[Diagnostic value of serum alpha-fetoprotein, alpha-fetoprotein variant and abnormal prothrombin in primary hepatocellular carcinoma].

Objective: To explore the diagnostic value of single or combined detection of serum tumor markers alpha-fetoprotein (AFP), α-fetoprotein (AFP)-L3 and abnormal clotting (PIVKA-II) in the primary hepatic carcinoma. Methods: Serum AFP, AFP-L3 and PIVKA-II of 56 cases with primary hepatic carcinoma, 46 cases with cirrhosis, 45 cases with other liver disease and 41 healthy persons (control group) were examined by chemiluminescence method, and the differences in the levels of AFP, AFP-L3 and PIVKA-II in each group were compared. Results: Serum level of AFP, AFP-L3 and PIVKA-II in patients with primary liver cancer was significantly higher than that of the cirrhosis, other liver disease and control groups, and the difference was statistically significant (P < 0.05). The receiver operating characteristic curve analysis showed that the areas under the curve for the diagnosis of primary hepatic carcinoma by AFP, AFP-L3 and PIVKA-II were 0.887, 0.846 and 0.885, respectively. The combined use of the three tumor markers for the diagnosis of primary hepatic carcinoma increased the area under the curve to 0.899. Among the single detection, AFP had the highest sensitivity of 91.07% and PIVKA-II had the highest specificity at 88.63%. In the combined detection, AFP/PIVKA-II combination had the highest sensitivity of 94.64 %, while the AFP + AFP-L3 + PIVKA-II combination had the highest specificity at 98.48%. Conclusion: Combined detection of AFP, AFP-L3 and PIVKA-II could improve the diagnostic specificity and the sensitivity of primary hepatic carcinoma; thereby make up the deficiency of single detection and improve the early diagnosis rate.

Expression profiles of the organic acid metabolism-associated genes during rat liver regeneration.

In this study, 55 of the organic acid metabolism-involved genes were primarily confirmed to be associated with liver regeneration (LR) by bioinformatics and gene expression profiling analysis. Number of the initially and totally expressed genes occurring in initiation phase of LR, G(0)/G(1), cell proliferation, cell differentiation and liver tissue structure-function reconstruction were 21, 5, 33, 1 and 40, 20, 174, 44, respectively, illustrating that genes were initially expressed mainly in initiation stage, and worked in different phases. 151 times up-regulation and 114 times down-regulation as well as 14 types of expression patterns showed the diversification and complication of genes expression changes. It is inferred from the above gene expression changes and patterns that acetate biosynthesis enhanced at forepart, propionate biosynthesis at forepart, prophase and early metaphase, pyruvate biosynthesis at forepart, metaphase and anaphase, succinate biosynthesis at forepart and anaphase; malate biosynthesis in metaphase and N-acetylneuraminate biosynthesis at 36, 66 and 96 h. Whereas, carnitine biosynthsis attenuates at forepart and prophase, enhancement at middle metaphase; isocitrate in the forepart, quinolinate at forepart and early metaphase, creatine at early metaphase and fumarate at anaphase perform the restrained biosynthesis, respectively; catabolisms of propionate and pyruvate were depressed in metaphase.

Conversion of atrial flutter by ibutilide is associated with increased atrial cycle length variability.

OBJECTIVES: This study was designed to test the hypothesis that conversion of atrial flutter in humans by ibutilide, a new class III antiarrhythmic agent, is characterized by an increase in atrial cycle length variability. BACKGROUND: Conversion of tachyarrhythmias has been associated with increased oscillations of cycle length. METHODS: Electrograms and monophasic action potentials from the right atrium in 35 patients with spontaneous, sustained atrial flutter were recorded before, during and after intravenous ibutilide (0.005 to 0.025 mg/kg body weight, n = 25) or placebo (n = 10). Atrial cycle length, cycle length variability (coefficient of variation), diastolic interval and diastolic interval variability were measured from 10 consecutive cycles at baseline and 3 min before, 1 min before, 30 s before and immediately before conversion. Similar measurements were made in patients who received ibutilide or placebo but did not convert. RESULTS: Ibutilide converted atrial flutter in 14 of 25 patients 25 +/- 16 min (mean +/- SD) after initiation of the infusion, whereas placebo converted no patients. Atrial cycle length was prolonged to the same extent in ibutilide converters and nonconverters (36 +/- 19 vs. 38 +/- 21 ms, p = NS) and was not affected by placebo. Beat-to-beat variability in atrial cycle length (baseline 1.2 +/- 0.7 vs. preconversion 7.3 +/- 4.9, p < 0.01) and diastolic interval (baseline 11 +/- 8 vs. preconversion 33 +/- 23, p < 0.05) increased significantly just before atrial flutter conversion and remained unchanged in ibutilide nonconverters and placebo group patients. CONCLUSIONS: Ibutilide prolongs atrial cycle length, but conversion of atrial flutter by ibutilide is characterized by increased variability in atrial cycle length and diastolic interval.

