The role of brain acetylcholine in cardiovascular regulation and hypertension: A minireview and therapeutic implications

Brezenoff, Henry E.; Coram, Willie Mae

doi:10.1002/ddr.430020305

Cited by 8 publications

(3 citation statements)

References 55 publications

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“…If the catecholaminergic-acetylcholinergic imbalance hypothesis of bipolar disorder, postulating that mania is characterized by overactivity of catecholaminergic (noradrenergic, dopaminergic) systems and depression is related to the overactivity of the acetylcholinergic system [ 21 ] is right and our assumption about the common nature of bipolar disorder and essential hypertension is correct, acetylcholine also should play a role in the regulation of blood pressure. Although this is true but the direction of the effect is the opposite to that which we would expect from our hypothesis: cholinergic manipulations like direct cholinomimetic agents as well as cholinesterase inhibitors increase blood pressure while the muscarinic antagonist scopolamine (an effective antidepressant) decreases blood pressure [ 26 - 28 ].…”

Section: Similarities and Differences Between Essential Hmentioning

confidence: 68%

Is Mania the Hypertension of the Mood? Discussion of A Hypothesis

Rihmer

Gonda²,

Döme³

2017

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Beyond both being biphasic/bidirectional disorders (hypo)mania and essential hypertension share a surprising number of similarities and an overlap between their genetics, biological background, underlying personality and temperamental factors, precipitating factors, comorbidity and response to treatment, indicating a possibly partially shared biological background. Based on theoretical knowledge, similarities related to characteristics, manifestation and course, and the results of pharmacological studies related to the effects and side effects of pharmacotherapies used in the treatment of these two distinct disorders, the authors outline a hypothesis discussing the similar origins of these two phenomena and thus mania being the hypertension of mood in memory of Athanasios Koukopoulos, one of the greatest researchers and theoreticists of mania of all time.

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Section: Similarities and Differences Between Essential Hmentioning

confidence: 68%

Is Mania the Hypertension of the Mood? Discussion of A Hypothesis

Rihmer

Gonda²,

Döme³

2017

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“…It has been shown in animal experiments that central muscarinic receptor stimulation plays an important role in cardiovascular regulation (1)(2)(3)(4)(5) . Intracerebral administration of muscarinic agonists into the posterior hypothalamic nucleus or medulla has been shown to increase arterial blood pressure, circulating catecholamine concentrations, and sympathetic neural outflow in rats.…”

Section: Introductionmentioning

confidence: 99%

Low-Dose Atropine Attenuates Muscle Sympathetic Nerve Activity in Healthy Humans.

et al. 2000

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and Ken-ichi KOBAYASHI Central muscarinic receptors play an important role in the regulation of cardiac vagal nerve activity. We studied the inhibition of central muscarinic receptors and sympathetic nerve function in humans, since very little information is currently available on this subject. We examined the effects of graded doses of atropine (five doses, range 0.001 to 0.016 mg/kg) on heart rate, arterial pressure, heart rate variability, and muscle sympathetic nerve activity in 13 healthy young volunteers. Atropine caused biphasic effects on heart rate and the high-frequency (HF) power of R-R interval variability. At lower doses (0.002 mg/kg for heart rate, 0.001 mg/kg for HF power), atropine decreased heart rate and increased HF power. In contrast, at higher doses, atropine increased heart rate and decreased HF power. Low-dose atropine significantly attenuated muscle sympathetic nerve activity, burst rate (bursts/min) by -30.5±6.0% and burst incidence (bursts/100 heart beats) by -23.8 ± 6.9% at 0.002 mg/kg. Systolic and diastolic arterial pressure did not change with atropine infusion. Low-dose atropine (0.002 mg/kg) did not significantly affect either low frequency (LF) power or LF/HF. These results suggest that central muscarinic receptors may modulate not only cardiac vagal nerve activity but also sympathetic nerve activity in the skeletal muscle vasculature.

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“…Previous reports strongly support the existence, in the rat, of a central cholinergic link in the control of peripheral blood pressure and define this system as pressor via increased central sympathetic outflow [Brezenoff and Rusin, 1974;Dirnhuber and Cullumbine, 1955;Varagic, 1955;Varagic and Krstic, 19661. A similar system appears to exist in humans [Aquilonius and Sjostrom, 1971;Nattel et al, 1979;Nutt et al, 1978;Risch et al, 19811. Activation of muscarinic mechanisms in the central nervous system (CNS) by acetylcholinesterase inhibitors or muscarinic agonists results in an acute hypertensive response in the rat and in humans [for review see Brezenoff and Coram, 1982;Brezenoff and Giuliano, 1982;Philippu, 19811. Evidence accumulated during recent years suggests that brain acetylcholine (ACh) may be involved in the development or maintenance of elevated blood pressure in the spontaneously hypertensive rat (SHR). The centrally mediated pressor response following physostigmine or carbachol administration is potentiated in this experimental model of hypertension [Hoffmann and Phillips, 1976;Hoffman et al, 1978;Kubo and Tatsumi, 19791 and the site mediating this potentiation resides in the CNS [Hoffman and Phillips, 1976;Hoffman et al, 1977;Buccafusco and Spector, 19801.…”

Section: Introductionmentioning

confidence: 99%

The antihypertensive effect of a selective central muscarinic cholinergic antagonist: N‐(4‐diethylamino‐2‐butynyl)‐succinimide

Coram¹,

Brezenoff²

1983

Drug Development Research

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Corarn, W.M., and H.E. Brezenoff:The antihypertensive effect of a selective central muscarinic cholinergic antagonist: N-(4-Diethylamino-2-butynyl)-succinimide. Drug Dev. Res. 3:503-516, 1983. N-(4-Diethylamino-2-butynyl)-succinimide (DKJQl), a cholinergic antagonist selective for muscarinic receptors in the central nervous system, has an antihypertensive effect in conscious spontaneously hypertensive rats (SHR) but not in normotensive Wistar-Kyoto (WKY) control rats. Intravenous doses over a range of 3.1 to 25.0 mglkg produced a dosedependent decrease in systolic blood pressure. This effect was still apparent 24 hr after drug administration, but blood pressure returned to predrug levels by 48 hr after injection of DKJ-21. In a dose-response study, the maximum antihypertensive response in a group receiving 25.0 mglkg was 43 & 8 mm Hg. Marked variability of the maximum response was observed in all age groups and with all doses. Decreases in blood pressure up to 75 mm Hg were obtained in individual animals. The magnitude of the antihypertensive effect is not age related since lo-, 15, 22-, and 36-week-old SHR responded to the same degree after injection of 25 mglkg DKJ-21. Smaller doses (50 pg) of DKJ-21 decreased blood pressure when administered into the lateral cerebral ventricle of SHR. Vascular responses to norepinephrine, acetylcholine, dimethylphenylpiperazinium, angiotensin I, and tyramine were not inhibited by i.v. injection of DKJ-21; however, the centrally mediated pressor response to physostigmine was reduced by 60%.

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The role of brain acetylcholine in cardiovascular regulation and hypertension: A minireview and therapeutic implications

Cited by 8 publications

References 55 publications

Is Mania the Hypertension of the Mood? Discussion of A Hypothesis

Is Mania the Hypertension of the Mood? Discussion of A Hypothesis

Low-Dose Atropine Attenuates Muscle Sympathetic Nerve Activity in Healthy Humans.

The antihypertensive effect of a selective central muscarinic cholinergic antagonist: N‐(4‐diethylamino‐2‐butynyl)‐succinimide

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