(Hypertension. 1995;25:266-271.)
© 1995 American Heart Association, Inc.
Articles |
Blood Pressure Response to the Valsalva Maneuver in Pheochromocytoma and Pseudopheochromocytoma
From the Second Department of Internal Medicine, Ehime (Japan) University School of Medicine (M.H., Y.S., K.H.), and the Hypertension Center, Kinki Central Hospital (Itami), Hyogo, Japan (M.M., Y.K., T.K.).
Correspondence to Mareomi Hamada, MD, The Second Department of Internal Medicine, Ehime University School of Medicine, Shigenobu, Onsen-gun, Ehime 791-02, Japan.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract To elucidate whether a difference in blood pressure reactivity exists between patients with pheochromocytoma (n=8) and pseudopheochromocytoma (n=22), we evaluated blood pressure changes during a Valsalva maneuver and baroreceptor reflex sensitivity. We also examined the effects of propranolol and prazosin on blood pressure reactivity during a Valsalva maneuver in patients with pseudopheochromocytoma. Pseudopheochromocytoma was defined as a paroxysmal rise in blood pressure accompanying pheochromocytoma-like symptoms and normal catecholamine values. The difference in systolic blood pressure between phase IV of the Valsalva maneuver and baseline (
SBP) was markedly smaller in the pheochromocytoma patients
(8.4±18.4 mm Hg) than in the essential hypertension patients (n=30,
30.9±19.4 mm Hg) and normotensive control subjects (n=10, 31.3±11.4
mm Hg), whereas SBP in the pseudopheochromocytoma patients
(77.8±11.2 mm Hg) was markedly greater than in the other three
groups. SBP was markedly suppressed by the administration of both
propranolol and prazosin. Baroreceptor reflex sensitivity index was
lower in the pheochromocytoma group than in the other three groups. In
conclusion, blood pressure reactivity responses to a Valsalva maneuver
are disparate between pheochromocytoma and pseudopheochromocytoma. The
high blood pressure reactivity to a Valsalva maneuver in
pseudopheochromocytoma is due to hyperactivity in both ß- and
1-adrenergic receptor functions, and the low blood
pressure reactivity to a Valsalva maneuver in pheochromocytoma seems to
be mainly due to the desensitization of both adrenergic systems
associated with chronic catecholamine excess. In addition, the impaired
baroreceptor function in pheochromocytoma is partially responsible for
it.
Key Words: pheochromocytoma • Valsalva's maneuver • hypertension, paroxysmal • prazosin • propranolol
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Pheochromocytoma is a rare but important cause of clinical hypertension because when unrecognized it is potentially lethal.1 In addition, pheochromocytoma is one of the most often suspected but least frequently confirmed causes of secondary hypertension. On the other hand, many patients have symptoms and signs suggestive of pheochromocytoma but have a different condition called pseudopheochromocytoma.2 Awareness of the existence of pseudopheochromocytoma may help physicians in choosing effective medication and preventing unnecessary surgical exploration in patients strongly suspected of harboring a pheochromocytoma.3 The clinical similarity of the sudden rise of blood pressure in pheochromocytoma and pseudopheochromocytoma creates a diagnostic dilemma. The diagnosis of pheochromocytoma is based on biochemical evidence of excessive release of catecholamines, but a minority of patients with pheochromocytoma have normal plasma catecholamine levels under resting conditions,4 and high plasma levels of catecholamines can be observed in many clinical conditions.5 6
Many patients with pseudopheochromocytoma are responsive to treatment with ß-adrenergic blocking drugs,3 but usually these patients are not responsive to them. This finding suggests that the procedures that stimulate the ß-adrenergic receptor can differentiate pseudopheochromocytoma from pheochromocytoma. During a Valsalva maneuver, a rapid and marked change of blood pressure occurs, and this change is markedly modified by the use of ß-adrenergic blocking drugs.7
In this study, we compared blood pressure reactivity during a Valsalva
maneuver between patients with pseudopheochromocytoma and
pheochromocytoma. The effects of ß- and 1-adrenergic
blocking drugs on the blood pressure response to a Valsalva maneuver
were also studied.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Subjects
Thirty patients were referred to our hospital because of symptoms and signs suggesting pheochromocytoma. Of the 30 patients, 22 did not have pheochromocytoma, based on diagnostic testing, including assays of catecholamines in plasma and urine and computed tomographic scans. Other secondary forms of hypertension were also eliminated. The remaining 8 patients (6 men and 2 women) had histologically proved pheochromocytoma. Clinical findings in 22 patients who had symptoms and signs suggesting pheochromocytoma but were determined to have pseudopheochromocytoma2 are shown in Table 1. Common findings in this group were a repetition of paroxysmal rise in blood pressure accompanying palpitation, chest pain, headache, faintness, sweating, nausea, or vomiting, and a normal range of plasma catecholamine values. Hypertension, defined as systolic blood pressure (SBP) greater than 160 mm Hg and/or diastolic blood pressure (DBP) greater than 95 mm Hg in the outpatient clinic,8 was observed in 8 patients (36%). A family history of hypertension was observed in 7 patients (32%).
