Biomedical subjects

S A Atlas

Publications and source records attributed to S A Atlas.

At least 19 recordsLinked to original sources

PubMed1992

Maintenance of forearm vasodilator action of atrial natriuretic factor in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Infusions of atrial natriuretic factor (ANF) are frequently associated with attenuated natriuretic and diuretic responses in patients with congestive heart failure. However, ANF infusions result in systemic vasodilation, suggesting that end organ responsiveness to ANF may not be uniformly decreased. To determine if the vasodilator effects of ANF were altered in heart failure, strain-gauge plethysmography was utilized to measure forearm blood flow responses to the intraarterial infusion of ANF using a dose range that was low enough to avoid systemic effects. In 9 control subjects, ANF infusions of 0.5, 1.0, 2.0 and 4.0 micrograms/min/100 ml forearm volume significantly increased forearm blood flow from 3.21 +/- 1.71 to 5.69 +/- 3.14, 6.20 +/- 2.57, 6.64 +/- 2.53 and 6.97 +/- 2.49 ml/min/100 ml forearm volume, respectively (all p less than 0.01). In 7 patients with heart failure, ANF infusion significantly increased forearm blood flow from 2.19 +/- 0.98 to 3.18 +/- 1.70, 3.76 +/- 2.0 and 4.42 +/- 2.80 ml/min/100 ml forearm volume for the 0.5, 1.0 and 2.0 micrograms doses, respectively (all p less than 0.05). By analysis of variance, the forearm blood flow responses pooled over all doses were not significantly different between the 2 groups. At the 2.0 micrograms dose, the peak increase in forearm blood flow in normal subjects represented a 107% increase over baseline compared with a 102% increase in patients with heart failure. In summary, these data demonstrate that intraarterial administration of ANF in patients with heart failure resulted in dose-related increases in forearm blood flow. The responses were not significantly different from normal subjects expressed both as an absolute response and as a percent increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1992

Inhibition of human renin by rat plasma. Rat angiotensinogen is a competitive inhibitor of the human renin-substrate interaction.

Human renin can cleave rat angiotensinogen, yet infusion of human renin into rats causes only a modest increase in blood pressure. We therefore investigated whether there is a factor in rat plasma which inhibits human renin activity. The addition of 20% normal rat plasma to human plasma had a slight, but not significant, inhibitory effect on the rate of angiotensin formation, while nephrectomized rat plasma, which had a seven-fold higher concentration of angiotensinogen, caused a dose dependent inhibition (20 to 70%). The rat plasma inhibitor copurified with angiotensinogen. Analysis of the kinetics of the human renin-human substrate reaction and of the human renin-rat substrate reaction revealed that the rate of angiotensin I production in the presence of both substrates could be entirely accounted for by assuming that rat and human angiotensinogens are competitive inhibitors of each other. These results show that human renin can cleave rat substrate but the reaction rate is extremely slow relative to the cleavage of human angiotensinogen. They also indicate that rat angiotensinogen is an effective competitive inhibitor of the human renin-substrate reaction. These results may be relevant to the development of renin inhibitors and to transfection studies involving heterologous renin or substrate genes.

Angiotensinogen↗

PubMed1992

Atrial natriuretic peptide synthesis in atrial tumors of transgenic mice.

Transgenic mice harboring a chimeric gene linking mouse protamine 1 5'-flanking sequence to the coding sequence of the simian virus 40 T-antigen develop spontaneous rhabdomyosarcomas of the right atria. The presence of the tumors is accompanied by dramatic elevations in plasma atrial natriuretic peptide (ANP) immunoreactivity (1,698 +/- 993 vs. 60 +/- 18 fmol/ml for controls) and hematocrit (56 +/- 8 vs. 51 +/- 2 for controls). The immunoreactive ANP (irANP) present in the tumors is similar in size to irANP found in normal mouse atria. ANP mRNA transcripts present in the tumors also appear to be very similar in overall size and 5'-termini to those produced in normal cardiac tissue. Microscopically, the tumors are composed of a disorganized array of densely packed abnormal-appearing cells. Immunocytochemistry and in situ hybridization analysis reveal considerable heterogeneity in ANP gene expression. ANP peptide and mRNA are detectable throughout the parenchyma of the tumors, but absolute levels of expression vary widely among different cells in the population. These tumors represent a potentially valuable model for the study of inappropriate ANP secretion and may provide a tissue source for the development of an ANP-producing atrial cell line.

