Atrial Natriuretic Peptide Group Research Articles

Risk of radiocontrast nephropathy in patients with and without diabetes mellitus

The present study was designed to test whether altered renovascular reactivity is associated with the increased risk of radio-contrast nephropathy (RCN) in diabetics. We studied 50 patients (24 diabetics, 26 nondiabetics) with chronic renal insufficiency undergoing cardiac catheterization. Patients were randomized to receive either saline, or one of three renal vasodilator/diuretic drugs--dopamine, atrial natriuretic peptide (ANP), or mannitol--by intravenous infusion during cardiac catheterization. Renal blood flow (RBF) was measured by thermodilution at various time points during cardiac catheterization. RCN was defined as an increase in PCr of at least 25% over baseline within 48 hours of cardiac catheterization. Baseline PCr and creatinine clearance were similar in diabetics and nondiabetics (2.6 +/- 0.2 mg/dl vs. 2.4 +/- 0.1 mg/dl, and 32 +/- 3 ml/min vs. 34 +/- 3 ml/min, respectively), but baseline RBF was significantly lower in diabetics (154 +/- 21 ml/min/kidney vs. 277 +/- 36 ml/min/kidney, P < 0.05). Diabetic patients exposed to the three vasodilator/diuretic drugs had the greatest increase in RBF throughout cardiac catheterization. The incidence of RCN among the diabetics receiving those drugs was 83%, 83% and 75%, in the dopamine, ANP and mannitol groups, respectively. In contrast, among the nondiabetics in each of those groups the incidence of RCN was zero (all P < 0.05, diabetics vs. nondiabetics). In the saline control group the rates of RCN in the diabetics and nondiabetics were 43% and 38%, respectively (NS). In conclusion, the increased risk of RCN among diabetics was associated with exaggerated renovascular reactivity: baseline vasoconstriction and enhanced vasodilation with vasodilator/diuretic drugs. These same drugs, however, reduced the risk of RCN in nondiabetic patients.

The interaction between atrial natriuretic peptide and cardiac parasympathetic function

We have demonstrated previously that atrial natriuretic peptide (ANP) inhibits hypotension-induced reflex tachycardia via a parasympathetic mechanism. The present study further defines that parasympathetic mechanism. We tested the hypothesis that ANP, during vagus nerve stimulation, acts as a physiological antagonist to interfere with α 1-adrenoceptor modulation of efferent cardiac vagal action. Sprague Dawley rats were divided into five groups, each group receiving a different infusion. Infusates included one of vehicle (Ringer's solution; RS), an α 1-adrenoceptor agonist (phenylephrine; PE), a combination of agonist and either a known α 1-adrenoceptor antagonist (prazosin; PE + PRZ) or the putative physiologic antagonist, ANP (PE + ANP). The fifth group received all three drugs, PE + PRZ + ANP. Under Inactin anesthesia (100 mg/kg i.p.), efferent autonomic input to the heart was surgically interrupted. Animals were also adrenalectomized to limit the effects of circulating catecholamines. We then monitored each group for the change in heart rate (ΔHR) in response to efferent vagus nerve stimulation at various frequencies (2 Hz, 5 Hz, 10 Hz). Infusion of PE significantly ( P < 0.01 by ANOVA) attenuated the magnitude of ΔHR when compared to the RS group. This attenuation of vagally-induced bradycardia was eliminated by the addition of the α 1-adrenoceptor antagonist, prazosin (PE + PRZ group). The PE + ANP group responded with results similar to those of the PE + PRZ group. There was no difference between ΔHR responses of the PE + PRZ + ANP group and the PE + PRZ group. The results show that, in a setting of experimentally manipulated autonomic input to the heart, ANP produces a response to vagus nerve stimulation that is equivalent to that seen with the α 1-adrenoceptor antagonist prazosin. Furthermore, in the presence of prazosin, ANP had no additional chronotropic effects. These results are consistent with our hypothesis that ANP influences parasympathetic control of heart rate by modifying the consequences of α 1-adrenergic receptor activation.

