Blood Pressure Responses to Adrenal Field Stimulation as a Measure of Adrenal Catecholamine Release

Clarke, David E.; Romanyshyn, W.M.

doi:10.1111/j.1476-5381.1976.tb07638.x

Cited by 5 publications

(2 citation statements)

References 9 publications

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“…It is well established that the adrenal medulla remains functional after chemical sympathectomy with 6-OHDA (Clarke & Romanyshyn, 1976) and, morevoer, several biochemical studies have shown increased activity of the adrenal medulla in sympathectomized animals. (Mueller, Thoenen & Axelrod, 1969;Mueller, 1971).…”

Section: Introductionmentioning

confidence: 99%

Reversal of 6‐hydroxydopamine‐induced hypotension in the rat without activation of the renin‐angiotensin system.

Bennett¹,

Gardiner²

1978

The Journal of Physiology

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1. Male Wistar rats were housed individually in glass metabolic cages for 5 days during which time their food and water intakes reached plateau levels and they developed a significant systolic arterial hypertension. 2. After the initial 5-day period, systolic blood pressure and water and electrolyte balances were measured for 4 days before and 7 days after I.P. injection of 6-hydroxydopamine (100 mg/kg). In a separate experiment, plasma renin activity and glomerular filtration rate were measured 1 and 3 days after injection of 6-hydroxydopamine. Haematocrit, plasma volume, osmolality and plasma concentrations of glucose, sodium, potassium and protein were also measured at intervals after treatment. 3. Systolic blood pressure fell within 24 hr after treatment with 6-hydroxydopamine but was restored to pretreatment levels within 7 days. There was also a transient fall in glomerular filtration rate. 4. Plasma volume was significantly expanded on the first day after treatment and there was a fall in haemotocrit together with changes in plasma constituents indicative of a haemodilution, although plasma glucose levels were elevated. 5. There was a significant water retention on the third, fourth and fifth days after treatment but this was not accompanied by any measurable sodium retention and could not be attributed to renal compensation. Furthermore, plasma renin activity showed no significant change following 6-hydroxydopamine treatment. 6. It is suggested that the return of systolic blood pressure to pre-treatment levels was chiefly due to the return of vasoconstrictor function. The changes in plasma composition and volume were probably due to a fall in capillary hydrostatic pressure and an increase in the osmolality of extracellular fluid due to the elevated glucose levels.

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Section: Introductionmentioning

confidence: 99%

Reversal of 6‐hydroxydopamine‐induced hypotension in the rat without activation of the renin‐angiotensin system.

Bennett¹,

Gardiner²

1978

The Journal of Physiology

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show abstract

“…Therefore, similar experiments were performed in a group of 6-hydroxydopamine (6-OHDA)-treated animals in order to determine whether adrenal medullary NE release could be modulated by the carotid sinus and cardiopulmonary reflexes. 6-Hydroxydopamine has been shown to destroy adrenergic nerve terminals effectively without destroying adrenal medullary catecholamine-containing cells or other nerves (Thoren and Tranzer, 1968;Prentice and Wood, 1975;Clark and Romanyshyn, 1976).…”

Section: Treatment With 6-hydroxydopaminementioning

confidence: 99%

Cardiovascular reflex modulation of plasma catecholamine concentrations in the anesthetized cat.

Heesch¹,

Bishop

1982

Circulation Research

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The purpose of this study was to examine the role of carotid sinus and cardiopulmonary mechanoreceptors in the reflex control of adrenal medullary catecholamine secretion. Afferent input from carotid sinus and cardiopulmonary mechanoreceptors was decreased by carotid occlusion or cervical vagal cold block, respectively. Increases in arterial pressure were significantly greater when either intervention was tested in the presence of the other, with the role of the carotid sinus baroreflex being dominant. Neither carotid occlusion nor vagal cold block resulted in a significant increase in plasma epinephrine or norepinephrine concentrations. However, carotid occlusion during vagal block caused a significant increase in plasma epinephrine (+87%) and norepinephrine concentrations (+128%). Likewise, vagal block during carotid occlusion increased plasma epinephrine (+82%) and norepinephrine concentrations (+73%). Similar experiments performed in a group of chemically sympathectomized animals (pre-treated with 50 mg/kg 6-hydroxydopamine) indicted that adrenal medullary norepinephrine as well as epinephrine release could be modulated by the carotid sinus and cardiopulmonary reflexes. Mean arterial blood pressure and heart rate were significantly lower in 6-hydroxydopamine-treated animals, compared with untreated controls. Although of lesser magnitude, responses to carotid occlusion and vagal block in 6-hydroxydopamine-treated animals were qualitatively similar to those in untreated animals. Plasma catecholamine concentrations did not increase from either manipulation. However, when the second manipulation was added to the first, significant increases occurred. We conclude from these data that both the carotid sinus and cardiopulmonary reflexes modulate the release of adrenal catecholamines. An interaction between the two reflexes exists whereby the influence of one reflex on catecholamine secretion is apparent only in the absence of the other input.

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Digitalis cardiotoxicity revisited

Lathers¹,

Roberts²

1980

Life Sciences

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Blood Pressure Responses to Adrenal Field Stimulation as a Measure of Adrenal Catecholamine Release

Cited by 5 publications

References 9 publications

Reversal of 6‐hydroxydopamine‐induced hypotension in the rat without activation of the renin‐angiotensin system.

Reversal of 6‐hydroxydopamine‐induced hypotension in the rat without activation of the renin‐angiotensin system.

Cardiovascular reflex modulation of plasma catecholamine concentrations in the anesthetized cat.

Digitalis cardiotoxicity revisited

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