Amino Acid Sequence↗

PubMed1992

Cardiac secretion of atrial natriuretic factor with exercise in chronic congestive heart failure patients.

We have previously reported a fivefold increase of plasma atrial natriuretic factor (ANF) in patients with congestive heart failure (CHF) compared with normal subjects. However, given the marked increase of ANF under basal conditions, the extent to which ANF secretion can further increase under physiological stress is not been clarified in CHF. We therefore evaluated ANF secretion during ergometric exercise in 11 patients with CHF, with peripheral venous ANF samples obtained at rest and peak exercise. In seven patients, simultaneous peripheral venous and right ventricular ANF samples were obtained to estimate myocardial ANF secretion. Hemodynamic characteristics of exercise included a significant increase of heart rate, mean arterial pressure, and cardiac output (all P < 0.01); reduction of systemic vascular resistance (P < 0.001); and increase of right atrial and pulmonary wedge pressures (P < 0.001). ANF was abnormally elevated at baseline (108 +/- 58 fmol/ml) yet increased further to 183 +/- 86 fmol/ml with exercise (P < 0.003). A step-up of right ventricular ANF, particularly during exercise, was consistent with active myocardial secretion, despite elevated baseline ANF levels.

Adult↗

PubMed1992

Hyperreninemia and secondary hyperaldosteronism in a patient with pheochromocytoma and von Hippel-Lindau disease.

In a 21-year-old Caucasian women with von Hippel-Lindau disease, norepinephrine-producing adrenal pheochromocytoma was identified as the underlying cause of severe hypertension. She was found to have extremely elevated levels of circulating renin and aldosterone, and she was markedly hypokalemic. Administration of captopril further enhanced renin secretion, while her blood pressure improved. The patient became normokalemic following tumor removal, and her blood pressure decreased to normal levels with reestablishment of normal circadian blood pressure rhythm. This case demonstrates that, in the absence of renovascular or malignant hypertension, pheochromocytoma can be the underlying cause for the clinical syndrome of hypertension associated with severe hypokalemia and hyperreninemic hyperaldosteronism.

Adrenal Gland Neoplasms↗

PubMed1992

In vivo left ventricular anatomy in rats with two-kidney, one clip and one-kidney, one clip renovascular hypertension.

OBJECTIVES: To evaluate differences in left ventricular structural changes related to different hemodynamic patterns. DESIGN: One-kidney, one clip (1K1C; volume-dependent hypertension) rats were two-kidney, one clip (2K1C; high-resistance hypertension) to determine whether these two types of Goldblatt rats showed different types of left ventricular adaptation. METHODS: M-mode echocardiography was used to study 28 2K1C and 19 1K1C Wistar rats 8 weeks after surgery and 55 age-matched control animals. RESULTS: Systolic blood pressure was equally high in the two models; the 1K1C rats had a larger left ventricular chamber and normal plasma renin activity (PRA), whereas in the 2K1C rats PRA was increased and the left ventricular chamber was normal. The atrial natriuretic factor was significantly increased only in the 2K1C rats and was related to PRA. The left ventricular mass index was increased in both models, but more in the 1K1C than the 2K1C rats. CONCLUSIONS: In both models the degree of left ventricular hypertrophy was associated with the interacting effects of the hemodynamic component superimposed on the primary hemodynamic pattern (i.e. blood pressure as an expression of pressure overload in the primarily volume-dependent 1K1C rats and the left ventricular chamber size as an expression of volume overload in the high-resistance 2K1C rats). The interaction between pressure and volume increased the left ventricular wall thickness in both models, with additional chamber enlargement in the 1K1C rats. In these rats, the increase in left ventricular mass was more pronounced due to the greater volume load on the heart.

Adaptation, Physiological↗

PubMed1991

Exercise-induced secretion of atrial natriuretic factor and its relation to hemodynamic and sympathetic stimulation in untreated essential hypertension.

