasma ANF in the presence of constant atrial dimensions. These results support the hypothesis that chronotropic stimulation can cause release of ANF by a mechanism that is independent of atrial stretch.

Sustained fetal pulmonary vasodilation with prolonged atrial natriuretic factor and GMP infusions

1991 ◽  
Vol 260 (1) ◽  
pp. H183-H192 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Atrial Natriuretic Factor ◽  
Pulmonary Blood Flow ◽  
Prostaglandin D2 ◽  
Pressure Flow ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Direct Acting ◽  
Atrial Natriuretic

To study mechanisms of vasodilation and factors that maintain high pulmonary vascular resistance in utero, we measured changes in blood flow and the pressure-flow relationship of the pulmonary circulation during prolonged exposures to direct-acting guanosine 3',5'-cyclic monophosphate (cGMP) vasodilators, atrial natriuretic factor (ANF), and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) and compared hemodynamic responses with other vasodilator stimuli in chronically prepared fetal lambs. The fetus was treated with 2 h of intrapulmonary infusions of ANF (0.15 micrograms/min), 8-BrcGMP (50 micrograms/min), prostaglandin D2 (PGD2, 0.4 micrograms/min), or acetylcholine (ACh, 1.5 micrograms/min) or increases in fetal Po2. Despite continued exposure to increased Po2, PGD2, and ACh, elevations of pulmonary blood flow and slopes of the pressure-flow relationship were not sustained, with both significantly decreased at 2 h from peak values. In contrast, pulmonary blood flow and pressure-flow slopes remained increased throughout 2 h of exposures to ANF and 8-BrcGMP. Adenosine 3',5'-cyclic monophosphate caused less change in blood flow than 8-BrcGMP within the dose range studied. We conclude that unlike other stimuli, direct-acting cGMP vasodilators are able to sustain vascular relaxation of the fetal pulmonary circulation.

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