Effects of atrial natriuretic peptide on glomerular filtration rate in essential hypertension: a radionuclide study

A number of studies show that atrial natriuretic peptide (ANP) raises renal sodium excretion with a concomitant increase in glomerular filtration rate (GFR) in both experimental animals and normal humans. Studies using indirect evaluation of GFR have provided less consistent results in hypertensive patients. We studied the effects of intravenously administered (iv) alpha-human ANP on GFR in patients with hypertension by a radionuclide technique using technetium 99m diethylenetriaminepenta-acetic acid. In six patients (ANP group), GFR was determined under control conditions, during iv ANP (initial bolus of 0.5 micrograms/kg followed by a 21-min maintenance infusion at 0.05 micrograms.kg-1.min-1) and during a recovery phase. In six other patients (control group), GFR was determined under control conditions, during saline iv infusion and during recovery. The two groups did not differ with respect to age, sex, basal blood pressure, heart rate or GFR. In the ANP group, the infusion of the peptide induced a significant decrease of mean blood pressure (from 133 +/- 5 to 120 +/- 5 mmHg, P less than 0.01), no change in heart rate and a significant increase in GFR (from 104 +/- 4 to 125 +/- 5 ml/min, P less than 0.01). During recovery, blood pressure, heart rate and GFR were not different from the values recorded under control conditions. No changes in blood pressure, heart rate or GFR (from 106 +/- 5 to 108 +/- 5 ml/min, n.s.) were detected during saline infusion in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Peptide in Habitual Snorers

We studied nocturnal and early morning variations in the concentration of plasma atrial natriuretic peptide (ANP) in 17 men who habitually snored. The subjects had a mean age of 51.0 +/- 5.8 years, range 41-62 y with a mean body mass index (BMI) of 32.9 +/- 7.3 kg/m2. The concentration of plasma ANP was measured by radioimmunoassay of venous samples at 10 p.m., midnight, 6 p.m. and 8 p.m. All night sleep recordings were conducted with the static charge sensitive bed to monitor body and breathing movements and a BIOX III Pulse Oximeter for the blood oxygen saturation level. Nine patients were defined as having the obstructive sleep apnea syndrome (OSAS). No significant diurnal variation for ANP concentrations was detected. At 8 a.m. five OSAS patients and two others had ANP concentrations above normal (70 pg/ml). Neither mean oxygen saturation during the night nor arterial hypertension discriminated between the high and low ANP groups at 8 a.m. The best discriminators for a high concentration of ANP at 8 p.m. were marked obesity (BMI greater than or equal to 30 kg/m2), over 400 movements lasting less than five seconds, and over 30% of active sleep per night. In a multivariate regression analysis age, percentage of active sleep during the night, BMI and the median oxygen saturation level during the night explained 76.4% of the total variance of ANP at 8 a.m. In a similar analysis the median oxygen saturation level during the night and BMI both explained the variance of ANP significantly. The whole model explained 53.7% of the variance of the ANP concentrations at 6 a.m.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of synthetic ANP on renal and loop of Henle functions in the young rat

The present studies were undertaken to determine, by recollection micropuncture, the effect of a synthetic atrial natriuretic peptide (ANP) on the absolute and fractional deliveries of water and sodium to the juxtamedullary end-descending limb. Two groups of young female Munich-Wistar rats were studied: control (n = 8) received the vehicle only; and ANP (n = 12) received a prime followed by the constant infusion of a synthetic rat atrial peptide (28 amino acids). With the infusion of ANP, clearance of p-[14C]aminohippurate [( 14C]PAH) and glomerular filtration rate (GFR) fell significantly. Despite this fall in GFR and renal plasma flow, ANP produced a 2-fold increase in urine volume and a 10-fold increase in sodium excretion. Absolute and fractional sodium deliveries to the end-descending limb increased by approximately 30% in the ANP group, whereas mean juxtamedullary single-nephron glomerular filtration rate (SNGFR) remained stable. In three additional rats prepared for micropuncture of the superficial end-accessible proximal tubule, ANP reduced cortical SNGFR by approximately 15%. By contrast, GFR did not decline in response to ANP in larger rats, when treated identically. We conclude that in young rats ANP can produce a natriuresis in the absence of a rise in GFR; the fall in GFR observed following ANP is due presumably to the immaturity of the animals used in these studies; and ANP produces a rise in absolute and fractional water and sodium deliveries to the end-descending limb that cannot be attributed to a change in SNGFR.(ABSTRACT TRUNCATED AT 250 WORDS)