This study evaluates the release of atrial natriuretic factor (ANF) during maximal exercise in 7 patients with untreated moderate to severe hypertension with invasive monitoring of hemodynamic characteristics in relation to sympathetic activity. Peripheral venous ANF (fmol/ml) was determined at rest and maximal exercise producing a respiratory exchange ratio of 1.14 +/- 0.10. In 5 of 7 patients, simultaneous right ventricular and peripheral venous ANF samples could be obtained to assess exercise myocardial secretion of ANF. With exercise, mean blood pressure increased from 150 +/- 26 to 192 +/- 29 mm Hg (p less than 0.001), pulmonary wedge pressure increased from 7 +/- 3 to 18 +/- 10 mm Hg (p less than 0.05) and ANF increased from 11.7 +/- 8.2 to 25.7 +/- 15.9 (p less than 0.02). This ANF response correlated weakly with pulmonary wedge pressure (r = 0.497, p = not significant), since patients without an increase in pulmonary wedge pressure had no increase in ANF. However, changes in pulmonary wedge pressure and plasma norepinephrine during exercise were inversely correlated (r = -0.811, p less than 0.02), with the greatest increase in norepinephrine occurring with a minimal increase in pulmonary wedge pressure. Similarly, ANF and plasma norepinephrine were inversely correlated during exercise (r = -0.869, p less than 0.05). A significant increase in right ventricular ANF indicated myocardial secretion. Plasma ANF therefore increased because of active myocardial production during exercise in patients with moderate to severe hypertension. These findings further suggest a directionally opposing relation between ANF release resulting from increased atrial tension and sympathetic nervous system influence on cardiac performance during exercise.

Adult↗

PubMed1990

Diurnal and postural variations in plasma atrial natriuretic factor, plasma guanosine 3':5'-cyclic monophosphate and sodium excretion.

1. We studied diurnal patterns of plasma atrial natriuretic factor, plasma guanosine 3':5'-cyclic monophosphate and urinary sodium excretion in normal subjects after 3 days on a 200 mmol of sodium/60 mmol of potassium diet. On the fourth day blood samples and urine were collected every 3 h. 2. Two studies were performed. In study 1, normal subjects (n = 8) were recumbent for 23 h from 09.00 hours to 08.00 hours the next day. In study 2, normal subjects (n = 10) were permitted to ambulate from 09.00 hours to 23.00 hours and then were recumbent until 08.00 hours the next day. 3. In study 1, assumption of the recumbent posture was associated with increases in plasma atrial natriuretic factor (P less than 0.01), plasma guanosine 3':5'-cyclic monophosphate (P less than 0.05) and urinary sodium excretion (P less than 0.05). 4. In contrast, in study 2 there were no significant changes in plasma atrial natriuretic factor during the day; instead, plasma atrial natriuretic factor increased overnight, reaching a peak at 24.00 hours after 1 h of recumbency (P less than 0.01). A smaller rise in plasma guanosine 3':5'-cyclic monophosphate (P less than 0.05) occurred; urinary sodium excretion decreased markedly (P less than 0.01) and there was no change in creatinine clearance. 5. In both studies, recumbency was associated with an initial drop, followed by a rise, in packed cell volume. 6. These data demonstrate that assumption of the supine position induces a rise in plasma atrial natriuretic factor and accounts for most of the observed variation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Relation of blood viscosity to demographic and physiologic variables and to cardiovascular risk factors in apparently normal adults.

Although increased blood viscosity occurs in several cardiovascular diseases, little is known of factors influencing blood rheology in normal adults. Accordingly, we examined the relations of whole blood viscosity (WBV) to its rheologic determinants (hematocrit level, plasma viscosity, protein concentration, and red cell aggregability and rigidity), to demographic and laboratory variables, and to cardiovascular risk factors in 128 normotensive employed adults. Hematocrit levels accounted for 67-84% of variability of WBV at shear rates from 208 to 0.1 sec-1 with lesser contributions from plasma viscosity, red cell aggregability, and rigidity (multiple r = 0.95-0.97); WBV was predicted accurately from standard measurements of hematocrit and total plasma protein levels (multiple r = 0.78-0.92 in "learning" and "test" analysis). Male sex, obesity, dietary Na+ intake, and increasing age had additive effects on WBV (multiple r greater than or equal to 0.59, p less than 0.00001); the last three of these factors and black race independently predicted plasma viscosity (multiple r = 0.36, p less than 0.001). Among regulators of plasma volume, plasma renin activity and urinary Na+ excretion bore independent positive relations to WBV. Diastolic and mean blood pressures were independent predictors of WBV and hematocrit levels (all p less than 0.05). Conventional risk factors (e.g., triglycerides, obesity, and cholesterol levels) were positively related to WBV or plasma viscosity. Thus, in apparently normal adults, 1) WBV or plasma viscosity are increased by male sex, obesity, high sodium intake, aging, and black race, 2) WBV is positively related to plasma renin activity, 3) WBV or plasma viscosity are related to diastolic and mean blood pressures, triglycerides and cholesterol concentrations, and 4) WBV can be predicted from simple measurements of hematocrit and total plasma protein levels.

