Atrial natriuretic factor attenuates sympathetic neuroeffector responses in hindlimb vasculature of rabbits

1989 ◽  
Vol 67 (9) ◽  
pp. 1101-1105 ◽  
Author(s):  
K. P. Patel
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Sympathetic Nerve Stimulation ◽  
Arterial Infusion ◽  
Natriuretic Factor ◽  
Before And After ◽  
Atrial Natriuretic

To determine whether atrial natriuretic factor (ANF) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or intra-arterial norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1–8 Hz), or administration of NE (50–200 ng), in an isolated constant flow-perfused hindlimb of chloralose-anesthetized rabbit before and after intra-arterial infusion of ANF (0.5 ng∙mL−1∙min−1). ANF significantly attenuated responses to LSNS (relative potency, RP = 0.65) and to NE (RP = 0.47). We conclude that ANF attenuates vasoconstrictor responses to both LSNS and NE. Thus ANF alters sympathetic nervous system mediated changes in vascular resistance possibly at the neuroeffector site.Key words: atrial natriuretic factor, sympathetic nerve stimulation, vasculature.

Adrenergic and nonadrenergic cotransmitters inhibit insulin secretion during sympathetic stimulation in dogs

1992 ◽  
Vol 263 (1) ◽  
pp. E72-E78
Author(s):  
J. Lorrain ◽  
I. Angel ◽  
N. Duval ◽  
M. T. Eon ◽  
A. Oblin ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Blocking Agent ◽  
Norepinephrine Release ◽  
Sympathetic Nerve Stimulation ◽  
K Channels ◽  
Adrenoceptor Antagonist

Vascular and biochemical responses to pancreatic sympathetic nerve stimulation were investigated in the blood-perfused pancreas of anesthetized dogs. During sympathetic nerve stimulation, pancreatic perfusion pressure and norepinephrine release increased, whereas insulin secretion decreased. The latter effect did not occur after pretreatment with the alpha 2-adrenoceptor antagonist idazoxan. However, after beta-adrenoceptor blockade with propranolol, neither single administration of idazoxan nor the alpha 1-adrenoceptor antagonist prazosin or glibenclamide, a blocker of ATP-modulated K+ channels, affected the decrease in insulin secretion induced by sympathetic nerve stimulation. In contrast, the combination of glibenclamide with idazoxan markedly antagonised the decrease in insulin release evoked by the latter procedure. After depletion of catecholamines with syrosingopine, the stimulation-induced inhibition of insulin secretion remained unchanged even though no increases in pancreas perfusion pressure or norepinephrine release were observed. In this preparation, glibenclamide inhibited the decrease in insulin release by 50%. In animals pretreated with the neuronal blocking agent bretylium, all of the responses to sympathetic nerve stimulation were abolished. These results indicate that the inhibitory effects exerted by the sympathetic nervous system on insulin secretion are mediated not only by the classical neurotransmitter norepinephrine acting on alpha 2-adrenoceptors but also by a nonadrenergic cotransmitter that can maintain transmission under conditions of catecholamine deficiency. The postulated nonadrenergic cotransmitter(s) acts, at least partly, via the opening of ATP-modulated K+ channels blockable by glibenclamide, and its release can be prevented by the neuronal blocking agent bretylium.

Influence of blood pressure, heart rate, age, and sex on concentrations of atrial natriuretic factor and cyclic GMP in 124 volunteers.

1989 ◽  
Vol 35 (7) ◽  
pp. 1519-1523 ◽  
Author(s):  
M Wencker ◽  
S Hauptlorenz ◽  
W Moll ◽  
B Puschendorf
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Confidence Interval ◽  
Atrial Natriuretic Factor ◽  
Blood Donation ◽  
Healthy Individuals ◽  
Natriuretic Factor ◽  
Before And After ◽  
Age And Sex ◽  
Atrial Natriuretic

