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Biomedical subjects

K Stepniakowski

Publications and source records attributed to K Stepniakowski.

At least 19 recordsLinked to original sources
PubMed1995

Additive effects of obesity and hypertension to limit venous volume.

The presence of reduced venous distensibility in obesity might have important hemodynamic effects and could indirectly implicate a role for metabolic factors in vascular control, because loading conditions are different in arterial and in venous vessels. Forearm blood flow and venous volume were measured plethysmographically in 58 subjects, including lean and obese hypertensives and normotensives. Venous volume at 30 mmHg (VV30) was decreased by both obesity and hypertension. This coincided with evidence for better preservation of central blood and stroke volumes with upright posture in obese than in lean subjects. Furthermore, obese hypertensives had lower VV30 than either lean hypertensives or obese normotensives. Postischemic forearm vascular resistance, a surrogate marker for structural luminal cross-sectional area, percent body fat, and fasting insulin each correlated independently with VV30 (P < 0.05) in multivariate analysis. Because nonesterified fatty acid levels are elevated in obese hypertensives and may have potent vascular effects, dorsal hand vein responses to coinfusion of Intralipid 10% and heparin to raise fatty acids locally were obtained in normal volunteers. The local infusion of Intralipid with heparin reduced hand vein distensibility, whereas dextrose and heparin did not (11 +/- 3% vs. 0 +/- 2%, respectively, P < 0.01). This study indicates that obesity and mild hypertension each reduce venous distensibility and that the coexistence of both conditions produces an even greater impairment in venous capacitance. The reduced venous distensibility in obesity appears to reflect structural as well as functional factors and to have systemic hemodynamic effects.

Adult↗
PubMed1995

Relationships among plasma aldosterone, high-density lipoprotein cholesterol, and insulin in humans.

To investigate the pathogenesis of hypertension in patients with obesity and insulin resistance and to explore the role of plasma lipids, we studied 30 subjects at the end of 7 days of low (20 mEq/d) then high (200 mEq/d) sodium diets. Glucose and insulin tolerance tests were performed at the end of each week and blood and urine collected for measurements of plasma aldosterone, renin activity, electrolytes, insulin, and lipoproteins. There was a strong negative correlation between plasma aldosterone and high-density lipoprotein cholesterol during both diets. There were weaker positive correlations between plasma aldosterone and insulin or triglycerides. When the aldosterone-renin ratio was the dependent variable and the correlation controlled for serum potassium, the inverse relationship with high-density lipoprotein cholesterol and the positive correlation with insulin remained, but only during the high salt diet. Subjects were divided into three groups based on high-density lipoprotein cholesterol. Subjects with the lowest high-density lipoprotein cholesterol levels showed the highest aldosterone, plasma triglycerides, body mass index, and waist-to-hip ratio. Those subjects also demonstrated the greatest resistance to insulin action on glucose and plasma unesterified fatty acids. There was a weak direct correlation between plasma aldosterone and systolic blood pressure during the high salt diet. These data suggest that high aldosterone levels may be a link between dyslipidemia, insulin resistance, and hypertension, a relationship made more evident by high salt intake.

Adult↗
PubMed1995

Glucose metabolism in abdominally obese hypertensive and normotensive subjects.

To determine whether the combination of obesity and hypertension results in additive defects in oxidative and nonoxidative glucose metabolism and the association of these changes with altered hemodynamic actions of insulin, we studied 11 abdominally obese hypertensive, 6 abdominally obese normotensive, and 7 lean normotensive nondiabetic subjects. Endogenous glucose production and glucose metabolized were calculated from a euglycemic clamp at 72 and 287 pmol insulin/m2 per minute. Glucose metabolized divided by insulin was lower at 72 pmol/m2 per minute in both obese groups than in lean normotensive subjects, at 148 +/- 14, 144 +/- 33, and 373 +/- 69 (mumol/m2 per minute)/(pmol/L), respectively (P < .01). Similar results were obtained during the higher insulin dose. Nonoxidative and oxidative glucose disposals by indirect calorimetry were lower in both abdominally obese groups (P < .05). Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Hemodynamic responses during the clamp were not significantly different among the three groups. Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Mild hypertension does not exacerbate these defects. Whereas the global impairment in glucose metabolism suggests the presence of an early defect or defects, including reduced tissue perfusion, systemic and regional hemodynamic responses to insulin were not altered. These findings do not support a direct role for insulin resistance in the pathogenesis of the hypertension associated with abdominal obesity.