Radiofrequency and cryoablation of atrial fibrillation in patients undergoing valvular operations.

BACKGROUND: Previous studies have shown that the maze operation can restore sinus rhythm and atrial transport function in patients with chronic atrial fibrillation. The purpose of this study was to test the feasibility of the application of radiofrequency and cryoablation as an alternative to the classic maze operation. METHODS: Twelve patients undergoing mitral valve procedures were included in this study. Radiofrequency and cryoablation were applied to create lesions in both atria to simulate the classic maze operation. RESULTS: There were two surgical deaths. At the mean follow-up of 10.25 months for the remaining 10 patients; 6 were in sinus rhythm, 2 in atrial rhythm, 1 in paroxysmal atrial tachycardia, and 1 in atrial fibrillation. Doppler echocardiography at 6-month follow-up showed emergence of biatrial transport function in 3 patients and right atrial contractility in 8. At 12-month follow-up of 5 patients, Doppler echocardiography showed biatrial transport function in 3 and right atrial contractility in 4. CONCLUSIONS: Our modified maze procedure during valvular operation is effective for achieving an acceptable success rate to restore sinus rhythm and atrial transport function in patients with chronic atrial fibrillation.

Impaired central mediation of the arterial baroreflex in chronic renal hypertension.

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

Abnormal baroreflex control in renal hypertension is due to abnormal baroreceptors.

We determined if baroreflex control (BC) of lumbar sympathetic nerve activity (LSNA) is preserved despite impaired control of heart rate (HR) in rabbits with 6 wk of renal hypertension (HT). Baroreflex responses were determined during transient or steady-state increases (phenylephrine, PE) or decreases (nitroglycerin or caval occlusion) in arterial pressure. Impaired BC of HR was confirmed in conscious and anesthetized HT rabbits with all baroreflexes intact. In contrast, BC of LSNA was preserved in anesthetized HT rabbits. We further determined whether this selective impairment of BC of HR but not of LSNA could be due to an abnormality in the central nervous system (CNS) or in the afferent limb of the baroreflex. With only the left aortic depressor nerve (ADN) intact (other arterial baroreceptor afferents cut), BC of both HR and LSNA in HT was significantly impaired during infusion of PE. However, responses of HR and LSNA to afferent electrical stimulation of the left ADN (all arterial baroreceptor afferents cut) were similar in HT and normotensive controls. We conclude that 1) BC of LSNA is preserved in renal HT even though control of HR is impaired; 2) selective impairment of BC of HR in HT results from an abnormality in the afferent limb of baroreflex and not in CNS; 3) this abnormality in the afferent limb is not sufficient to impair BC of LSNA when all baroreflexes are intact but is sufficient after partial arterial baroreceptor denervation.

Baroreflex regulation of hindquarter vascular resistance during acute blood volume expansion.

The baroreflex control of hindquarter vascular resistance in response to a 30% blood volume expansion (BVE) was examined in constant-flow perfused hindlimbs of chloralose-urethan-anesthetized rats. Volume expansion initially increased both systemic arterial pressure (SAP) and central venous pressure (CVP) while decreasing hindquarter vascular resistance. After these initial changes, there was a parallel return of hindquarter-vascular resistance and CVP to pre-expansion levels, suggesting that cardiopulmonary afferents play a major role in the vascular resistance adjustments to volume expansion. This notion was supported in a separate set of experiments in which CVP was elevated selectively while SAP was held constant. This manipulation elicited a decrease in hindquarter vascular resistance, which was significantly attenuated following vagal cardiopulmonary denervation. The return of hindquarter vascular resistance following BVE also occurred in the presence of elevated SAP in rats with vagotomy and aortic nerve denervation, i.e., only the carotid sinus baroreflexes intact, but the time course was much faster compared with preparations with cardiopulmonary receptors intact. No response of hindquarter vascular resistance to BVE was observed in rats with both sinoaortic and cardiopulmonary baroreceptors denervated. These findings suggest that the return of hindquarter vascular resistance following BVE involves a gradual increase in sympathetic outflow to the hindquarters resulting from both a decrease in cardiopulmonary afferent activity and a rapid adaptation of arterial baroreflexes.

