Recruitment of the Sympathetic Nervous System in the Hypertension of Pheochromocytoma

Prokocimer, Philippe; Rosenbaum, J.; Viokery, R. G.; Hoffman, B B; Haze, M.

doi:10.1097/00000542-198609001-00407

Cited by 3 publications

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“…3,6,9 -11 Although external comparisons between data obtained in a limited number of subjects (often demographically unmatched) should be made with caution, this further supports the conclusion of a central sympathoinhibitory state in this form of secondary hypertension. It also may account, however, for the depressor and vasodilatating responses that have been reported in pheochromocytoma after the administration of a centrally acting agent such as clonidine, 2,20,21 which, despite the sympathoinhibitory state, may further inhibit residual sympathetic nerve traffic in patients with pheochromocytoma. Second, MSNA provides a sensitive and reproducible measure of central sympathetic outflow 8 that is restricted, however, to the skeletal muscle district.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic Nerve Traffic Responses to Surgical Removal of Pheochromocytoma

1999

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Abstract-Pheochromocytoma is usually characterized by a marked increase in peripheral catecholamine secretion.Whether this is accompanied by an alteration in central sympathetic drive has not been clarified. In 6 patients with adrenal pheochromocytoma (meanϮSEM age, 49.3Ϯ7.2 years), we measured systolic and diastolic blood pressure (photoplethysmographic device), heart rate (ECG), venous plasma catecholamines (high-performance liquid chromatography), and postganglionic muscle sympathetic nerve activity (microneurography) before and 78.3Ϯ13 days after surgical removal of the tumor. In each experimental session, measurements were performed during (1) a 60-minute resting period to compare several values of sympathetic nerve traffic at similar blood pressures before and after surgery and (2) voluntary end-expiratory apnea, ie, a maneuver inducing sympathetic activation. Tumor removal significantly (PϽ0.05 at least) reduced plasma catecholamines, blood pressure, and heart rate. In contrast, muscle sympathetic nerve activity was significantly (PϽ0.01) increased, both when quantified as bursts per minute (from 28.1Ϯ5.7 to 54.3Ϯ7.5) and as bursts per 100 heartbeats (from 33.4Ϯ5.6 to 65.1Ϯ6.5). This was also the case when data were evaluated in periods of 2 experimental sessions characterized by similar diastolic blood pressure values. The apnea maneuver induced sympathetic nerve traffic responses that were significantly (PϽ0.05) greater after surgery than before surgery. These data provide the first direct evidence that in pheochromocytoma central sympathetic outflow is markedly reduced and that this reduction cannot be ascribed to a reflex inhibitory response to elevated blood pressures. It is likely that this sympathoinhibition is rather due to a central depression of sympathetic outflow induced by high circulating catecholamines. (Hypertension. 1999;34:461-465.)Key Words: nervous system, sympathetic Ⅲ catecholamines Ⅲ nervous system, autonomic T he contribution of sympathetic nerve activity to blood pressure (BP) levels in pheochromocytoma is controversial. This is because it has been widely assumed that in this condition the BP elevation and the high level of circulating catecholamines should lead to a depression of sympathetic outflow by reflex mechanisms and direct stimulation of central adrenergic receptors, respectively. It has been reported, however, that in rats harboring a pheochromocytoma, pithing is accompanied by a clear-cut BP reduction, 1 pointing toward a sizable neural contribution to the BP elevation characterizing this condition. Furthermore, evidence has been produced that central sympathoinhibition by clonidine causes a similar BP reduction in patients with pheochromocytoma and with essential hypertension, 2 suggesting a similar degree of tonic sympathetic activity in both conditions.We have previously shown that muscle sympathetic nerve traffic as quantified by microneurography is much greater in patients with essential hypertension than in patients with a pheochromocytoma. 3 In the present study ...

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Section: Discussionmentioning

confidence: 99%

Sympathetic Nerve Traffic Responses to Surgical Removal of Pheochromocytoma

1999

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“…It is noteworthy that the fall in blood pressure occurred in the presence of very high circulating concentrations of norepinephrine suggesting the possibility that captopril enhances the action of a vasodilating factor. Alternatively, as we have previously found that sympathetic nervous system plays an important role in the maintenance of hypertension in rats harboring pheochromocytoma, 6 it may be that effects of captopril on the autonomic nervous system are of importance in lowering blood pressure in these rats. These possibilities will require further experimental testing.…”

Section: Discussionmentioning

confidence: 88%

“…3 ' 5 We found that the sympathetic nervous system plays an important role in the maintenance of hypertension in NEDH rats harboring pheochromocytoma. 6 Those studies were stimulated by observations in patients with pheochromocytoma that demonstrated that the centrally acting antihypertensive drug clonidine lowered blood pressure in these individuals without changing the circulating concentrations of plasma catecholamines.…”

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confidence: 99%

Captopril improves hypertension and cardiomyopathy in rats with pheochromocytoma.

