Central Effects of Dopamine and Bromocriptine on Vasopressin Release and Blood Pressure

Kimura, Tokihisa; Share, Leonard; Wang, Bin C.; Crofton, J. T.

doi:10.1159/000123259

Cited by 25 publications

(7 citation statements)

References 15 publications

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“…The potential for cocaine to enhance dopaminergic neurotransmission also did not seem to explain the central sympathoexcitatory action of the drug. This is because dopamine and other dopaminergic agonists such as bromocriptine decrease blood pressure upon central administration (Kimura et al, 1981;Park et al, 1991;Tangri et al, 1993). Moreover, the results of the present studies were not consistent with a major role for dopamine receptors in mediating the pressor action of cocaine.…”

Section: Discussioncontrasting

confidence: 65%

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

Buccafusco¹,

Davis²,

Shuster³

et al. 2004

J Pharmacol Exp Ther

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After intracisternal injection, 140 nmol (48 g) of cocaine (but not lidocaine or procaine) evoked an increase in mean arterial pressure (MAP) of 41 mm Hg. The increase in MAP began within 1 min after injection and lasted 10 to 15 min. The pressor response to intracisternal injection of cocaine was not mediated through central ␣-adrenergic receptors, but intracisternal pretreatment with D1 or D2 dopamine receptor antagonists shortened the duration of the response. Pretreatment with intracisternal injection of hemicholinium-3 to deplete medullary acetylcholine produced a dose-dependent inhibition of the pressor and tachycardic responses to intracisternal injection of cocaine. Central pretreatment with hemicholinium-3 also inhibited the pressor response to intravenous injection of 0.5 mg/kg cocaine. Atropine pretreatment was only partly effective in blocking the pressor and tachycardic responses to intracisternal injection of cocaine. However, a single intracisternal injection of the nicotinic ganglionic receptor blocker hexamethonium inhibited the pressor response to cocaine administered intracisternally 24 h later, and on each of the following 4 days. The blocking effect of hexamethonium was not mimicked by the ␣7 selective antagonist methyllycaconitine or by the ␣4␤2 subtype-preferring antagonist dihydro-␤-erythroidine. The data suggest that the pressor response to cocaine is mediated by medullary acetylcholine release on to nicotinic receptors of the ganglionic type, enhancing the output of bulbospinal sympathetic premotor neurons. Our results provide new evidence for the prolonged inactivation of relevant central nicotinic receptors by nicotinic receptor antagonists, and suggest that such compounds might be used safely for cocaine overdose, as well as for antiabuse issues without the concern for autonomic side effects.The ability of cocaine to increase systemic blood pressure usually is considered to be commensurate with drug's pharmacological classification as an indirect-acting sympathomimetic amine. Whereas cocaine conforms to this classification both in the peripheral and central nervous systems, the role of the CNS in terms of blood pressure alterations has been debated (Knuepfer et al., 1993;Gillis et al., 1995;Bernards, 1996). In fact, agonists at central ␣ 2 -adrenergic receptors such as clonidine and ␣-methyldopa are effective antihypertensive drugs; and levodopa and other dopaminergic antiParkinson agents often produce orthostatic hypotension as a side effect. Also, systemic administration of cocaine has been reported to decrease sympathetic nervous activity (Knuepfer and Branch, 1992;Gillis et al., 1995;Abrahams et al., 1996). Yet, there have been instances when cocaine has been administered directly into the CNS, usually via the cerebrospinal fluid, that the drug elicits an increase in arterial blood pressure. However, based upon the requirement for relatively high doses to elicit a pressor response via the lateral ventricular route (Knuepfer et al., 1993), it is unlikely that forebrain str...

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Section: Discussioncontrasting

confidence: 65%

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

Buccafusco¹,

Davis²,

Shuster³

et al. 2004

J Pharmacol Exp Ther

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“…Thus, the extent of AVP reduction during /3-adrenergic blockade closely correlated with the initial level of plasma AVP. Since /3-blockers increase plasma dopamine levels and dopamine inhibits AVP release, 52 this might be an alternative explanation of reduced AVP during /3-adrenergic blockade. This alternative is not the most likely, however, since dopamine was equally stimulated by the two /3-blockers while only oxprenolol significantly reduced the plasma AVP concentration.…”

Section: Discussionmentioning

confidence: 99%

Increased plasma vasopressin in low renin essential hypertension.