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity.

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

Junctional tachycardia during radiofrequency ablation of the slow pathway in patients with AV nodal reentrant tachycardia: effects of autonomic blockade.

INTRODUCTION: The autonomic nervous system richly innervates the peri-AV nodal region and may be activated during radiofrequency (RF) ablation for AV nodal reentrant tachycardia, resulting in the generation of junctional tachycardia. The purpose of this prospective study was to determine the role of the autonomic nervous system in the genesis of junctional tachycardia. METHODS AND RESULTS: We compared the characteristics of junctional tachycardia in patients with (n = 10) and without (n = 10) autonomic blockade undergoing RF ablation for AV nodal reentrant tachycardia. Intravenous administration of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) were used to block the autonomic nervous system. There were no differences in clinical variables and baseline electrophysiologic characteristics between the two groups except for slightly longer effective refractory periods of the fast pathway and of the atrium in the autonomic blockade group. The autonomic blockade shortened the baseline sinus cycle length and effective refractory period of the ventricle only but not other electrophysiologic characteristics of the AV node. The junctional tachycardia was observed during ablation in each patient, but its occurrence and cycle length, as well as numbers of consecutive junctional beats, were not altered by the autonomic blockade. CONCLUSION: Our results indicate that the muscarinic and beta-adrenergic components of the autonomic nervous system play no role in the genesis of junctional tachycardia.

Different effects of vasopressin and angiotensin II on baroreflexes.

Our data indicate that vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity by two mechanisms: it sensitizes baroreceptors locally and shifts the stimulus-response curve so that a lower carotid sinus pressure results in a certain level of reflex sympathetic inhibition; it also produces a corresponding shift when given i.v. and excluded from baroreceptors implicating a second, central mechanism for facilitation of baroreflexes. In contrast, angiotensin II attenuates baroreflex inhibition of peripheral sympathetic function and this is accounted for totally by a central action. Why these differences occur present challenging new questions for future investigation.

Sites at which vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity.

We recently reported that intravenous vasopressin in anesthetized rabbits facilitates baroreflex inhibition of lumbar sympathetic nerve activity. The purpose of this study was to determine the possible sites of this facilitation. We found that intravenous infusion of vasopressin (16-32 mU X kg-1 X min-1) caused greater inhibition of lumbar sympathetic nerve activity than did phenylephrine for a given increase in aortic baroreceptor activity, suggesting a "central" action of vasopressin. A central action was supported also by the observation that the carotid baroreflex inhibition of lumbar sympathetic nerve activity was augmented by intravenous infusion of vasopressin when the carotid sinuses were isolated, filled with saline, and distended (aortic depressor and vagal nerves were cut). On the other hand, vasopressin also facilitated baroreflex inhibition of lumbar sympathetic nerve activity through an influence on arterial baroreceptors, because intravenous vasopressin caused greater afferent activity of the aortic depressor nerve per unit rise in arterial pressure than did phenylephrine. In a separate group of rabbits, intravenous infusion of vasopressin also elevated the level of afferent aortic depressor activity during increases in arterial pressure induced by intra-aortic balloon inflation. Furthermore, when vasopressin was confined to the isolated carotid sinuses, the reflex inhibition of lumbar sympathetic nerve activity during distension of carotid sinuses was augmented. We conclude that circulating vasopressin facilitates baroreflex inhibition of sympathetic nerve activity through a central nervous system action as well as through an effect on arterial baroreceptors.

Paroxysmal atrial tachycardia with second-degree atrioventricular block.

Paroxysmal atrial tachycardia with atrioventricular block usually indicates potentially dangerous overdigitalization, and serious heart disease is almost universally present. In this report, we describe a patient with a structurally normal heart who manifested spontaneously intra-atrial reentrant tachycardia with Wenckebach atrioventricular block in the absence of medications. In this patient, the longest atrial paced cycle length that induced atrioventricular nodal block was 390 ms, and the atrial cycle length during tachycardia ranged from 360 to 400 ms. The electrophysiologic study in our patient demonstrated that second-degree atrioventricular block during atrial tachycardia may occur in patients without structural heart diseases or taking any medication.