Abstract The significance of increased atrial natriuretic factor (ANF) in relation to blood pressure and age is still controversial. We investigated the influence of blood pressure, age, and some other variables on ANF and its putative second messenger, cGMP. Samples for ANF and cGMP detection were taken from 124 ostensibly healthy individuals who were donating blood. Samples were also collected from 27 volunteers before and after blood donation, to study the influence of bleeding. During blood donation, ANF increased from 78.9 to 87.4 ng/L (P = 0.0035), whereas cGMP remained unchanged. ANF concentrations in 124 healthy individuals, corrected for the influence of bleeding, were 61.5 (SD 26.1) ng/L, with a 95% confidence interval of 10.0 to 112.1 ng/L. Mean cGMP concentrations in plasma were 2.9 (SD 1.45) nmol/L, with a 95% confidence interval of 0.4 to 5.75 nmol/L. Multivariance analysis revealed no significant influence of blood pressure, age, heart rate, or sex on concentrations of either ANF or cGMP in plasma.

Trout vascular and renal responses to atrial natriuretic factor and heart extracts

1986 ◽  
Vol 251 (3) ◽  
pp. R639-R642 ◽  
Author(s):  
D. W. Duff ◽  
K. R. Olson
Keyword(s):  
Flow Rate ◽  
Atrial Natriuretic Factor ◽  
Pressor Response ◽  
Aortic Pressure ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Natriuretic Factor ◽  
Long Duration ◽  
Before And After ◽  
Atrial Natriuretic

Dorsal aortic pressure (DAP), urine flow rate, and urinary K+, Na+, and Cl- were monitored in chronically catheterized unanesthetized rainbow trout before and after injection of saline, tissue extracts, or synthetic (rat, Ile-26) atrial natriuretic factor (ANF). Synthetic ANF (1.0 and 10.0 micrograms/kg body wt) and extracts from trout atria and ventricles increased DAP, urine flow rate, and electrolyte excretion. Saline, skeletal muscle extracts, and 0.1 microgram/kg body wt synthetic ANF had no effect on DAP and only minor effects on renal water and ion excretion. The slow-onset long-duration pressor response to ANF and heart extracts contrasted with a rapid short-acting pressor effect of epinephrine. Synthetic ANF (10 micrograms/kg body wt) and ventricular extracts produced marked increases in Na+ and Cl- excretion but only a mild diuresis. Much of the increase in urine flow rate appears to be due to solvent injection. These results show that trout hearts contain an ANF-like material and that mammalian and piscine ANF produce hemodynamic and renal effects upon intra-arterial injection.

Effects of renal perfusion pressure on the natriuresis induced by atrial natriuretic factor

1987 ◽  
Vol 253 (2) ◽  
pp. F234-F238
Author(s):  
A. A. Seymour ◽  
S. G. Smith ◽  
E. K. Mazack
Keyword(s):  
Vascular Resistance ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Natriuretic Factor ◽  
Renal Vascular ◽  
Atrial Natriuretic

Synthetic atrial natriuretic factor (ANF 101-126) was infused at 1, 5, 25, and 125 pmol X kg-1 X min-1 into the renal artery of anesthetized, one-kidney dogs. During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). When base-line RPP was lowered to 101 +/- 5 mmHg by tightening a suprarenal aortic constriction, the same doses raised FENa to only 5.6 +/- 1.6 and 5.1 +/- 1.6%. A larger reduction of beginning RPP to 82 +/- 4 mmHg suppressed the natriuretic responses to 25 and 125 pmol X kg-1 X min-1 of ANF 101-126 to only 1.4 +/- 0.8 and 0.8 +/- 0.3%, respectively.During the peak natriuretic dose of 25 pmol X kg-1 X min-1, renal vascular resistance (RVR) fell from 0.88 +/- 0.10 to 0.68 +/- 0.07, from 0.78 +/- 0.10 to 0.68 +/- 0.12, and from 0.60 +/- 0.06 to 0.61 +/- 0.06 mmHg X ml-1 X min-1 at RPP = RPP = 112, 101, and 82 mmHg, respectively. ANF 101-126 did not affect glomerular filtration rate (GFR) at any level of RPP tested. In conclusion, the natriuretic responses to ANF 101-126 occurred without changes in GFR and were modulated by the prevailing levels of renal perfusion pressure and renal vascular resistance.