|
Table 2 profiles 8 patients with pheochromocytoma. One patient (patient 7) had almost normal baseline catecholamine levels but showed a positive glucagon test. Another patient (patient 5) had a family history of pheochromocytoma.
|
Thirty patients (21 men and 9 women) with essential hypertension who had no such symptoms and signs as observed in patients with pseudopheochromocytoma served as controls. The mean age of this group was 47±10 years. Mean SBP and DBP values in this group were 174±20 and 103±16 mm Hg, respectively. Ten normotensive volunteers (8 men and 2 women) who had no history of hypertension and no abnormalities on physical examinations, electrocardiogram, chest x-ray film, or echocardiogram also served as controls. The mean age of this group was 48±6 years.
Of 8 patients with pheochromocytoma, 1 patient had received 20 mg/d nifedipine; 1 had received a combination of 25 mg/d captopril, 1.5 mg/d prazosin, and 20 mg/d nifedipine; 1 had received 10 mg/d carteolol; and 1 had received 25 mg/d captopril. The other 4 patients had received no medical treatment. The hemodynamic testing for the former 4 patients was carried out when patients were asymptomatic after medication had been discontinued for at least 1 week. Hemodynamic testing in patients with pseudopheochromocytoma and essential hypertension who had received medical therapy was carried out after medication had been discontinued for at least 1 week.
All subjects participated in this study after giving informed consent.
Blood Pressure Measurement and Valsalva Maneuver
Blood pressure during a Valsalva maneuver was measured directly
with a catheter introduced percutaneously into the left brachial
artery. The Valsalva maneuver was begun after subjects had rested 15
minutes after insertion of the catheter. Blood pressure was not
significantly different before and after catheter insertion. The
subject was told how to perform the Valsalva maneuver and then asked to
perform the maneuver at the end of an inspiratory effort. The
effectiveness of the procedure was assessed by noting whether the
subject developed a florid face, distended neck veins, and increased
abdominal muscle wall tone. After 10 seconds, the subject was
instructed to relax the abdomen and resume normal quiet breathing.
After the first study, 20 patients with pseudopheochromocytoma, 26
patients with essential hypertension, and 10 normotensive control
subjects rested for at least 15 minutes or until heart rate and blood
pressure had returned to control levels. Thereafter, propranolol (0.1
mg/kg body wt IV) was administered over 5 minutes, and the subject was
allowed to rest for 10 minutes. Then, an identical Valsalva maneuver
was performed. After the first study, 1 mg prazosin was administered
orally to 2 patients with pseudopheochromocytoma and 4 patients with
essential hypertension. The patients were allowed to rest for 60
minutes, after which an identical study was performed.
From the blood pressure response to a Valsalva maneuver, two indexes
were measured as shown in Fig 1. One was change in SBP
(SBP), which was calculated as the difference between peak SBP at
phase IV and SBP at control level. The other was "recovery time,"
defined as the interval from the point of peak SBP to the point at
which SBP returned to control levels.
|
Measurement of Baroreceptor Reflex Sensitivity Index
Baroreceptor reflex sensitivity index was calculated from phase
IV of the Valsalva maneuver as reported by Palmero et al.9
A first Valsalva maneuver was recorded at a lower paper speed to
evaluate the hemodynamic response, and a second one was recorded at 50
mm/s to determine the change of the RR interval of the
electrocardiogram and SBP. Each SBP measurement was plotted against the
RR interval following it. The linear relation between SBP and RR
interval was calculated where the regression coefficient corresponded
to the index of baroreceptor sensitivity.