Differential baroreflex control of heart rate and vascular resistance in rabbits. Relative role of carotid, aortic, and cardiopulmonary baroreceptors.

We assessed the relative roles of aortic (ABR), carotid sinus (CBR), and vagal cardiopulmonary baroreceptors in the reflex control of heart rate and vascular resistance during changes in arterial blood pressure. Injections of phenylephrine (PE) and nitroglycerin (NG) were given intravenously to anesthetized rabbits (chloralose-urethane). Reflex, heart rate responses were impaired significantly by denervation (X) of either CBR or ABR. In contrast, reflex vascular responses in the hindlimb (perfused at constant blood flow) were preserved except for a slight impairment of reflex vasoconstriction after ABRX. Vagotomy with intact CBR and ABR impaired only the reflex bradycardia. After vagotomy, neither CBRX nor ABRX altered significantly the reflex heart rate or vascular responses except, again, for an impairment of reflex vasoconstriction after ABRX. Combined CBRX and ABRX eliminated all reflex responses except for a small bradycardia and a biphasic change in perfusion pressure (constrictor-dilator) during PE. Vagotomy eliminated the bradycardia and the dilator phase; the constrictor phase persisted and was abolished by lumbar sympathectomy. The results indicate that (1) reflex control of heart rate may be impaired when reflex control of hindlimb resistance is preserved; thus reflex changes in heart rate may not be used as a reliable index of the integrity of arterial baroreceptor control of the total circulation; (2) one set of arterial baroreceptors does not compensate for the absence of the other with respect to activation of vagal neurons; in contrast, one set of baroreceptors compensates fully for the absence of the other with respect to inhibition of sympathetic neurons; (3) cardiopulmonary and other baroreceptors contribute minimally to reflex responses only during large PE-induced increases in arterial pressure.

Effect of digoxin and amino sugar cardiac glycoside (ASI-222) on plasma antidiuretic hormone activity.

Digoxin acts at central neural (CNS) as well as peripheral sites after intravenous administration. In contrast, the analog, 3-beta-O(4-amino-4,6-dideoxy-beta-D-galactopyranosyl)-digitoxigenin (ASI-222), cannot cross the blood-brain barrier so it acts only at sites outside the CNS. The effects of these two agents on plasma antidiuretic hormone activity (ADH) were investigated in conscious dogs. Despite previous evidence that digoxin produces reflex decreases in sympathetic nerve activity by activating ventricular receptors with vagal afferents, no decreases in ADH were detected when either digoxin (25 and 50 micrograms/kg) or ASI-222 (38.5 micrograms/kg) were administered intravenously even with preexisting high levels of plasma ADH. In contrast, both digoxin (50 micrograms/kg) and ASI-222 (38.5 micrograms/kg) resulted in increased ADH levels, but only in association with emesis and behavioral changes suggestive of nausea. Cerebroventricular (IVT) injections of digoxin were given, starting with a dose of 0.1 microgram, that were intended to produce a comparable cerebrospinal fluid (CSF) concentration to that associated with the 50 micrograms/kg intravenous dose. Only the highest dose of digoxin, 1 micrograms, but not 0.1 and 0.3 micrograms, produced increases in ADH and emesis when given into the lateral cerebral ventricle. This is further evidence that a site accessible to blood but not to CSF was involved. These results suggest that digoxin and ASI-222 may activate pathways in the area postrema and produce increases in ADH as well as emesis.

Atrial size reduction as a predictor of the success of radiofrequency maze procedure for chronic atrial fibrillation in patients undergoing concomitant valvular surgery.