Billingham

Tuck

et al. 1990

Hypertension

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Hypertension and cardiomyopathy are prominent findings in humans and rats harboring pheochromocytomas, tumors that can secrete enormous quantities of catecholamines. We have previously found that a-and /J-adrenergic receptor antagonists may ameliorate the hypertension and cardiomyopathy found in New England Deaconess Hospital rats implanted with pheochromocytoma. The present studies were designed to determine the possible action of the angiotensin converting enzyme inhibitor captopril on these changes in rats harboring pheochromocytomas. Rats were implanted with transplantable pheochromocytomas and treated with captopril dissolved in the drinking water (1 mg/ml) for 4 -6 weeks. Systolic blood pressure was monitored by using the tail-cuff technique. In the rats with pheochromocytoma, blood pressure progressively increased to 184±3 mm Hg after the tumor was implanted. However, in rats with pheochromocytoma treated with captopril in the drinking water before the development of hypertension, blood pressure did not increase (137±3 mm Hg). In rats with pheochromocytoma with established hypertension, captopril normalized the systolic blood pressure. Plasma norepinephrine was markedly elevated to a similar extent in both groups compared with unimplanted control rats. Plasma renin activities were slightly lower in rats with pheochromocytoma compared with unimplanted control rats. Treatment with captopril of rats with pheochromocytoma did not modify contraction of isolated rings of thoracic aorta exposed in vitro to either phenylephrine or angiotensin H, Treatment with captopril markedly attenuated the cardiomyopathy induced by pheochromocytoma. These results demonstrate that captopril prevents the development of hypertension despite markedly elevated concentrations of catecholamines. In addition, captopril attenuates catecholamine-induced cardiomyopathy in pheochromocytoma. To what extent these effects of captopril reflect actions on local renin-angiotensin systems or other mechanisms requires further study. (Hypertension 1990;15:210-215) P heochromocytoma is a rare but dramatic cause of human hypertension. 1 These tumors typically secrete large quantities of norepinephrine. Hypertension in patients with pheochromocytoma may be severe; also, many patients with this tumor have been found to have a cardiomyopathy that is highly suggestive of lesions induced by cateFrom the

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“…Fourth , Tsujimoto and coworkers7 reported that elimination of sympathetic nerve activity by pithing caused a greater reduction of blood pressure in pheochromocytoma‐bearing rats than in age‐matched, unimplanted rats. Additionally, Prokocimer and coworkers found that both clonidine and chlorisondamine, a ganglion blocker, markedly decreased blood pressure in intact rats with pheochromocytoma 8. However, the observation that the blood pressure in pithed pheochromocytoma rats is further reduced by phentolamine, an alpha‐adrenergic antagonist, suggests that high concentrations of circulating catecholamines are also involved in the maintenance of elevated blood pressure.…”

Section: Pathophysiologymentioning

confidence: 99%

Pheochromocytoma

Bravo

2002

Annals of the New York Academy of Sciences

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Pheochromocytoma and paragangliomas are rare tumors of chromaffin tissue that secrete catecholamines either intermittently or continuously, producing hypertension with a constellation of symptoms and signs that can be frightening to the patient and that continue to provide perplexing problems for clinicians. With surgical treatment, symptoms will be relieved and hypertension normalized or ameliorated for patients who do not have malignant tumors. Appropriate antihypertensive drugs are used to manage hypertension, to control associated cardiovascular symptoms, and to prepare patients for operation. The question debated most often regarding medical therapy of pheochromocytoma is whether antihypertensive treatment regimens other than nonspecific alpha-blockade are just as effective and safe. Understanding the pathophysiologic mechanisms that sustain the hypertension and the pharmacology of antihypertensive agents allows better selection of antihypertensive therapy.

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Recruitment of the Sympathetic Nervous System in the Hypertension of Pheochromocytoma

Cited by 3 publications

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Sympathetic Nerve Traffic Responses to Surgical Removal of Pheochromocytoma

Sympathetic Nerve Traffic Responses to Surgical Removal of Pheochromocytoma

Captopril improves hypertension and cardiomyopathy in rats with pheochromocytoma.

Pheochromocytoma

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