Measurement of Plasma Norepinephrine and Epinephrine
Blood samples for measurement of plasma norepinephrine and
epinephrine levels were drawn through an indwelling plastic catheter
inserted into the left brachial artery. Plasma norepinephrine and
epinephrine were measured using high-speed ion-exchange column
chromatography.10
Measurement of Hemodynamic Parameters
Echocardiographic studies were carried out using an SSD-870
echocardiograph with a 3.5-MHz transducer (ALOKA, Tokyo, Japan). M-mode
echocardiographic recordings were made while the cardiac anatomy was
visualized by two-dimensional echocardiography. Electrocardiogram,
phonocardiogram, carotid pulse tracing, and M-mode echocardiogram were
simultaneously recorded at a paper speed of 100 mm/s. Mean velocity of
circumferential shortening (mVCF), ejection fraction (EF), stroke
volume (SV), cardiac output (CO), and preejection period (PEP) were
calculated from the following formulas: mVCF=Dd-Ds/DdxLVET, where Dd,
Ds, and LVET are left ventricular end-diastolic and
end-systolic dimensions and left ventricular ejection time,
respectively; EF=EDV-ESV/EDV, where EDV and ESV are
end-diastolic and end-systolic volumes measured by
Teichholz's method; SV=EDV-ESV; CO=SVxHR, where HR is heart rate;
and PEP=Q-II-LVET, where Q-II is electromechanical systole. SV and CO
were corrected by body surface area (stroke index and cardiac index,
respectively).
Statistical Analysis
Values in the text and tables are mean±SD. Statistical
evaluation was performed by ANOVA, and subsequent comparisons between
group mean values were performed using Duncan's multiple range test. A
value of P<.05 was considered significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Fig 2 shows the representative patterns of Valsalva reactions in a normotensive control subject, an essential hypertension patient, a pseudopheochromocytoma patient, and a pheochromocytoma patient. A marked elevation of blood pressure in overshoot phase was observed in the pseudopheochromocytoma patient, and no significant overshoot was observed in the pheochromocytoma patient. Fig 3 shows
SBP in normotensive control subjects and
essential hypertension, pseudopheochromocytoma, and pheochromocytoma
patients. SBP in pseudopheochromocytoma patients was significantly
greater than in normotensive control subjects and essential
hypertension patients, but SBP in pheochromocytoma patients was
significantly smaller than in normotensive control subjects and
essential hypertension patients. There was no overlap in SBP between
patients with pheochromocytoma and pseudopheochromocytoma. Of the
pheochromocytoma patients, only one patient, whose norepinephrine level
was normal and epinephrine level was slightly high at baseline, showed
a normal blood pressure response to the Valsalva maneuver. A marked
reduction in overshoot in pheochromocytoma patients returned to normal
in approximately 1 month after the operation. SBP in all
pseudopheochromocytoma patients was greater than 50 mm Hg. On the
other hand, SBP of greater than 50 mm Hg was observed in only 5 of
30 (17%) essential hypertension patients.
|
|
Recovery time was significantly longer in pseudopheochromocytoma patients (85±38 milliseconds) than in normotensive control subjects (20±12 milliseconds) and essential hypertension patients (22±23 milliseconds) but was markedly shorter in pheochromocytoma patients (8±15 milliseconds) than in the other three groups.
Plasma norepinephrine and epinephrine levels under basal conditions were 156±65 and 61±43 pg/mL, respectively, in pseudopheochromocytoma patients, 155±58 and 64±40 pg/mL in essential hypertension patients, and 165±46 and 59±27 pg/mL in normotensive control subjects. There were no significant differences in plasma norepinephrine and epinephrine levels among pseudopheochromocytoma and essential hypertension patients and normotensive control subjects. Both catecholamine levels during the attack episode in pseudopheochromocytoma patients were higher than at rest, but both remained within normal limits as shown in Table 1.
