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S A Atlas

Publications and source records attributed to S A Atlas.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1987

Altered renin and aldosterone excretion in patients treated for metastatic germ cell tumours.

Twenty-four patients with metastatic germ cell tumours were studied for abnormalities in the renin-aldosterone axis and for persistent abnormalities of renal function 9+ to 54+ months following completion of cisplatin based chemotherapy. Increased plasma renin activity and aldosterone were identified in fourteen of nineteen (79%) patients. The mean serum magnesium was subnormal. Statistically lower serum phosphorus levels, and higher urea and creatinine levels were also observed. No patients was hypertensive or on diuretics at the time of study. Since vascular toxicity has been reported after cisplatin based chemotherapy and hypomagnesaemia and increased plasma renin activity have been linked to cardiovascular events, these data imply that germ cell tumour patients treated with cisplatin based chemotherapy should be carefully observed for delayed cardiovascular toxicity.

Aldosterone↗
PubMed1987

The cat: an animal model for studies of inactive renin.

Inactive renin, prorenin, is found in high concentrations in human plasma. We report herein the characteristics of trypsin-activated inactive renin from cat kidney and plasma. Cat and human plasma inactive renin were activated by similar concentrations of trypsin. As in humans, there was more inactive than active renin in cat plasma; also, inactive renin was low but detectable after nephrectomy. Trypsin-activated renal inactive renin, purified on Cibacron blue agarose and pepstatin-amino-hexyl-Sepharose chromatography, was inhibited by pepstatin and by a renin inhibitor similarly to cat and human active renins. The pH optimum of cat renin was biphasic: the higher peak of active renin was at pH 5.7, whereas that of activated inactive renin was at pH 7.5. As in humans, active and inactive plasma renin increased during sodium depletion and inactive renin increased during beta-adrenergic blockade, while active renin decreased. These results demonstrate that cat inactive renin is similar to human prorenin. Therefore, the cat may be a useful model for the study of prorenin.

Adrenergic beta-Antagonists↗
PubMed1987

Relationship of increased plasma atrial natriuretic factor and renal sodium handling during immersion-induced central hypervolemia in normal humans.

Although maneuvers augmenting atrial volume and/or stretch also augment plasma levels of atrial natriuretic factor (ANF), the role of ANF in modulating renal sodium and water handling has not been defined. Water immersion to the neck (NI) was employed to assess the ANF response to acute volume expansion in 13 seated sodium-replete normal subjects. ANF increased promptly and markedly from 7.8 +/- 1.8 to 19.4 +/- 3.8 fmol/ml, then declined to 6.3 +/- 1.4 fmol/ml after 60 min recovery. Concomitantly, NI increased urine flow rate (V) (2.0 +/- 0.6 to 7.0 +/- 0.9 ml/min; P less than 0.001) and sodium excretion (UNaV) (92 +/- 12 to 191 +/- 15 mu eq/min; P less than 0.001), and decreased PRA (-66 +/- 3%) and plasma aldosterone (-57 +/- 6%). Increases of plasma ANF ranged from less than 20% to over 12-fold. Similarly, the natriuretic response to NI varied markedly from none to 500%. There was a strong correlation between peak ANF and peak UNaV (r = 0.67; P less than 0.025), but none between peak V and peak plasma ANF (r = -0.10; P greater than 0.5). These findings suggest that an increase in plasma ANF contributes to the natriuretic response to NI, implying a physiological role for ANF in modulating volume homeostasis in humans.

Adult↗
PubMed1987

Elevated levels of plasma prorenin (inactive renin) in diabetic and nondiabetic patients with autonomic dysfunction.

We measured plasma inactive renin (prorenin) levels in 46 diabetic patients, 4 nondiabetic patients with idiopathic autonomic dysfunction, and 115 normal subjects. Plasma inactive renin levels were normal in the diabetic patients who had no complications (n = 6) and in those with microvascular disease (n = 8) who did not have coexistent autonomic dysfunction. Plasma inactive renin was either grossly elevated or in the upper limit of the normal range in diabetic patients with autonomic dysfunction (n = 18). No correlation was found between plasma inactive renin and glycemic control, as measured by hemoglobin A1c. High plasma inactive renin levels were also found in the 4 nondiabetic patients with idiopathic autonomic dysfunction. These data suggest that increased plasma inactive renin levels in diabetic patients are a consequence of coexistent autonomic dysfunction. This finding is consistent with other evidence that suggests autonomic regulation of the processing of prorenin to renin within the kidney.

Adult↗
PubMed1987

Ovarian prorenin.

We review here recent evidence that the ovaries synthesize and secrete prorenin and we explore the possible reasons why prorenin, and not active renin, is formed almost exclusively in this extra-renal site. Very high concentrations of prorenin are present in the human ovary in the fluid inside mature follicles. This ovarian prorenin appears to be secreted into the circulation since plasma prorenin increases in normal women for two to three days at mid-menstrual cycle, at the time of ovulation. No change in plasma active renin occurs at this time. Plasma prorenin increases much more at mid-cycle in women whose ovaries have been hyperstimulated with gonadotropins. Their mid-cycle increment in plasma prorenin (after hCG) is directly related to the number of ovarian follicles. Plasma prorenin also increases markedly (10-fold) in pregnant women within two weeks after conception, in parallel with the rise in endogenous hCG. The ovaries are the apparent source of the increase in plasma prorenin during pregnancy since no such increase occurred in a woman with ovarian failure who conceived after receiving a donor egg. These results suggest that the ovaries synthesize and secrete prorenin in response to stimulation by gonadotropic hormones. Future studies will investigate the potential role of ovarian prorenin in human reproductive function. We postulate the existence of a prorenin receptor which activates prorenin and, in consequence, activates a local renin-angiotensin system. The functioning of this system may be regulated by changes in prorenin and its receptor.

Animals↗
PubMed1987

Effects of atrial natriuretic factor on the kidney and the renin-angiotensin-aldosterone system.

ANF is a peptide hormone with peripheral and central effects on several physiologic control systems, which suggests broad involvement in the regulation of intravascular volume and cardiovascular homeostasis. ANF acts directly on the kidney to modulate renal vascular resistance, increase glomerular filtration rate, and decrease inner medullary hypertonicity. These hemodynamic effects act in concert to promote marked natriuresis and diuresis and to inhibit renin secretion by the kidney; the potential role of direct effects on tubular transport and on the juxtaglomerular cells remains to be clarified. ANF also inhibits steroidogenesis, most prominently affecting agonist-induced aldosterone biosynthesis by the adrenal cortex. ANF exerts a smooth muscle relaxant effect on isolated vessels constricted with various hormonal agonists. ANF causes especially pronounced antagonism of the adrenal and vascular actions of angiotensin II and antagonizes the latter peptide's central nervous system effects. Although complex systemic hemodynamic mechanisms are involved, ANF-induced vasorelaxation may contribute to its depressor action, particularly in states characterized by angiotensin II-induced vasoconstriction. Distention of the atria is a major stimulus to ANF release and evokes many responses that are mimicked by ANF infusion. Although ANF is not the sole or even dominant mediator of the responses to atrial distention, available data suggest that it plays a role in the renal and hormonal responses to intravascular volume expansion. Definitive assessment of its physiologic and pathophysiologic significance must await development of specific antagonists, but further studies on the mechanisms of action of ANF at the molecular, cellular, and systemic levels are likely to contribute significantly to our understanding of the complex process of volume regulation and cardiovascular homeostasis.

Animals↗