Os¹,

Kjeldsen²,

Skjøtø³

et al. 1986

Hypertension

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SUMMARY Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 ± 2.2 [SE] vs 7.5 ± 1.0 pg/ml; p < 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 ± 0.04 vs 0.46 ± 0.06 Goldblatt units X 10 4 /ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 ± 12 vs 68 ± 6 pg/ml; p < 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 ± 0.8 vs 3.5 ± 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective /3-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 ±6.4 to 13.5 ±4.2 pg/ml (p < 0.01). After 6 weeks of treatment with the /3,-selective agent atenolol in another 11 men with low renin hypertension, plasma vasopressin level fell from 16.3 ± 3.3 to 13.1 ±3.1 pg/ml, but this reduction was not significant. In pooled groups treated with /3-adrenergic blockade, plasma vasopressin level decreased more the higher its initial concentrations (r= 0.79, p< 0.001, n = 22). These findings suggest that plasma vasopressin is increased in low renin essential hypertension and may be related to sympathetic adrenal overactivity. (Hypertension 8: 506-513, 1986) KEY WORDS • blood pressure • catecholamines • sodium • osmolality • /3-adrenergic blockade • pituitary • antidiuretic hormone A RGININE vasopressin (AVP) may increase /\ blood pressure primarily by volume reten-A. \. tion, but it is also a powerful vasoconstrictive agent, even more potent than angiotensin.1 It may also participate in cardiovascular regulation, both centrally 2 and peripherally, 3 and stimulate the gain of baroreceptor reflexes. 4 Potentiation of the vasoconstrictor effect of catecholamines has been established. with mineralocorticoid excess. 6 -9 "" Deoxycorticosterone-salt hypertension will not develop in the Brattleboro rat, which lacks AVP because of a genetic defect. Blockade by either specific antiserum or competitive antagonists of AVP substantially attenuates both the development and severity of preexisting deoxycorticosterone-salt hypertension. Most recently, observations by Hay wood et al.12 point to the sy...

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“…Conflicting results have been obtained; different investigators have variously reported inhibition, 10 ' l2 stimulation, 9 -"• * both, 37 ' 38 or neither. 39 These discrepancies undoubtedly result from differences in animal species and experimental design.…”

Section: Discussionmentioning

confidence: 99%

Role of dopamine in the inhibition of vasopressin secretion by L-dopa in carbidopa-treated dogs.

Reid¹,

Chou²,

Chang³

et al. 1986

Hypertension

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SUMMARY Elevation of brain catecholamine levels by systemic administration of L-dopa in dogs pretreated with the dopa decarboxylase inhibitor carbidopa inhibits the secretion of vasopressin and adrenocorticotropic hormone (ACTH) and decreases arterial blood pressure. The aim of the present study was to determine 1) whether the inhibition of vasopressin secretion is mediated by dopamine or norepinephrine, both of which have been implicated in the control of vasopressin secretion, and 2) whether the decrease in vasopressin secretion contributes to the suppression of ACTH secretion and fall in blood pressure produced by L-dopa. This was accomplished by comparing the effects of dopamine and a-adrenergic receptor antagonists on vasopressin, ACTH, and blood pressure responses to L-dopa. The effect of a specific antagonist of the vasoconstrictor action of vasopressin also was studied. Injection of L-dopa (20 mg/kg i.v.) in dogs pretreated with carbidopa (20 mg/kg i.v.) caused reductions in plasma vasopressin concentration (from 16.0 ± 4.8 to 3.8 ± 0.9 pg/ml; p<0.05), plasma ACTH concentration (from 96.0 ± 20.4 to 49.2 ± 10.0 pg/ml; p<0.05), and mean arterial pressure (from 121 ± 6 to 78 ± 5 mm Hg; p<0.05). Pretreatment with pimozide (1 mg/kg i.p.) completely blocked the inhibition of vasopressin secretion by L-dopa but failed to block the suppression of ACTH secretion (57.6 ± 11.8 to 34.0 ± 5.1 pg/ml; p<0.05) or the decrease in mean arterial pressure (126 ± 5 to 93 ± 7 mm Hg; p<0.05). The antihypertensive effect of L-dopa was reduced by prazosin (97 ± 3 to 82 ± 6 mm Hg; p<0.05) and blocked by yohimbine, but neither drug blocked the suppression of plasma vasopressin or ACTH. Administration of a vasopressin antagonist did not decrease arterial pressure and caused only a small, delayed reduction in plasma ACTH concentration. These studies provide evidence that the inhibition of vasopressin secretion by L-dopa is mediated by dopamine rather than by norepinephrine. The failure of a vasopressin antagonist to significantly decrease blood pressure or ACTH secretion and the dissociation of the effects of L-dopa on vasopressin release, blood pressure, and ACTH secretion argue against a major role for vasopressin in the blood pressure and ACTH responses to L-dopa. Received December 13, 1985; accepted April 15, 1986. variety of stimuli. 3 4 In addition, the release of vasopressin can be altered by central administration of catecholamines, other adrenergic agonists, and adrenergic blocking drugs.5 " 9 Although there is general agreement that central catecholamines are involved in the control of vasopressin release, there is still controversy concerning the nature of this control. Many investigators have concluded that brain catecholamines act to inhibit vasopressin release, 6 ' '• 10~15 while others have presented evidence for a stimulatory effect. 8 ' l6~18 In addition, the relative importance of dopamine and norepinephrine is not clear.In a previous investigation in this laboratory, we reported that intravenous administratio...

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Central Effects of Dopamine and Bromocriptine on Vasopressin Release and Blood Pressure

Cited by 25 publications

References 15 publications

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

Increased plasma vasopressin in low renin essential hypertension.

Role of dopamine in the inhibition of vasopressin secretion by L-dopa in carbidopa-treated dogs.

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