Adult↗

PubMed1990

Angiotensin II-induced atrial natriuretic factor release in dogs is not related to hemodynamic responses.

Angiotensin II (Ang II) and atrial natriuretic factor (ANF) appear to act as functional antagonists in the regulation of fluid and electrolyte homeostasis and blood pressure. To further define the relations between these hormones in vivo, we investigated the effect of low doses of Ang II (1-10 ng/kg/min) on plasma ANF levels. We also evaluated the influence of ANF release on the renal and hormonal responses to ANG II. Studies were performed in anesthetized and conscious instrumented dogs during sustained saline load and converting enzyme inhibition. In the anesthetized dogs, Ang II significantly increased plasma ANF levels and ANF arteriovenous difference without changing either atrial pressures or hematocrit. In both conscious and anesthetized dogs, ANF increases were not correlated with blood pressure responses to Ang II and did not occur in control groups when Ang II was replaced by vehicle. Ang II-induced sodium retention and stimulation of aldosterone production were attenuated, and renin suppression was enhanced in dogs having the largest changes in plasma ANF in response to converting enzyme inhibition or Ang II. These results demonstrate that in volume-replete dogs Ang II can promote ANF release independently of changes in atrial pressures or systemic hemodynamics, suggesting that Ang II may exert a significant modulatory effect on ANF secretion. The results also show significant relations between ANF and renal and adrenal responses to Ang II, which may suggest that, in turn, endogenous ANF modulates the effects of Ang II.

Adrenal Glands↗

PubMed1990

[Hormonal control of the endocrine function of the heart].

Previous studies demonstrate that high doses of angiotensin II (Ang II) increase the release of ANF from atrial cells but it is not known whether this is a direct effect of Ang II or due to the induced hemodynamic changes. We report the effects of low doses of Ang II (1, 2.5, 5, 10 ng/kg/min) in anesthetized, instrumented dogs after volume load (2.5% body weight) and converting enzyme inhibition. During Ang II infusion we found an increase in mean blood pressure (from 147 +/- 3 to 160 +/- 3 mmHg, p less than 0.05) and arterial ANF (from 32 +/- 6 to 80 +/- 23 fmol/ml, p less than 0.05), while left and right atrial pressures did not change significantly. In a second group of dogs (n = 4) that underwent a similar protocol with the infusion of vehicle alone we failed to find any statistical difference in the above mentioned parameters. The Ang II induced ANF release was not related to the hemodynamic changes. Changes in plasma ANF levels were, in turn, related to the effects of Ang II on hormones and kidney, thus suggesting a role for endogenous ANF. In a separate study we found an increase of ANF production (+129 +/- 18, +176 +/- 46, +210 +/- 66% basal value) from isolated atrial minces exposed to Ang II concentration of 1, 10, and 100 nM, respectively.

Aldosterone↗

PubMed1989

Relationship of atrial natriuretic factor to left ventricular volume and mass.

Although atrial natriuretic factor is primarily of atrial origin, recent observations indicate that the hormone is also synthesized by hypertrophied left ventricular myocardium. To assess the separate influences of left ventricular and left atrial dilatation and left ventricular hypertrophy on human atrial natriuretic factor levels, left atrial dimension and volume and left ventricular dimension and mass were compared in 49 normal subjects, in 33 patients with chronic aortic regurgitation, and in 15 patients with chronic mitral regurgitation. When compared with normal subjects, patients with chronic aortic and mitral regurgitation had similarly dilated and hypertrophied left ventricles (p less than 0.0005), while only mitral regurgitation patients had significantly enlarged (p less than 0.0005) mean left atrial dimension and volume. Likewise, plasma atrial natriuretic factor was elevated among patients with mitral regurgitation (60.3 +/- 47.0 fmol/ml) but was normal in patients with aortic regurgitation (19.0 +/- 11.0 fmol/ml versus 12.4 +/- 5.2 fmol/ml in normals; both p less than 0.0005 versus mitral regurgitation). Among all 97 subjects, atrial natriuretic factor levels correlated more closely with left atrial dimension and volume (r = 0.62 and 0.64, p less than 0.0005) than with left ventricular dimension (r = 0.44, p less than 0.0005) or mass (r = 0.40, p less than 0.0005). In addition, multivariate analysis indicated that left atrial volume bore a stronger independent relationship to plasma atrial natriuretic factor levels than either age or left ventricular variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗

PubMed1989

Atrial natriuretic factor in normal and hypertensive pregnancy.