INTRODUCTION: Previous studies showed that the surgical maze procedure can restore sinus rhythm and atrial transport function in patients with chronic atrial fibrillation (AF). However, no previous studies discussed the association of atrial size reduction and the success of sinus conversion by the radiofrequency (RF) maze procedure for chronic AF. METHODS AND RESULTS: A total of 119 chronic AF patients undergoing valvular operations were included in this study. Sixty-one patients received RF and cryoablation to create lesions in both atria to simulate the surgical maze II or III procedure (RF maze II or RF maze III; 13 patients, group 1) or a modified maze pattern (RF maze "IV"; 48 patients, group 2). The other 58 patients who underwent valvular operations alone without the maze procedure served as control (group 3). At 3-month follow-up after operation, sinus rhythm was restored in 73%, 81%, and 11% of patients in groups 1, 2 and 3, respectively. Preoperative left and right atrial sizes were not statistically significant predictors of sinus conversion by the RF maze procedure. However, as a result of postoperative reduction of atrial sizes, postoperative left atrial diameter was significantly smaller in patients who had sinus conversion by the RF maze procedure than in patients who did not regain sinus rhythm (45.0+/-7.0 mm vs 51.0+/-8.0 mm; P = 0.03). Postoperative right atrial area of patients who had sinus conversion by the RF maze procedure also was significantly smaller than that of patients who did not regain sinus rhythm (18.1+/-4.4 cm2 vs 28.5+/-8.2 cm2; P = 0.008). CONCLUSION: Atrial size reduction appears to predict the success of sinus conversion with the RF maze procedure used in conjunction with valvular surgery.

Underutilization of anticoagulation therapy in chronic atrial fibrillation.

Atrial fibrillation, the most common chronic arrhythmia, results in an increased risk of stroke. Anticoagulation therapy can reduce this risk, but appears to be underused. The objective of this study was to examine the use of warfarin and prevalence of stroke in patients with rheumatic, nonrheumatic valvular and nonvalvular atrial fibrillation. Between January 1993 and December 1998, 457 chronic atrial fibrillation patients with continuous follow-up in our hospital were identified as having rheumatic heart disease (n = 114): nonrheumatic valvular disease (n = 65); or nonvalvular disease (n = 278). Warfarin was used less often in patients with nonrheumatic valvular (16.7%) and nonvalvular diseases (20.1%) than in those with rheumatic heart disease (81.6%, p < 0.001). In contrast, the prevalence of stroke among patients with nonvalvular disease was 40.3% which was similar to the 33.3% found in patients with rheumatic heart disease but significantly higher than the 24.6% found in patients with nonrheumatic valvular disease (p < 0.05). A history of stroke did not alter the trend of use of warfarin among the three groups of patients. Only 20.6% of patients on warfarin received monthly monitoring of prothrombin time. In conclusion, the anticoagulation therapy in our patients with chronic atrial fibrillation, regardless of their associated valvular diseases, is significantly underutilized. This underuse could account for a high prevalence of stroke. This risk of stroke, however, is less in patients with nonrheumatic valvular discase than in those with nonvalvular atrial fibrillation.

Unexpected loss of bipolar pacing with implanted dual chamber pacemakers.

Bipolar leads are most commonly used in the current practice of pacemaker therapy. In our study of 124 patients implanted with Guidant/Cardiac Pacemakers (CPI) Vigor dual chamber pacemakers, 5 patients had unexpectedly abrupt increases in bipolar lead impedance and pacing threshold 2 weeks to 18 months postimplantation without changes in sensing function. With the lead configuration reprogrammed to unipolar, the lead impedance and pacing threshold were restored to appropriate ranges. The changes in bipolar lead parameters can be caused by the CPI's "Quick Connect" (QC1) header lead system incorporated in these pacemakers.

Mycotic aneurysm leading to iliac arteriovenous fistula diagnosed by vascular duplex color scan.

Arteriovenous fistula between common iliac vessels is uncommon. Most of the reported cases are secondary to lumbar disc surgery. Mycotic aneurysm of iliac vessels caused by bacterial infection is even rarer. We describe the case of a 63 year old man with dyspnea, abdominal pain, bipedal edema, chills and fever. He had a right common iliac AVF as a result of a ruptured salmonella mycotic aneurysm, and the diagnosis was made by vascular duplex color scan.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity.

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

Role of vasopressin in cardiovascular and blood pressure regulation.

At low concentrations and in physiologic states vasopressin is a potent antidiuretic hormone. Its cardiovascular effects have been more complex and their role in circulatory adjustments to hypovolemia and hypotension difficult to define with precision. Although recognized as a powerful vasoconstrictor, its pressor effect in intact animals, even at high concentrations, is minimal. The reasons for this blunted pressor response have been explored. This report is a review of previously published work from our laboratories which highlights the direct and indirect vasodilator actions of this hormone in animals and humans. The indirect vasodilator effect is caused by inhibition of sympathetic efferents, and facilitation of the baroreflex through a central action of the hormone and its sensitization of arterial baroreceptors as well as cardiac afferents.