Abdomen↗
PubMed1994

Central cardiovascular effects of AVP and ANP in normotensive and spontaneously hypertensive rats.

The purpose of the present study was to compare influence of central arginine vasopressin (AVP) and of atrial natriuretic peptide (ANP) on control of arterial blood pressure (MAP) and heart rate (HR) in normotensive (WKY) and spontaneously hypertensive (SHR) rats. Three series of experiments were performed on 30 WKY and 30 SHR, chronically instrumented with guide tubes in the lateral ventricle (LV) and arterial and venous catheters. MAP and HR were monitored before and after i.v. injections of either vehicle or 1, 10 and 50 ng of AVP and 25, 125 and 500 ng of ANP. Sensitivity of cardiac component of baroreflex (CCB), expressed as a slope of the regression line was determined from relationships between systolic arterial pressure (SAP) and HR period (HRp) during phenylephrine (Phe)-induced hypertension and sodium nitroprusside (SN)-induced hypotension. CCB was measured before and after administration of either vehicle, AVP, ANP, or both peptides together. Increases of MAP occurred after LV administration of 1, 10 and 50 ng of AVP in WKY and of 10 and 50 ng in SHR. ANP did not cause significant changes in MAP in both strains as compared to vehicle, but it abolished AVP-induced MAP increase in WKY and SHR. CCB was reduced in WKY and SHR after LV administration of AVP during SN-induced hypotension. In SHR but not in WKY administration of ANP, AVP and ANP + AVP decreased CCB during Phe-induced MAP elevation. The results indicate that centrally applied AVP and ANP exert differential effects on blood pressure and baroreflex control of heart rate in WKY and SHR and suggest interaction of these two peptides in blood pressure regulation at the level of central nervous system.

Animals↗
PubMed1994

Renin and aldosterone are higher and the hyperinsulinemic effect of salt restriction greater in subjects with risk factors clustering.

Separate lines of evidence suggest that abdominal obesity, insulin, and renin are independent risk factors for coronary heart disease. Since insulin levels are higher in abdominally obese subjects and may enhance renin and aldosterone production, these risk factors may not be entirely independent. Moreover, the renin-angiotensin system may contribute to insulin resistance. These observations suggest that some inconsistencies in the literature regarding the effects of salt restriction on insulin may be explained by baseline anthropometric and metabolic differences in the subjects studied. To examine these issues, 29 volunteers with a range of risk factors were studied after 1 week each on isocaloric 20 and 200 mmol/day NaCl diets. Measurements included ambulatory blood pressures, plasma renin and aldosterone, and responses to oral glucose and intravenous insulin. Subjects were divided into three groups based on a composite score reflecting the risk factor cluster associated with abdominal obesity and hyperinsulinemia. The nine subjects with the highest scores had significantly greater values for renin and aldosterone on both the high and low salt diets than the nine subjects with the lowest scores. Fasting insulin and triglycerides, the insulin response to oral glucose, and plasma aldosterone all rose significantly more with salt restriction in the high than in the low risk subjects. Plasma renin activity also tended to increase more on the low salt diet in the high risk group. Ambulatory blood pressures were greater on the low than the high salt diet only in the high risk group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Elevated blood pressures in obese young men with mild hypertension are sustained during the day and night.

The major goal of this study was to determine if the elevated blood pressures in obese men < 45 years old with mild hypertension persist outside the clinic. A secondary aim was to determine if hyperinsulinemia is associated with accentuated diurnal changes of blood pressure. To address these objectives, the clinic and ambulatory blood pressures as well as a 75-g, 2-h oral glucose tolerance test measurements were obtained from 9 lean normotensive, 9 lean hypertensive, and 22 obese hypertensive men < 45 years old. The week before study, volunteers ate an isocaloric diet with 220 mEq of NaCl/day. Obese hypertensives, subdivided by high (n = 11) and low (n = 11) insulin areas-under-the-curve (AUCs) in response to oral glucose, and lean hypertensives maintained higher ambulatory blood pressure than lean normotensives (130 +/- 3/74 +/- 1, 136 +/- 4/78 +/- 2, 132 +/- 5/77 +/- 3 v 118 +/- 4/65 +/- 2 mm Hg, respectively, P < .05). As expected, the insulin AUC during the glucose tolerance test was higher in obese hypertensives with higher insulin AUCs than in obese hypertensives with lower insulin AUCs, lean hypertensives, or lean normotensives (13.9 +/- 1.2 v 7.9 +/- 0.3, 7.2 +/- 0.7, 5.7 +/- 0.7 mU-min/dL, P < .05). Insulin AUCs were not significantly different in obese hypertensives with lower insulin levels, lean hypertensives, or lean normotensives. The diurnal increases of systolic and diastolic blood pressure as well as heart rate and pressure-rate product were similar in all four groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension.