Atrial natriuretic factor may play a role in the regulation of blood pressure, renal function, and volume homeostasis in normal and pathologic states. Atrial natriuretic factor and plasma renin activity were measured by radioimmunoassay in pregnant women with normal blood pressure (n = 29), chronic hypertension (n = 17), and preeclampsia (n = 18) during the first, second, and third trimesters and in the postpartum period. Serial data were obtained in 11 patients. Nonpregnant age-matched women were used as controls (n = 14). In normal gestation and in chronic hypertension, atrial natriuretic factor levels were in the same range as that in the control group. Mean atrial natriuretic factor was significantly higher in the antepartum and postpartum periods in severe preeclampsia. There was an inverse relationship between atrial natriuretic factor and plasma renin activity in pregnancies complicated by chronic hypertension or preeclampsia. Although fluctuations in atrial natriuretic factor levels did not predict preeclampsia, atrial natriuretic factor did correlate with the severity of the disease.

Atrial Natriuretic Factor↗

PubMed1989

Plasma atrial natriuretic factor in essential hypertension: relation to cardiac size, function and systemic hemodynamics.

To evaluate determinants of elevated plasma atrial natriuretic factor levels in patients with hypertension, immunoreactive plasma atrial natriuretic factor in 54 normal subjects and 40 untreated hypertensive patients was compared with echocardiographic measurements of cardiac size, function and systemic hemodynamics. In normal subjects, plasma atrial natriuretic factor was related to age, systolic blood pressure and left atrial and ventricular chamber sizes, but only age and ventricular size were independent predictors. In untreated hypertensive patients, atrial natriuretic factor was directly related to age, atrial size, systolic pressure, peripheral resistance and ventricular systolic performance; age, atrial size and peripheral resistance were independent predictors. Eight patients with elevated atrial natriuretic factor values (greater than 25 fmol/ml) were significantly (p less than 0.01) older and had greater atrial and ventricular size and higher systolic pressure and function than normal subjects or patients with normal natriuretic factor levels. Plasma atrial natriuretic factor was inversely related to peak diastolic filling rate in normal subjects (r = -0.59; p less than 0.001), whereas it was positively related to the proportional contribution of atrial systole to left ventricular filling in hypertensive patients (r = 0.77; p less than 0.001). These findings suggest that in normal subjects, impairment of ventricular relaxation with age may contribute to atrial natriuretic factor secretion by increasing left atrial afterload; the correlation with left ventricular size may reflect physiologic fluctuations in plasma volume. In patients with uncomplicated hypertension, left atrial enlargement and consequent stronger atrial contraction contributed to increased atrial natriuretic factor release, whereas no independent relation existed with left ventricular hypertrophy or systolic function. Because ventricular relaxation was normal and ventricular size and systolic performance were increased in hypertensive patients with high atrial natriuretic factor levels, the observed increase in left atrial size and atrial contribution to ventricular filling might reflect a primary increase in venous return in this subset of hypertensive patients.

Adult↗

PubMed1989

Increased plasma atrial natriuretic factor and reduced plasma renin in patients with poorly controlled diabetes mellitus.

1. To investigate atrial natriuretic factor (ANF) and its relationship to the renin system in diabetes, we measured plasma immunoreactive ANF and plasma renin activity (PRA) in 27 non-ketotic diabetic patients without evidence of cardiac or overt renal disease, and compared them with 26 age- and sex-matched normal subjects. 2. Diabetic patients were divided prospectively into poor (PGC, n = 14) or moderate (MGC, n = 13) glycaemic control depending on their concurrent plasma glycohaemoglobin (HbA1) levels (greater than 9% or less than 9%, respectively). Plasma ANF was elevated in PGC diabetic patients (15.7 +/- 1.8 fmol/ml, mean +/- SEM) compared with MGC diabetics (9.9 +/- 0.8 fmol/ml, P less than 0.001) and normal subjects (10.1 +/- 1.3 fmol/ml, P less than 0.05). 3. In contrast, PRA was lower in the PGC diabetic patients (1.3 +/- 0.3 pmol of angiotensin 1 h-1 ml-1) compared with the other groups (2.5 +/- 0.5 and 2.1 +/- 0.2 pmol of angiotensin I h-1 ml-1, P less than 0.05). Diabetic groups had proportionally more patients with high prorenin values (over 30 ng h-1 ml-1) than the normal group, but there was no difference between the diabetic groups. 4. Among the diabetic patients, ANF was directly related to HbA1 (r = 0.49, P less than 0.005) and urinary albumin excretion (r = 0.40, P less than 0.02), and was inversely related to PRA (r = 0.36, P less than 0.04) and plasma creatinine (r = -0.42, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗

PubMed1988

Renal responses to atrial natriuretic factor in patients with congestive heart failure.

It is now recognised after many years of speculation regarding the role of mammalian atria in the direct regulation of intravascular volume, that atrial myocites produce a peptide hormone that results in natriuresis and diuresis, under the condition of atrial distention. This atrial natriuretic factor (ANF) is secreted in normal subjects and is increased in patients with congestive heart failure. Atrial natriuretic factor may be administered exogenously and the results of studies performed by our group indicate that natriuresis and diuresis are induced in normal subjects but not in patients with congestive heart failure. These findings, when taken together, suggest that ANF is increased in heart failure patients in response to the atrial distention associated with ventricular dysfunction and intrinsic renal insufficiency. The mechanism for the blunted renal response to atrial natriuretic factor in heart failure patients requires further clarification.

Atrial Natriuretic Factor↗

PubMed1988

Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.

The effects of endogenous activation of sympathetic nervous system on systemic and regional hemodynamics and on plasma levels of atrial natriuretic factor (ANF) were studied in subjects with essential hypertension. Stimulation of sympathetic nervous system was reflex-induced by a selective deactivation of carotid baroreceptors obtained by increasing external neck-tissue pressure (NTP) by means of a neck chamber. The effects of graded levels (+30, +45, and +60 mm Hg) and one single and sustained level (+45 mm Hg for 15 min) of NTP were studied. As expected, NTP caused reflex increases in blood pressure, heart rate, and forearm vascular resistance, whereas atrial pressures did not change significantly and cardiac output tended to increase. In the studies based on graded levels of NTP, immunoreactive ANF (irANF) progressively fell (from 31.7 +/- 10 to 13.3 +/- 4 fmol/ml; p less than .05) and the changes in irANF were significantly correlated with those observed in FVR (r = -.671, p less than .001). Both hemodynamic and irANF changes were prevented by adrenergic blockade (phentolamine + propranolol). During +45 mm Hg NTP for 15 min, the levels of irANF fell both in the pulmonary artery and in the inferior vena cava. The irANF arteriovenous difference also fell during this maneuver. These data show that, in hypertensive patients, factors other than atrial wall tension may influence ANF release. They also show that endogenous sympathetic activation may reduce ANF release.

Atrial Natriuretic Factor↗

PubMed1988

Atrial natriuretic hormone: a regulator of blood pressure and volume homeostasis.

An explosion of research over the last seven years has led to the discovery and characterization of a peptide, originating in the heart's atria, that possesses impressive vasorelaxant and natriuretic properties. Although the several atrial peptides that have been isolated by researchers working in different laboratories vary in length, all contain the same core sequence. Cardionatrin I, a 28-amino acid peptide, is the likely active circulating hormone. In the atrial peptide's action on vascular smooth muscle, it appears especially to counter the effects of angiotensin II. The peptide's effects on renal hemodynamics and sodium excretion include a marked increase in glomerular filtration rate. Atrial hormone also induces impressive natriuresis in experimental animals, for which an increase in glomerular filtration rate may be a necessary component. Atrial hormone has been found to reduce arterial blood pressure in both animals and humans. In experimental animals, the peptide appears to lower blood pressure by different mechanisms in high- and low-renin forms of hypertension, and to lower pressure to a greater degree and with lower doses in the former as compared with the latter. In patients with essential hypertension, primary aldosteronism, congestive heart failure, renal failure, and perhaps ascitic cirrhosis, plasma ANH levels tend to be higher than they are in normotensive individuals. Atrial hormone causes marked and sustained suppression of renal renin secretion and, thus, of plasma renin levels. In addition, atrial hormone blocks aldosterone secretion and opposes the vasoconstrictive effects of angiotensin II and the sodium-retaining action of aldosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