Baroreceptor reflex sensitivity index showed no significant differences among pseudopheochromocytoma and essential hypertension patients and normotensive control subjects, as shown in Fig 4. However, baroreceptor reflex sensitivity index was significantly lower in pheochromocytoma patients than in the other three groups.
|
Data of hemodynamic parameters in normotensive control subjects and essential hypertension and pseudopheochromocytoma patients are shown in Table 3. Preejection period in essential hypertension patients was longer than in normotensive control subjects and pseudopheochromocytoma patients, but other hemodynamic parameters showed no significant differences among the three groups. Pseudopheochromocytoma patients did not show the hyperdynamic contraction.
|
Effects of propranolol on SBP and baroreceptor reflex sensitivity
index were examined. Both SBP and DBP were unchanged after the
administration of propranolol. As shown in Fig 5, SBP
decreased in all subjects. Baroreceptor reflex sensitivity index showed
no significant change before and after the administration of
propranolol in pseudopheochromocytoma and essential hypertension
patients and normotensive control subjects (Fig 4). After the
administration of prazosin, SBP decreased from 153.0±11.0 to
135.5±8.5 mm Hg, and DBP decreased from 91.3±6.3 to 82.7±7.1
mm Hg. As shown in Fig 6, SBP was markedly
suppressed by the oral administration of prazosin. SBP in patients
21 and 22 with pseudopheochromocytoma was changed from 96 to 26 mm Hg
and from 90 to 18 mm Hg, respectively. Mean SBP in four essential
hypertension patients was also decreased from 32.2±5.4 to 14.4±2.6
mm Hg by the oral administration of prazosin.
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Our results indicate that blood pressure reactivity responses to a Valsalva maneuver are disparate between patients with pheochromocytoma and pseudopheochromocytoma. Blood pressure response in phase IV to the Valsalva maneuver in pseudopheochromocytoma patients was greater, and inversely that in pheochromocytoma patients was smaller than that in normotensive control subjects and essential hypertension patients. The exaggerated blood pressure response in pseudopheochromocytoma patients was attenuated by the administration of both propranolol and prazosin. This increased blood pressure response in pseudopheochromocytoma patients is not related to basal plasma catecholamine levels, cardiac function and performance, or baroreceptor reflex sensitivity. On the other hand, the decreased blood pressure response in pheochromocytoma patients may be partially related to impaired baroreceptor function.
Clinical profiles of the pseudopheochromocytoma patients in this study are similar to those in patients reported by Kuchel et al2 3 and Takabatake et al11 and are different from those in patients with a hyperdynamic ß-adrenergic circulating state12 13 or hyperkinetic type of borderline hypertension14 15 in several ways. First, a characteristic in our patients is the paroxysmal elevation of blood pressure accompanied by various symptoms imitating pheochromocytoma. This paroxysmal hypertension is not observed in patients with a hyperdynamic ß-adrenergic circulating state or hyperkinetic type of borderline hypertension. Second, the age of pseudopheochromocytoma patients is widely distributed, as shown in the present study, but patients who are in a hyperdynamic ß-adrenergic state are usually young. Third, cardiac function and performance in our pseudopheochromocytoma patients and patients reported by Takabatake et al11 were normal, but in patients showing a hyperdynamic ß-adrenergic state or hyperkinesis of the left ventricle, cardiac function and performance are in a high-output state. Incidentally, hemodynamic characteristics in pheochromocytoma patients include a marked shortening of electromechanical systole and left ventricular ejection time and normal preejection period. Low cardiac index, low stroke index, and high total peripheral resistance index are also characteristics in pheochromocytoma.16 Fourth, the blood pressure response to a Valsalva maneuver in our patients was markedly exaggerated but was within normal limits in patients reported by Frohlich et al.13 Thus, there is a marked difference in pathophysiological condition between patients with pseudopheochromocytoma and patients with a hyperdynamic state, although ß-adrenergic blocking drugs are effective in both types of patients.
It is known that ß-adrenergic blocking drugs influence hemodynamic
responses to a Valsalva maneuver such as the attenuation of the
increase in blood pressure during the overshoot7 and the
prevention of Valsalva-induced ventricular arrhythmia in patients with
long QT syndrome.17 The decrease in myocardial
contractility and heart rate caused by the administration of
ß-adrenergic blocking drugs seems to be closely related to the
decrease in stroke volume and cardiac output, resulting in a decrease
in blood pressure overshoot. It is also known that SBP during a
Valsalva maneuver is markedly influenced by the condition of the heart.
The height of SBP overshoot is also related to the left ventricular
ejection fraction, and the overshoot is not observed in patients with
heart failure.18 As shown in Table 3, however, there were
no differences in left ventricular ejection fraction, stroke index,
cardiac index, and basal catecholamine levels among
pseudopheochromocytoma and essential hypertension patients and
normotensive control subjects. The difference in overshoot among the
three groups seems to be mainly caused by the difference in
ß-adrenergic receptor function in each group. Thus, the exaggerated
blood pressure response to a Valsalva maneuver in
pseudopheochromocytoma patients seems to be mainly caused by the
hyperactivity of the ß-adrenergic receptor–mediated system.