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

Animals↗
PubMed1994

Prolonged stimulation of intrarenal V1 vasopressin receptors results in sustained hypertension.

In an earlier study, we reported that chronic intravenous administration of the V1 agonist [Phe2,Ile3,Orn8]vasopressin (V1AG) results in sustained hypertension. The present study was designed to determine whether V1-induced hypertension may be related specifically to intrarenal actions of this peptide. Chronic infusion of the V1 agonist into the medullary interstitial space of a single remaining kidney of normal, conscious Sprague-Dawley rats at the rate of 2 ng.kg-1.min-1 for 14 days resulted in a sustained rise of 18 mmHg of mean arterial pressure (MAP). After withdrawal of V1AG, MAP returned to the baseline level. During the first day of V1AG infusion, there was a net loss of body sodium and no evidence of fluid retention throughout the period of hypertension. Plasma osmolality, sodium and potassium concentration, and water intake and body weight were not significantly affected by medullary interstitial infusion of V1AG. Renal medullary interstitial infusion of an equimolar amount of arginine vasopressin (AVP) did not affect MAP. Chronic medullary interstitial infusion of the selective V1 antagonist d(CH2)5[Tyr(Me)2,Ala-NH(2)9]AVP in equimolar amounts (2.5 ng.kg-1.min-1) prevented the MAP increase elicited by intravenous V1AG. However, intravenous administration of the V1 antagonist at the same rate together with V1AG (n = 7) failed to prevent hypertension. The results indicate that hypertension can be elicited by chronic stimulation of renal medullary V1 vasopressin receptors. They also suggest that some V2 agonistic properties of AVP may restrict the hypertensive action of this hormone. The mechanism for the rise of arterial pressure remains to be determined.

Animals↗
PubMed1994

Insulin levels are similar in obese salt-sensitive and salt-resistant hypertensive subjects.

Evidence supports the hypothesis that hyperinsulinemia, especially in obesity, contributes to salt-sensitive hypertension by enhancing sodium retention and blunting the normal reduction of sympathetic drive and vascular resistance that occurs during a high versus low NaCl diet. To address these issues, we studied 18 obese (body mass index, > 27 kg/m2) subjects younger than 45 years old with mild hypertension to determine if the salt-sensitive versus salt-resistant subset had higher insulin levels, retained more volume, and failed to suppress sympathetic drive and vascular tone normally on a high (approximately 200 mEq/d) versus low (20 mEq/d) NaCl diet for 7 days each. Six obese subjects were salt sensitive, with an 8.4 +/- 2.1 (SEM) mm Hg increase of ambulatory mean blood pressure on the high versus low NaCl diet. Ten obese subjects were salt resistant, with a 7.1 +/- 0.9 mm Hg reduction of ambulatory mean blood pressure on high versus low NaCl. The salt-sensitive and salt-resistant groups had similar values, respectively, for the insulin area under the curve during an oral glucose tolerance test on low (14.6 +/- 1.8 versus 14.0 +/- 1.4 mU x min/dL, P = NS) and high (10.6 +/- 1.5 versus 10.6 +/- 1.0, P = NS) salt diets. Although insulin levels were similar, insulin raised calf blood flow in salt-resistant subjects (P < .05) but not in salt-sensitive subjects on the high NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Compensatory hyperinsulinemia and the forearm vasodilator response during an oral glucose-tolerance test in obese hypertensives.