Direct evidence for the role of neuropeptide Y in sympathetic nerve stimulation-induced vasoconstriction

1998 ◽  
Vol 274 (1) ◽  
pp. H290-H294 ◽  
Author(s):  
Songping Han ◽  
Chun-Lian Yang ◽  
Xiaoli Chen ◽  
Linda Naes ◽  
Bryan F. Cox ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Biological Action ◽  
Sympathetic Nerve Stimulation ◽  
Low Frequencies ◽  
Vascular Bed ◽  
Potentiation Effect ◽  
Mesenteric Vascular Bed

Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter with norepinephrine (NE) in sympathetic nerve terminals and is thought to be involved in sympathetic nerve stimulation (SNS)-induced vasoconstriction. Using BIBP-3226, a Y1 receptor selective antagonist, we examined this hypothesis in the isolated and perfused mesenteric vascular bed. SNS produced a frequency-dependent increase in perfusion pressure and concomitant overflow of NPY immunoreactivity in the perfusate. [Leu31,Pro34]NPY potentiated NE-induced and ATP-induced vasoconstriction, indicating the presence and biological action of Y1 receptors in this vascular bed. The potentiation effect of [Leu31,Pro34]NPY of the increase in perfusion pressure by NE, ATP, or SNS was prevented by BIBP-3226. In addition, SNS-induced vasoconstriction at both high and low frequencies was significantly attenuated by BIBP-3226 at a concentration that completely blocked the [Leu31,Pro34]NPY-induced potentiation of the NE- or ATP-induced vasoconstrictor effect. These results suggest that ∼30% of vasoconstriction produced by SNS depends on NPY in the mesenteric vascular bed.

Antagonism of vasoconstriction by muscle contraction differs with alpha-adrenergic subtype

1993 ◽  
Vol 264 (3) ◽  
pp. H892-H900 ◽  
Author(s):  
L. R. Dodd ◽  
P. C. Johnson
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Second Order ◽  
Sartorius Muscle ◽  
Receptor Subtypes ◽  
Sympathetic Nerve Stimulation ◽  
Adrenergic Antagonist ◽  
Prejunctional Inhibition

It has been suggested that muscle contraction causes prejunctional inhibition of transmitter release from sympathetic nerves. In accordance with this, we found that second-order (50 microns ID) arterioles of the cat sartorius muscle dilate 40-80% more with muscle contraction during 2-, 4-, or 8-Hz sympathetic nerve stimulation than during equivalent constriction produced by intravenous norepinephrine injection. However, when constriction was to the selective alpha 1-agonist phenylephrine, the magnitude of dilation induced by muscle contraction was similar to that seen with sympathetic nerve stimulation, suggesting that prejunctional inhibition is not involved. Alternatively, different receptor subtypes may be activated by sympathetic nerve stimulation and exogenous norepinephrine. In support of this explanation, we found that approximately 50% of the vasoconstrictor effect of sympathetic nerve stimulation (8 Hz) was blocked by prazosin, an alpha 1-adrenergic antagonist, but no further diminution of tone was seen with addiction of yohimbine, an alpha 2-adrenergic antagonist. In contrast, the vasoconstrictor response to exogenous norepinephrine was not affected by prazosin, while addition of yohimbine almost completely blocked the response. These findings suggest that muscle contraction selectively attenuates vasoconstriction mediated by junctional receptors in second-order arterioles.

Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs

1978 ◽  
Vol 235 (6) ◽  
pp. H803-H808
Author(s):  
E. Y. Tong ◽  
A. A. Mathe ◽  
P. W. Tisher
Keyword(s):  
Electrical Stimulation ◽  
Pulmonary Artery ◽  
Monoamine Oxidase ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Systemic Circulation ◽  
Inhibitory Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Mao Inhibitor

Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.

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