Furthermore, this is the reason why ß-adrenergic blocking drugs are
effective in the treatment of pseudopheochromocytoma patients.
Previously, we reported that 1-adrenergic receptor
function was closely related to the blood pressure response to
isometric handgrip exercise and that the increased
1-adrenergic receptor function was mainly responsible
for the exaggerated blood pressure response to handgrip exercise in
essential hypertension patients.19 In the present
study, we showed that blood pressure change during phase IV of a
Valsalva maneuver was also related to 1-adrenergic
receptor function. Blood pressure overshoot in phase IV was markedly
suppressed in both pseudopheochromocytoma and essential hypertension
patients. This finding indicates that sufficient vascular tone mediated
by 1-adrenergic receptors was necessary to maintain
blood pressure during phase IV of the Valsalva maneuver. However,
further examination must be done to determine whether the augmented
1-adrenergic receptor function itself is one of the
responsible factors for the exaggerated blood pressure response during
phase IV in pseudopheochromocytoma patients.
On the other hand, blood pressure response during phase IV of the Valsalva maneuver is markedly suppressed in pheochromocytoma patients. Decreased baroreceptor reflex sensitivity index in pheochromocytoma patients seems to be one of the reasons for the suppression of blood pressure elevation in response to a Valsalva maneuver. In addition, it is acknowledged that desensitization of adrenergic functions is observed in pheochromocytoma patients.20 This is another reason why the lack of overshoot in blood pressure during a Valsalva maneuver is observed in pheochromocytoma patients. Only one of the pheochromocytoma patients whose norepinephrine level was normal showed a normal blood pressure response. In addition, an abnormal blood pressure response during the Valsalva maneuver returned to normal in more than 1 month after the resection of the pheochromocytoma. These findings support the fact that the abnormal blood pressure response to a Valsalva maneuver is closely related to malfunctions of adrenergic receptor–mediated systems associated with chronic catecholamine excess from pheochromocytoma, such as the homogeneous and heterogeneous desensitizations of the adrenergic receptor system.
In the present study, we showed that there was a marked difference
in the mechanism for the appearance of symptoms or signs of
pseudopheochromocytoma and pheochromocytoma. Symptoms or signs in the
former are due to the hyperactivity in both ß- and
1-adrenergic receptor functions, and those in the latter
may be due to the desensitization of the ß- and
1-adrenergic systems associated with chronic
catecholamine excess. Thus, ß- or 1-adrenergic
blocking drugs are helpful in relieving symptoms in
pseudopheochromocytoma patients. On the other hand, the use of
ß-adrenergic blocking drugs alone in pheochromocytoma patients is
dangerous because of the stimulation of the -adrenergic
receptor–mediated system. The Valsalva maneuver is easy to perform;
therefore, it may be useful in assessing the effect of treatment with
ß-blocking drugs of pseudopheochromocytoma patients.
Received November 8, 1993; first decision December 14, 1993; accepted October 17, 1994.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Kaplan NM. Pheochromocytoma (with a preface about incidental adrenal masses). In: Clinical Hypertension. Baltimore, Md: Williams & Wilkins; 1990:350-367.
2.
Kuchel O. Pseudopheochromocytoma.
Hypertension. 1985;7:151-158.
3.
Kuchel O, Buu NT, Hamet P, Larochelle P, Bourque M, Genet J.
Essential hypertension with low conjugated catecholamines imitates
pheochromocytoma. Hypertension. 1981;3:347-355.
4.
Grossman E, Goldstein DS, Hoffman A, Keiser HR.
Glucagon and clonidine testing in the diagnosis of pheochromocytoma.
Hypertension. 1991;17:733-741.
5. Kopin IJ, Lake RC, Ziegler M. Plasma levels of norepinephrine. Ann Intern Med. 1978;88:671-680.
6. Plouin PF, Duclos JM, Menard J, Comoy E, Bohuon C, Alexandre JM. Biochemical tests for diagnosis of pheochromocytoma: urinary versus plasma determinations. Br Med J. 1981;282:853-854.