OBJECTIVE: To determine whether obese hypertensive patients manifest a diminished regional vasodilator response to an oral glucose challenge. METHODS: Nineteen obese hypertensives (body mass index 34.1 +/- 1.3 kg/m2, blood pressure 144 +/- 3/96 +/- 2 mmHg) and 13 lean controls (23.6 +/- 0.3 kg/m2, 127 +/- 4/83 +/- 3 mmHg) were studied. After 1 week on a standard diet, forearm blood flow (plethysmography), systemic hemodynamics (impedance cardiography), glucose and insulin levels were measured at baseline and again at 15, 30, 60, 90 and 120 min during an oral glucose-tolerance test (OGTT). RESULTS: Forearm blood flow increased after the oral glucose ingestion in obese hypertensives and lean controls. The rise in forearm blood flow was greater in obese hypertensives than in lean controls during the 2-h OGTT. Insulin levels also increased more in obese patients after the glucose load. During the second hour of the OGTT the ratio of changes in forearm blood flow and insulin level, an index of vascular insulin resistance, was similar in both groups. In contrast to the regional hemodynamic findings, total systemic vascular resistance decreased in lean controls but did not change in obese hypertensives during the second hour of the OGTT. CONCLUSION: The forearm vasodilator response to oral glucose in overweight, non-diabetic hypertensives is not impaired. If dynamic increases in flow are indeed important to insulin-mediated glucose disposal, then these observations raise the possibility that the greater increase of regional blood flow during an OGTT in obese hypertensives represents a component of the compensatory response for their defect in glucose metabolism.

Adult↗
PubMed1994

Ketanserin's sympatholytic and serotonin2-receptor blocking actions precede the hypotensive effects.

The hypotensive action of ketanserin in humans remains incompletely defined but may be mediated by factors unrelated to vascular alpha 1 or serotonin2-receptor blockade. We examined the effects of ketanserin on indices of sympathetic drive, alpha 1- and serotonin2-receptor responses, and sympathetic tone in 13 elderly men with mild hypertension. Studies were performed after ten days and six weeks of double-blind assignment to placebo and ketanserin 40 mg twice daily. An eight week long single-blind, placebo washout period separated the double-blind phases. In the entire group, ketanserin lowered BP and heart rate significantly after six weeks but not at ten days. In contrast, plasma noradrenaline, an index of sympathetic drive, and platelet aggregation in response to 1 microM serotonin, an index of serotonin2-receptor antagonism, declined significantly after both ten days and six weeks (P < 0.05) on ketanserin versus placebo. Mean BP after six weeks on ketanserin fell to > 10% in seven patients (responders) and to < 10% in six subjects (nonresponders). Responders had higher baseline SBPs and heart rates compared with nonresponders. Even in responders, BP was reduced at six weeks but not after ten days on ketanserin versus placebo. Plasma and platelet noradrenaline, plasma renin activity, and platelet responses to serotonin at baseline and during ketanserin did not distinguish between responders and nonresponders. Ketanserin reduces sympathetic drive and antagonizes serotonin2-receptors in the short term. The relationship of these actions to the hypotensive effect of ketanserin, which is delayed and dependent on the initial BP, is unclear.

Double-Blind Method↗
PubMed1993

Effects of enalapril on the hyperinsulinemic response to severe salt restriction in obese young men with mild systemic hypertension.

Hypertension in obese patients is associated with hyperinsulinemia and salt sensitivity. Very low salt diets may exacerbate hyperinsulinemia, perhaps by activating the renin-angiotensin system. Therefore, the effects of a low salt diet alone and with enalapril on blood pressure and the insulin response to an oral glucose tolerance test were studied in 9 obese (body mass index 35 +/- 2 kg/m2) men with mild hypertension. Measurements were first obtained after a 2-week high-salt (20 mEq/day sodium diet+eleven 1 g salt tablets per day) baseline period. The same measurements were repeated after 2 weeks on a low salt diet (20 mEq/day) and after 2 weeks on low salt diet with enalapril in random sequence. The insulin area under the curve increased from 12.8 +/- 3.0 mU-min/dl during high salt to 16.6 +/- 3.2 mU-min/dl (p < 0.001). Plasma renin activity also increased with salt restriction from 1.4 +/- 0.2 to 3.0 +/- 0.5 ng/ml/hour, p = 0.01. With addition of enalapril to the low sodium chloride diet, the insulin area under the curve (14.5 +/- 2.6 mU-min/dl) was not significantly different from that during the high sodium chloride phase. Mean blood pressure in the laboratory was 105 +/- 1 mm Hg with high salt versus 99 +/- 1 mm Hg with low salt, p < 0.05. Addition of enalapril to the low-salt diet reduced mean blood pressure to 87 +/- 1 mm Hg (p < 0.01 vs low salt), largely by reducing total systemic resistance (p < 0.05). Salt restriction decreases laboratory BP while raising insulin levels in obese men with mild hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Increased prevalence of abnormal signal-averaged electrocardiograms in older patients who have hypertension with low diastolic blood pressure.

Greater mortality in hypertensive patients with the lowest diastolic blood pressure (DBP) values has been reported and may be partially explained by more fatal arrhythmias. The records of 135 patients were reviewed to determine whether the prevalence of an abnormal signal-averaged electrocardiogram (SAECG+), a risk marker for ventricular arrhythmias, was greater in patients who have hypertension with DBP < 85 mm Hg. SAECG+ was present in 31 (39%) of 80 patients with hypertension and 13 (24%) of 55 subjects with normotension p < 0.05. Hypertensive patients were more likely than normotensive subjects to have left ventricular hypertrophy (LVH, p = 0.01) and LV dysfunction (p < 0.01). In multivariate analysis only age and systolic dysfunction emerged as significant predictors of SAECG+. Among 68 hypertensive patients and for whom recent DBP data were available, SAECG+ was present in 18 of 37 with DBP < 85 mm Hg (group 1), 1 of 12 with DBP 85 to 94 mm Hg (group 2, p < 0.05 vs group 1), and 4 of 19 with DBP > 95 mm Hg (group 3, p < 0.05 vs group 1, p = 0.08 vs group 2). There were no significant differences between the three groups of hypertensive patients for coronary artery disease, LVH, systolic dysfunction, or left-sided cardiac chamber enlargement. Multivariate analysis in hypertensive patients indicated that age and DBP were each independently predictive of SAECG+, whereas the indexes of heart disease were not. Within group 1, those with SAECG+ were significantly older (68 +/- 1 vs 59 +/- 1 years, p < 0.01) and more likely to have LVH (p < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1993

Improved baroreflex sensitivity in elderly hypertensives on lisinopril is not explained by blood pressure reduction alone.

OBJECTIVE: The major goals of this study were to determine whether lisinopril and nifedipine lowered blood pressure and improved carotid baroreflexes in older hypertensives. DESIGN: The effects of lisinopril at 10-40 mg/day versus nifedipine gastrointestinal therapeutic system (GITS) at 30-90 mg/day on blood pressure and baroreflex sensitivity were studied after 3 weeks each on (1) single-blind placebo, (2) double-blind assignment to either lisinopril or nifedipine, (3) single-blind placebo, and (4) crossover to double-blind lisinopril or nifedipine. Measurements at the end of the four phases included 24-h blood pressure using the Accutracker, laboratory hemodynamics with the Dinamap and impedance cardiography, baroreflex sensitivity with the pneumatic neck chamber, and plasma samples for neurohumoral and metabolic activity. PATIENTS: Thirteen patients aged 55 years or older (mean +/- SEM 65 +/- 1 years) with mild-to-moderate hypertension completed the study. MAIN OUTCOME MEASURES: The primary data for analysis across the four study phases included ambulatory blood pressure values, laboratory hemodynamics, and baroreflex sensitivity. RESULTS: Compared with the preceding placebo, lisinopril and nifedipine lowered 24-h blood pressure significantly. In the laboratory, the effects of both compounds on blood pressure, cardiac output, calculated total systemic resistance, and the stroke volume-pulse pressure relationship, an index of arterial compliance, were similar. Lisinopril was associated with a relative increase in the standing systolic blood pressure compared with nifedipine (P < 0.05). This coincided with an enhanced heart-rate (R-R interval) response to neck pressure, which also decreased carotid transmural pressure, with lisinopril versus nifedipine (P < 0.05). CONCLUSIONS: Lisinopril and nifedipine were both effective as monotherapy for controlling blood pressure in these elderly patients. Despite similar effects on blood pressure and systemic hemodynamics, baroreflex sensitivity in response to a reduction in carotid transmural pressure was greater with lisinopril than with nifedipine.

Aged↗
PubMed1993

Insulin does not reduce forearm alpha-vasoreactivity in obese hypertensive or lean normotensive men.