7. Frohlich ED, Dunn FG, Messerli FH. Pharmacologic and physiologic considerations of adrenoceptor blockade. Am J Med. 1983:75:9-14.
8. Report of a WHO Expert Committee. Arterial hypertension. WHO Tech Rep Ser. 1978;628:9.
9. Palmero HA, Caeiro TF, Iosa DJ, Bas J. Baroreceptor reflex sensitivity index derived from phase 4 of the Valsalva maneuver. Hypertension. 1981;3(suppl II):II-134-II-137.
10. Ueda E, Yoshida N, Nishimura K, Joh T, Antoku S, Tsukada K, Ganno S, Kokubu T. A semi-automated measurement of urinary catecholamines using high-speed ion-exchange column chromatography. Clin Chim Acta. 1977;80:447-453. [Medline] [Order article via Infotrieve]
11. Takabatake T, Yamamoto Y, Ohta H, Nakamura S, Hara H, Ishida Y, Hashimoto N, Hattori N. Blood pressure variability and hemodynamic response to stress in patients with paroxysmal elevation of blood pressure. Clin Exp Hypertens A. 1985;7:235-242. [Medline] [Order article via Infotrieve]
12.
Frohlich ED, Dustan HP, Page IH. Hyperdynamic beta-adrenergic
circulatory state. Arch Intern Med. 1966;117:614-619.
13.
Frohlich ED, Tarazi RC, Dustan HP. Hyperdynamic ß-adrenergic
circulatory state: increased ß-receptor responsiveness. Arch
Intern Med. 1969;123:1-7.
14.
Julius S, Pascual AV, London R. Role of parasympathetic
inhibition in the hyperkinetic type of borderline hypertension.
Circulation. 1971;44:413-418.
15. Gillum RF, Teichholz LE, Herman MV, Gorlin R. The idiopathic hyperkinetic heart syndrome: clinical course and long-term prognosis. Am Heart J. 1981;102:728-734. [Medline] [Order article via Infotrieve]
16. Hamada M, Ito T, Hiwada K, Kokubu T, Genda A, Takeda R. Characteristics of systolic time intervals in patients with pheochromocytoma. Jpn Circ J. 1991;55:417-426. [Medline] [Order article via Infotrieve]
17.
Mitsutake A, Takeshita A, Kuroiwa A, Nakamura M. Usefulness of
the Valsalva maneuver in management of the long QT syndrome.
Circulation. 1981;63:1029-1035.
18.
Zema MJ, Restivo B, Sos T, Sniderman KW, Kline S. Left
ventricular dysfunction-bedside Valsalva manoeuvre. Br Heart
J. 1980;44:560-569.
19. Hamada M, Kazatani Y, Shigematsu Y, Ito T, Kokubu T, Ishise S. Enhanced blood pressure response to isometric handgrip exercise in patients with essential hypertension: effects of propranolol and prazosin. J Hypertens. 1987;5:305-309. [Medline] [Order article via Infotrieve]
20.
Valet P, Damase-Michel C, Chamontin B, Durand D, Chollet F,
Montastruc JL. Platelet 2- and leucocyte ß2-adrenoceptors in
phaeochromocytoma: effect of tumour removal. Eur J Clin
Invest. 1988;18:481-485.[Medline]
[Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  T. Ketch, I. Biaggioni, R. Robertson, and D. Robertson Four Faces of Baroreflex Failure: Hypertensive Crisis, Volatile Hypertension, Orthostatic Tachycardia, and Malignant Vagotonia Circulation, May 28, 2002; 105(21): 2518 - 2523. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ohtsuka, M. Hamada, G. Hiasa, O. Sasaki, M. Suzuki, Y. Hara, Y. Shigematsu, and K. Hiwada Effect of beta-blockers on circulating levels of inflammatory and anti-inflammatory cytokines in patients with dilated cardiomyopathy J. Am. Coll. Cardiol., February 1, 2001; 37(2): 412 - 417. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Mann Severe Paroxysmal Hypertension (Pseudopheochromocytoma): Understanding the Cause and Treatment Arch Intern Med, April 12, 1999; 159(7): 670 - 674. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. P. Holschneider, O. U. Scremin, K. P. Roos, D. R. Chialvo, K. Chen, and J. C. Shih Increased baroreceptor response in mice deficient in monoamine oxidase A and B Am J Physiol Heart Circ Physiol, March 1, 2002; 282(3): H964 - H972. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||