Evidence supports the hypothesis that an impaired capacity of insulin to antagonize norepinephrine-induced vasoconstriction increases alpha-adrenergic tone in overweight young men with insulin resistance and mild hypertension. Therefore, the effects of regionally infused insulin at 100 microU/mL on forearm blood flow (milliliters per deciliter per minute) and responses to norepinephrine were measured in seven obese hypertensive and eight lean normotensive men younger than 45 years old. The obese hypertensive men were hyperinsulinemic and insulin resistant compared with the normotensive men, as evidenced by abnormal values for fasting insulin (15.5 +/- 1.6 versus 7.2 +/- 0.8 microU/mL, P < .001), the insulin area under the curve in response to a 2-hour oral glucose tolerance test (12.0 +/- 1.5 versus 6.7 +/- 1.1 mU x min/dL, P < .01), and the disappearance rate of glucose during a 15-minute insulin tolerance test (2.7 +/- 0.3 versus 4.1 +/- 0.3 mg%/min, P < .05). The logarithm of the norepinephrine EC50 was not significantly different in obese hypertensive men (mean, 95% confidence interval: -8.15, -8.42 to -7.87) versus lean normotensive men (-7.91, -8.23 to -7.59). The 2-hour regional insulin infusion at 100 microU/mL did not significantly alter the EC50 for norepinephrine in either group. Insulin at this concentration induced significant and similar increases of forearm blood flow in the hypertensive and normotensive groups (1.7 +/- 0.4 versus 1.7 +/- 0.6 mL/100 mL per minute, P = NS). At approximately 100 microU/mL, insulin does not antagonize norepinephrine-induced vasoconstriction in the forearm circulation of either obese hypertensive or lean normotensive men.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Plasma atrial natriuretic peptide (ANP) concentration in patients with pheochromocytoma.

The interaction between catecholamines (CA) and ANP is not clearly established. The effects of excess endogenous CA on ANP secretion can be investigated in patients with pheochromocytoma. We studied 27 patients with surgically and histologically proven pheochromocytoma (P) aged 19-70 years. In 16 of these patients plasma ANP study was repeated after surgical removal of the tumour. The control group (C) consisted of 20 healthy volunteers aged 21-48 years. Moreover, 42 patients with uncomplicated mild to moderate essential hypertension (EH) aged 18-48 years were also studied. In P higher plasma ANP concentration versus C, EH was found (51.9 +/- 8.1; 25.5 +/- 1.5; 19.3 +/- 1.5 fmol/ml, respectively). In 16 patients with P, increased plasma ANP level (mean 63.3 +/- 12.6 fmol/ml) declined after surgical removal of the tumour (mean 22.4 +/- 2.9 fmol/ml). In the P patients no relationship was found between plasma ANP and hormonal patterns of the tumour or between plasma ANP and plasma catecholamines, whereas significant positive correlations between plasma ANP and both systolic and diastolic blood pressure and heart rate were demonstrated. These results suggest that excess CA produced by the chromaffin tumour induce ANP secretion via stimulation of adrenergic receptors. However, influence of the haemodynamic changes evoked by CA cannot be excluded. It is suggested that increased secretion of ANP may be of some importance in maintaining blood pressure homeostasis in patients with pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1992

Effect of vasopressin and V1 receptors blockade on hypotensive action of ANP in normotensive (WKY) and spontaneously hypertensive rats.

The aim of the study was to find out whether vasopressin (AVP) modifies hypotensive and heart rate accelerating effects of atrial natriuretic peptide (ANP) in normotensive (WKY) and spontaneously hypertensive (SHR) conscious rats. The effect of i.v. administration of 1; 2 and 4 micrograms of ANP on blood pressure (MP) and heart rate (HR) was compared during i.v. infusion of 0.9% NaCl (NaCl), NaCl+AVP (1.2 ng kg-1 min-1) and NaCl+dEt2AVP (V1 receptors antagonist, 0.5 microgram kg-1 min-1). AVP increased MP in SHR and WKY and decreased HR in SHR. V1 antagonist decreased MP and increased HR only in SHR. In SHR ANP decreased MP and increased HR during NaCl, AVP and V1 antagonist infusion. In WKY these effects were observed only during AVP administration. In each experimental situation hypotension and tachycardia induced by ANP were greater in SHR than in WKY. In both strains ANP induced changes in MP and HR were enhanced during AVP in comparison to NaCl infusion. V1 antagonist did not modify effects of ANP in WKY and SHR. The results indicate that ANP abolishes hypertensive response induced by blood AVP elevation and that the basal levels of endogenous vasopressin acting through V1 receptors does not interfere with hypotensive action of ANP neither in WKY nor in SHR.

Animals↗